| 1. |
- Blix, Arnoldus S, et al.
(författare)
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Cardiac receptors in ducks--a link between vasoconstriction and bradycardia during diving.
- 1976
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 97:1, s. 13-9
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Tidskriftsartikel (refereegranskat)abstract
- It has been demonstrated that cardiac receptors, most likely of the left ventricular type, are present also in the duck's heart. These receptors and their reflex responses (i.e. bradycardia and hypotension) could be blocked by intrapericardial administration of lidocaine. Initially, usch receptor blockade did not affect efferent vagal control of heart rate, as revealed by undiminished bradycardia in response to a standardized vagal stimulation. After cardiac receptor blockade, however, the duck's normal bradycardia response to head immersion was greatly reduced. The cardiovascular response to submersion was now instead characterized by a marked rise in arterial pressure, with superimposed bouts of intensified bradycardia and pressure reduction, evidently induced reflexly from the arterial baroreceptors. Meanwhile, the bradycardia response to standarized efferent vagal stimulation was still the same as before intrapericardial lidocaine injection. These results suggest that the marked rise in cardiac filling pressure following the intense shemo-receptor-induced constriction of both resistance and capacitance vessels, activates ventricular stretch receptors signalling in vagal afferents. Apparently, the activation of these receptors contributes crucially to the bradycardia and reduction of cardial output, which balance off the greatly increased peripheral resistance in the diving duck.
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| 2. |
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| 3. |
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| 4. |
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| 5. |
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| 6. |
- Lisander, Björn, 1940, et al.
(författare)
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Baroreceptor-induced decrease in muscle blood flow upon propranolol administration.
- 1978
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Ingår i: European journal of pharmacology. - 0014-2999. ; 50:3, s. 275-8
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Tidskriftsartikel (refereegranskat)abstract
- The acute effects of propranolol, 1 mg/kg i.v., were studied in chloralosed, vagotomized cats. The vascularly isolated but innervated calf muscles were perfused from another animal. In one group of experiments, the carotid baroreceptors were exposed to ambient arterial pressure. Here, propranolol caused a fall in heart rate and an increase in resistance of the isolated muscle bed. In other experiments, the carotid sinuses were perfused at a constant pressure. In these animals, no increase in muscle flow resistance was observed after the drug. It is concluded that the increase in total peripheral resistance, seen initially upon propranolol administration, may be reflexly induced via the baroreceptors.
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| 7. |
- Little, R, et al.
(författare)
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Aspects of the central integration of arterial baroreceptor and cardiac ventricular receptor reflexes in the cat.
- 1975
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Ingår i: Acta physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 93:1, s. 85-96
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Tidskriftsartikel (refereegranskat)abstract
- The possible central integrative mechanisms, responsible for the earlier reported, differentiated reflex engagement of the renal and muscle vessels and the heart from cardiac ventricular receptors and arterial baroreceptors, respectively, were analyzed in atropinized cats. The reflux renal vessel, muscle vessel and heart rate responses, expressed as per cent of maximum, to graded activations of arterial baroreceptors (sinus pressure variations) and stimulations of ventricular receptor afferents in the cardiac nerve were systematically compared. Cardiac nerve stimulation with low frequencies was found to elicit more pronounced reflex renal vessel responses than muscle vessel and heart rate responses. In contrast, elevations of sinus pressure induced equally pronounced renal and muscle vessel responses. High frequency cardiac nerve stimulation elicited maximal reflex renal vessel responses, but only submaximal effects on muscle vessels and heart rate, while intense baroreceptor stimulation induced maximal reflex effector responses throughout. The submaximal heart rate response to cardiac nerve stimulation is probably due to a simultaneous activation of excitatory afferents. On the other hand, the less pronounced muscle than renal vessel responses when the cardiac nerve was stimulated probably reflect a relatively sparse innervation of muscle vasomotor neurons by ventricular receptor afferents, which seem instead to be preferentially oriented towards renal vasomotor and, possibly, cardiac motor neurons.
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| 8. |
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| 9. |
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| 10. |
- Wennergren, Göran, 1947, et al.
(författare)
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Cardiac receptors activated during the hypothalamic defence reaction.
- 1977
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 101:2, s. 241-6
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Tidskriftsartikel (refereegranskat)abstract
- The increases of arterial blood pressure, cardiac inotropy and venous return seen during the hypothalamic defence reaction are likely to lead to concomitant excitation of left ventricular receptors with nonmedullated afferents. The integrated efferent pattern of response resulting from the central interaction between the defence reaction and influences from the mentioned cardiac receptors was recently analyzed. These two, essentially opposing influences on the circulation were then seen to interact in such a way as to produce an optimal cardiovascular response with respect to increases in cardiac output and blood supply to the skeletal muscles. However, direct electrophysiological recordings from nonmedullated cardiac efferents during defence area stimulation have hitherto been lacking. The present experiments, performed on chloralose-anesthetized cats and utilizing electrophysiological recordings, clearly demonstrate that the left ventricular receptors are activated by the cardiovascular readjustments induced by the defence reaction. Defence area stimulation increased the activity of these receptors, which work within a very narrow, low frequency range, from 1.1 +/- 0.3 imp/s to 2.7 +/- 0.7 imp/s associated with rises in systolic blood pressure (afterload) and heart rate. Normally such a receptor activation would induce considerable bradycardia and sympathetic inhibition, but particularly the reflex bradycardia is centrally supressed by a concomitant defence area activation. The marked bradycardia often seen immediately upon interruption of the defence area stimulation is, however, probably to a great extent initiated from the excited ventricular receptors.
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| 11. |
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| 12. |
- Wennergren, Göran, 1947, et al.
(författare)
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Interaction between the hypothalamic defence reaction and cardiac ventricular receptor reflexes.
- 1976
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Ingår i: Acta physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 96:4, s. 532-47
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Tidskriftsartikel (refereegranskat)abstract
- The interference with regard to the cardiovascular and gastric motility responses which follows stimulation of the hypothalamic defence area (D.A.) and a simultaneous afferent input from cardiac ventricular receptors was analysed in chloralose-anesthetized cats. In spinalized animals with only the vagal efferent innervation of autonomic effectors from supraspinal structures intact, a D.A. stimulation increased the heart rate to the same level irrespective whether the cardiac receptor afferents were stimulated or not. This suggests that the vagal component of the reflex bradycardia of cardiac receptor origin was completely suppressed by the D.A. stimulation. The reflex gastric relaxation to cardiac receptor activation, mediated via vagal efferent non-adrenergic fibres, was similarly completely blocked by D.A. stimulation. In contrast, the reflex inhibition of the sympathetic outflow to the heart and vessels from cardiac receptors was still effective during a D.A. stimulation, a phenomenon which seems compatible with a simple summation of excitatory D.A. and inhibitory cardiac receptor influences on the sympathetic neurons. The modifying influence from ventricular receptors on D.A. responses closely resembles that exerted by the arterial baroreceptors. The two reflex mechanisms thus work in concert and synergistically with the hypothalamic influences to produce maximal cardiac output and skeletal muscle perfusion without undue increases of pressure load on the pump during a defence reaction.
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| 13. |
- Wennergren, Göran, 1947, et al.
(författare)
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Studies on the central integration of excitatory chemoreceptor influences and inhibitory baroreceptor and cardiac receptor influences.
- 1976
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 96:1, s. 1-18
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Tidskriftsartikel (refereegranskat)abstract
- Experiments were performed on cats to explore the integrated cardiovascular responses when excitatory (chemoreceptor) and inhibitory (baroreceptor or cardiac receptor) influences are simultaneously presented to the medullary cardiovascular areas. At a given sinus pressure in the low or medium pressure range, the systemic blood pressure and the vascular resistance were higher when the chemoreceptors were stimulated, while a high, pulsating sinus pressure, i.e.a strong baroreceptor stimulation, could suppress completely even an intense chemoreceptor activation. Thus, the set point and the gain of the baroreflex were increased by a concomitant chemoreceptor activation. These effects are compatible with a simple, mutual 'summation' of excitatory and inhibitory influences on a common population of central vasomotor neurons. The reflex vasodilator effects elicited via vagal cardiac afferents were found to be more effectively suppressed by a concomitant chemoreceptor stimulation than were the baroreceptor effects, provided a primary chemoreceptor response (bradycardia) was at hand, while the heart rate responses were essentially uninfluenced by the prevailing chemoreceptor activity. This chemoreceptor suppression of the reflex vasodilatation from cardiac receptors, which may be of great importance in hypoxic situations, e.g. during a dive, suggests a more complex, neuronal interaction between the two reflex mechanisms in the CNS.
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| 14. |
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| 15. |
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| 16. |
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| 17. |
- Johansson, B, et al.
(författare)
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Effects of Tris on vascular smooth muscle
- 1979
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Ingår i: American Journal of Physiology - Heart and Circulatory Physiology. - 1522-1539. ; 237:3, s. 409-411
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Tidskriftsartikel (refereegranskat)
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| 18. |
- Johansson, B, et al.
(författare)
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Responses of smooth muscle to quick load change studied at high time resolution
- 1978
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Ingår i: Blood Vessels. - 0303-6847. ; 15:1-3, s. 65-82
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Tidskriftsartikel (refereegranskat)abstract
- Quick-release and quick-stretch experiments have been performed on preparations of smooth muscle from rat portal vein and rabbit urinary bladder. The low equivalent mass of the isotonic lever (8 mg) implied that inertial oscillations were limited to the first 5-10 msec after the load step. The high time resolution achieved in this way enabled us to separate three components in the length response to a step change in force: (1) an immediate passive elastic recoil, (2) an isotonic velocity transient lasting 50-75 msec and (3) shortening of the contractile element after its full adjustment to the new load. The maximal series elastic recoil was about 10% of the total muscle length in portal vein but only some 3% in urinary bladder. Stiffness of series elasticity increased in proportion to force and was about 3 times higher in bladder than in portal vein at any force level. Force-velocity relations for loads less than Po could be fitted to Hill's equation; Vmax in 4 AC-stimulated portal veins was 0.53 +/- 0.03 muscle lengths/sec and in 8 K+-activated bladder preparations 0.18 +/- 0.01 muscle lengths/sec. Application of loads greater than Po produced rates of lengthening greater than expected from an extrapolation of Hill's hyperbola. The nature of the transient component is discussed in the light of recent studies of force and velocity transients in skeletal muscle.
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| 19. |
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| 20. |
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| 21. |
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| 22. |
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| 23. |
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| 25. |
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| 26. |
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| 27. |
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| 28. |
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| 29. |
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| 30. |
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| 31. |
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| 32. |
- Gerdin, Bengt, 1947-, et al.
(författare)
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Deposition and clearance of fibrin in the rat lung following acute haemorrhage.
- 1979
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Ingår i: Circulatory shock. - 0092-6213. ; 6:4, s. 357-64
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Tidskriftsartikel (refereegranskat)abstract
- The effect of acute haemorrhage on the deposition and clearance of fibrin in the rat lung after thrombin-induced intravascular coagulation was investigated. Haemorrhage was followed by less embolization of fibrin to the lungs and delayed elimination from the lungs. As lung tissue fibrinolysis was not diminished, the peripheral and pulmonary circulatory disturbance was probably in itself responsible for the observed effects.
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| 33. |
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| 34. |
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| 35. |
- Hellstrand, Per, et al.
(författare)
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Analysis of the length response to a force step in smooth muscle from rabbit urinary bladder
- 1979
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 106:2, s. 221-238
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Tidskriftsartikel (refereegranskat)abstract
- Responses to isotonic quick release of AC-stimulated smooth muscle strips from rabbit urinary bladder were analysed. Releases were performed at the peak of contraction and at a preset tension level in the contraction and relaxation phase. In other expts. responses at 37 degrees C and 27 degrees C were compared. The length response always consisted of 3 parts: (1) elastic recoil, (2) rapid length change (isotonic transient), (3) steady length change. Qualitatively, phases (1)-(3) could be distinguished also in responses to isotonic quick stretch. The immediate elastic recoils, phase (1), were described by exponential stress-strain relations. Stiffness was found to be somewhat lower during relaxation than during contraction. No effect of temperature on the elastic recoil was seen. The initial velocity in phase (2) was 2-3 times greater than the velocity 100 ms after release. By means of computer analysis of the length records during phases (2) and (3) two decaying exponential processes with widely different time constants could be separated. The time constant of the faster process was of the order of 15-30 ms at 37 degrees C. It decreased with increasing force steps and with increasing temperature. The amount of shortening associated with this process was correlated with the size of the force step, reaching a maximum of about 1.2% of the muscle length. The shortening velocities in phase (3), measured 100 ms after release, were described by Hill's equation. Vmax in the rising part and at the peak of contraction were 0.7 and 0.6 L/s respectively at 37 degrees C. Lower values were found during relaxation and at 27 degrees C. We suggest that part of the elastic recoil in phase (1) occurs in structures associated with the individual cross-bridges, that phase (2) is dominated by a change in the distribution of conformations of bridges in the attached position and that the shortening rate in phase (3) is determined by the entire cycle of events during turnover of bridges after the muscle has adapted to the new load. Observations on the force response to length steps and on shifts from isometric to afterloaded isotonic contraction and vice versa are consistent with this interpretation.
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| 36. |
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| 37. |
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| 38. |
- Hellstrand, Per, et al.
(författare)
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Mechanical, electrical, and biochemical effects of hypoxia and substrate removal on spontaneously active vascular smooth muscle
- 1977
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 100:1, s. 69-83
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Tidskriftsartikel (refereegranskat)abstract
- Effects of hypoxia and glucose-free solution on the isolated rat portal vein were studied. Decrease of extracellular PO2 below 50 mm Hg caused graded inhibition of spontaneous mechanical activity; below 7 mm Hg, inhibition was complete in most preparations. Contracture force of depolarized portal vein was less sensitive to decreases in PO2. Responses to noradrenaline at all concentrations were markedly depressed at extreme hypoxia. Sucrose-gap experiments showed that hypoxia reduced the spontaneous electrical spike discharge. Mean tissue contents of PCr, ATP and glycogen (expressed as glucose) were 3.02, 2.47 and 5.07 micromol/g cell wt. in spontaneously active control muscles and 1.07, 1.65 and 1.83 after 20 min anoxia. Physiological variations in PO2 may influence myogenic activity of vascular smooth muscle largely through an action at the membrane level and this mechanism may participate in local blood flow control. Caculations indicated that the graded response to hypoxia in the present in vitro experiments was not due to diffusion limitation. Spontaneous mechanical activity was relatively well maintained even after prolonged exposure to glucose-free solution, whereas the responses to K+ and noradrenaline were markedly suppressed. Electrophysiological recordings during spontaneous activity indicated desynchronization and impaired conduction. PCr and ATP were maintained at control levels and glycogen reduced by 50 per cent after 2 h in glucose-free medium. Indications of the use of amino acids (glutamate) as substrate under these conditions were obtained.
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| 39. |
- Hellstrand, Per
(författare)
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Oxygen consumption and lactate production of the rat portal vein in relation to its contractile activity
- 1977
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 100:1, s. 91-106
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Tidskriftsartikel (refereegranskat)abstract
- Energy turnover in the isolated rat portal vein was investigated by measurement of oxygen consumption (JO2) and lactate production (JLA) under simultaneous recording of mechanical activity. In spontaneous activity under aerobic conditions and at optimal muscle length JO2 and JLA were 0.55 and 0.62 micromol/min X g, respectively, corresponding to an ATP-production of 4.3 micromol/min X G. When muscle length was changed, an approximately linear relation was found between energy turnover and mean isometric tension. The tension-indpendent part of ATP-production was 3.0 micromol/min X g. In Ca2+-free solution the metabolic rate was 20% lower still. JO2 was nearly equal in isometric contractions and in afterloaded isotonic contractions from the same initial muscle length. During a maximal tonic contracture in 5+-depolarized portal vein JO2 increased to about twice that in spontaneous activity. Changes in contracture force by variations in muscle length or in [Ca2+]0 were associated with identical linear relations between JO2 and active tension. This relation was less steep than the corresponding relation for spontaneous activity. The anaerobic lactate production of the portal vein was 2.7 times theaerobic leve. The accelerated glycolysis did not compensate for eliminated oxidative metabolism. Under substrate-free aerobic conditions no lactate was produced by the muscle and compared to the control situation JO2 declined more than could be accounted for by reduced mechanical activity alone. The metabolic turnover rate in relation to isometric tension is high in the rat portal vein compared to that of tonic vascular smooth muscle from larger vessels. This correlates with differences in dyanmic mechanical properties. At comaparable tension levels in the portal vein, the rate of cross-bridge turnover may be higher in spontaneous phasic activity than in sustained contracture.
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| 40. |
- Hellstrand, Per, et al.
(författare)
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The force-velocity relation in phasic contractions of venous smooth muscle
- 1975
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 93:2, s. 157-166
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Tidskriftsartikel (refereegranskat)abstract
- The force-velocity relation of the rat portal vein has been studied during regular spontaneous contractions induced by elevated levels of [K-+]O AND [Ca-2+]o. No satisfactory description of the force-velocity relation was obtained by measuring shortening velocity in afterloaded isotonic contractions. Therefore the method of isotonic quick release was used, as this permits mechanical studies at specified instants of the contraction-relaxation cycle. The temporal development of the force-velocity relation in the phasic response was investigated. During a time interval in the rising phase of the contraction, at about the time for maximal dP/dt, the force-velicity curves were practically identical, suggesting a plateau in the intensity of active state. At later stages of the twitch the curves were progressively displaced towards the origin, the intercepts on both the force and the velocity axis becoming smaller. At the time of the isometric peak the maximal shortening velocity had declined relatively more than the isometric force. This is presumably caused by inhomogeneous activation of the muscle at the beginning of relaxation, The maximal force-velocity relation in the rising phase of the contraction can be described by Hill's (1938) equation with the following parameters (at 37 degrees tc): a/Po = 0.73 plus or minus 0.04, b = 0.54 plus or minus 0.04 lengths/s, Vmax = 0.74 plus or minus 0.02 lengths/s (n = 7, mean plus or minus S.E,). The force-velocity relation of the portal vein in comparison with other kinds of muscle is discussed.
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| 41. |
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| 42. |
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| 43. |
- Johansson, B, et al.
(författare)
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Isometric and isotonic relaxation in venous smooth muscle
- 1975
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 93:2, s. 167-174
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Tidskriftsartikel (refereegranskat)abstract
- The time course of relaxation under isometric and isotonic conditions was studied in preparations of rat portal vein which maintained regular phasic contractions in solutions with increased [K-+] and [Ca-2+]. It was found that the smooth muscle during isotonic lengthening was able to carry the afterload for a period of time which was longer than expected from the control isometric response. The difference was largest for afterloads corresponding to about half the isometric peak force. The terminal decline in force was identical in afterloaded and purely isometric responses. Inhibitory influences of isotonic shortening causing increased rates of relaxation, as reported for striated muscles, were not observed. The differences in the course of relaxation between isotonic and isometric responses of portal vein could not be attributed to variations in membrane excitation. It also appears that the differences are not due to changes in release or uptake of activator calcium, or to presence of viscous elements in the tissue. It is suggested that the ability of the smooth muscle to carry load over a relatively long period during isotonic relaxation may be attributed to the characteristics of the instantaneous force-velocity relations in the force range above Po.
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| 44. |
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| 45. |
- Jonsson, Olof, 1941, et al.
(författare)
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The distribution of sodium in aortic walls from spontaneously hypertensive and normotensive rats.
- 1975
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 93:4, s. 548-52
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Tidskriftsartikel (refereegranskat)abstract
- The contents of exchangeable sodium, bound sodium and total water and the extracellular space of thoracic aortas from normotensive and spontaneously hypertensive rats were measured. The aortas from the hypertensive rats contained more sodium than those from the normotensive animals while the total water content and extracellular space in the two groups were the same. The capacity to bind sodium in an osmotically inactive form was greater in the aortas from the hypertensives than in those from the normotensives. The difference in binding capacity was of the same order of magnitude as the difference in sodium content, indicating that the excess sodium in the thoracic aortas from the hypertensive rats was osmotically inactive and thus unable to cause water logging.
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| 46. |
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| 47. |
- Lisander, Björn, 1940, et al.
(författare)
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The role of cardiac receptors in clonidine-induced vagal bradycardia.
- 1979
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Ingår i: European journal of pharmacology. - 0014-2999. ; 54:1-2, s. 109-18
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Tidskriftsartikel (refereegranskat)abstract
- In chloralosed, spinalized and beta-blocked cats, clonidine, 10 microgram/kg i.v. caused a vagally mediated bradycardia which was further analysed with particular attention to cardiopulmonary receptors. Cardiovascular deafferentiation, with preservation of vagal cardiac efferents, abolished the bradycardia. However, in animals with arterial baroreceptors denervated but with vagal cardiopulmonary pathways intact, clonidine decreased heart rate simultaneously with an increase in left atrial pressure to an extent known to activate cardiac receptors with unmyelinated vagal efferents. Clonidine somewhat enhanced the bradycardia to efferent vagal stimulation and also had a slight positive chronotropic effect on the non-innervated heart. The reflex bradycardia from electrical stimulation of unmyelinated cardiac afferents was augmented by the drug but not more than could be accounted for by the changed neuroeffector sensitivity. The data suggest that clonidine can reflexly augment vagal tone on the heart by an increased activity in vagal cardiac afferents, secondary to the drug's peripheral vasoconstrictor action, whereas no evidence for any central facilitation of these reflexes has been found.
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| 48. |
- Olsson, Kurt Å., 1940-
(författare)
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Hypothalamic and cortical control of jaw reflexes
- 1979
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The subject of the thesis is a study of the projections from low threshold oral and face afferents to the cerebral cortex and of descending motor control mechanisms originating in the cerebral cortex or the hypothalamus and influencing the jaw reflexes.Cats anaesthetized with chi oral ose were used for the experiments. Ipsi- and contralateral nerves from the oral cavity and the face were stimulated electrically. Cortical potentials were averaged and recorded. The location of the projections was related to the cytoarchi-tectonic areas of the cerebral cortex. It was found that the afferents projected to separate maximum points in areas 3a, 3b, 5a and 6aß. The projections to areas 3a and 3b were somatotopically organized, but the layout of the projections on the cortex was not facelike.The effect of monopolar anodal stimulation of the cerebral cortex on the monosynaptic jaw closing and the di synaptic jaw opening reflexes was investigated. A sequence of facilitation and inhibition of both reflexes was elicited by cortical stimulation. The effects were of short latency (2.5 ms) and could start with either facilitation or inhibition. The timecourse of the sequence was sinuslike with a period of 10 ms. The largest effect originated in the "sensory" areas 3a and 3b and not in the "motor" areas 4y and 6ag. It is suggested, that a tri gemino-cortico-tri geminai loop via area 3a may function in reflex modulation of jaw movements.The hypothalamic effects on the jaw reflexes were evoked by electrical stimulation in those parts of the hypothalamus, which are w known to generate defence, attack or feeding responses. A tenfold facilitation of the jaw closing reflex and a facilitation followed by almost complete inhibition of the jaw opening reflex were observed in the anaesthetized animal with intact cerebral cortex. The effects remained but were diminished in amplitude after cortical ablation. The descending path was located in the ventral midbrain tegmentum.It is suggested that the observed hypothalamo-tri geminai mechanism may exercise a tonic influence on the trigeminal motoneurones, thereby controlling the set points of the biting force and the rest position. The implications of this hypothesis on the etiology of bruxism and the myofascial pain-dysfunction are discussed.
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| 49. |
- Persson, A E, et al.
(författare)
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The hydraulic conductivity of the rat proximal tubular wall determined with colloidal solutions
- 1975
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Ingår i: Pflügers Archiv. - 0031-6768 .- 1432-2013. ; 360:1, s. 25-44
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Tidskriftsartikel (refereegranskat)abstract
- The hydraulic conductivity of the rat proximal tubular wall was determined using colloidal solutions perfused in short (50--200 mum) (SMP) or long (90--200 mum) (LMP) proximal tubular segments. In SMP human serum albumin (HSA) or polyvinylpyrrolidone (PVP) was added to raffinose solutions. A Lp of 0.019 nl-min-1-mm-1-mm Hg-1 was found when high colloid concentrations were used while values of 0.055--0.092 were found when low colloid concentrations were used. In other experiments, the Lp was determined by perfusing short tubular segments with pure raffinose solutions. A value of 0.015 nl-min-1-mm-1-mm Hg-1 was found. This is twice the value found when raffinose solutions were perfused through long tubular segments and it is concluded that the short microperfusion technique overestimates Lp with a factor of two. When microperfusions of long tubular segments were conducted, PVP was added to an equilibrium solution consisting of NaCl (110 mM) and raffinose (80 mM). Lp was found to be 0.018--0.021 when high colloid concentrations were used, while a value of 0.029 was found when a low colloid concentration was used. As found in both SMP and LMP a decrease in Lp's with increasing colloid concentrations indicates that a significant influence of radial concentration differences is highly probable. It is therefore suggested that the highest Lp derived when using the lowest colloid concentrations represents the best estimate. With this Lp value (0.03--0.05 nl-min-1-mm-1-mm Hg-1) and the existing transtubular hydrostatic and oncotic pressure difference it can be calculated that these passive forces might constitute the driving force for 1/3 of the fluid reabsorbed in the proximal tubule.
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| 50. |
- Rammer, L, et al.
(författare)
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Protection against the impairment of renal function after intravascular coagulation in the rat kidney by increased ingestion of sodium chloride.
- 1975
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Ingår i: Nephron. Clinical practice. - 1660-8151 .- 2235-3186. ; 14:6
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Tidskriftsartikel (refereegranskat)abstract
- Rats were kept for 4 weeks on a dietary regimen with a low or high sodium intake to increase or reduce, respectively, the renin activity of the kidneys and plasma. Fibrinolysis was inhibited by intravenous injection of AMCA and thrombin was infused into the jugular vein, giving rise to heavy intravascular fibrin deposition in the kidneys. Shortly after the thrombin infusion the glomerular filtration rate (GFR) decreased equally in saline-loaded and normal rats. 48 h after the thrombin infusion the GFR was still markedly reduced in saline-deprived and normal rats but had returned to preinfusion values in the saline-loaded rats. The results might indicate that the renin-angiotensin system is involved in the presistence of the renal functional impairment after intravascular coagulation in the rat kidney.
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