| 1. |
- Bentzer, Peter, et al.
(författare)
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Supersensitivity in rat micro-arteries after short-term denervation
- 1997
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 161:2, s. 125-133
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Tidskriftsartikel (refereegranskat)abstract
- Contractile responses to phenylephrine and high-K+ were investigated in vitro in microvascular preparations from the rat medial plantar artery, a branch from the saphenous artery, obtained after short-term denervation in vivo. Two groups of animals were studied: (1) animals undergoing surgical resection of the saphenous nerve, and (2) animals undergoing surgical resection of both the sciatic and saphenous nerves. The animals were operated on one side only. Microvascular preparations (diameter about 325 microns) were obtained 10 days after surgery. Vessels from the non-operated side served as controls. Immunocytochemistry showed a decreased number of both neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP) immunoreactive nerve fibres in vessels after resection of the saphenous nerve only. Resection of both the saphenous and the sciatic nerve caused a complete loss of immunoreactive nerve fibres. Mechanical measurements were performed using a wire myograph. In vessels subjected to resection of the saphenous nerve the sensitivity to phenylephrine was similar to controls. Vessels denervated by resection of both the saphenous and sciatic nerves showed significant increases in phenylephrine and potassium sensitivity. When depolarized in high-K+ solution the denervated vessels showed an increased sensitivity to extracellular Ca2+. The results show that complete short-term denervation of the rat medial plantar artery in vivo causes a pronounced supersensitivity in the vascular smooth muscle. The supersensitivity appears not to be restricted to the sympathetic alpha-receptors but also associated with changes in the cellular excitation-contraction coupling. Such altered reactivity of the vascular smooth muscle may contribute to vascular disturbances observed in vivo after nerve damage or surgical denervation.
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| 2. |
- Ekelund, Ulf, et al.
(författare)
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Effects of the combined ETA and ETB receptor antagonist PD145065 on arteries, arterioles, and veins in the cat hindlimb
- 1995
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Ingår i: Journal of Cardiovascular Pharmacology. - 1533-4023. ; 26:Suppl. 3, s. 211-213
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to describe in quantitative terms the effects of ETA and ETB receptor blockade on vascular tone (resistance) in large-bore arterial resistance vessels (> 25 microns), small arterioles (< 25 microns), and veins in the cat gastrocnemius muscle in vivo. In the muscle vascular bed, the combined ETA and ETB receptor antagonist PD145065 (1 mg/kg/min, intra-arterially) abolished the biphasic vascular responses (dilatation followed by constriction) to both ET-1 (0.4 microgram/kg/min, intra-arterially) and to the selective ETB receptor agonist IRL1620 (3.2 micrograms/kg/min, intra-arterially). In the cat femoral artery and vein in vitro, PD145065 competitively inhibited the contractile responses to both ET-1 and IRL1620. The contractile response to the latter agonist could be evoked only after long-term incubation of the vessels (37 degrees C for 5 days). These results indicate that PD145065 is a potent antagonist at both ETA and ETB receptors in vivo and in vitro. Therefore, this antagonist may prove useful for elucidating the possible physiologic and/or pathophysiologic roles of the endothelins. For example, it was shown that PD145065 had no effect on vascular tone in the resting state, indicating no role for the endothelins in the regulation of basal vascular tone in cat skeletal muscle.
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| 3. |
- Ekelund, A, et al.
(författare)
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Additional colloids have only a minor haemodilutive effect after surgery for aneurysmal subarachnoid haemorrhage
- 1999
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Ingår i: British Journal of Neurosurgery. - : Informa UK Limited. - 0268-8697 .- 1360-046X. ; 13:4, s. 399-404
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Tidskriftsartikel (refereegranskat)abstract
- Haemodilution is commonly used as prophylaxis, as well as treatment for cerebral ischaemia after aneurysmal subarachnoid haemorrhage (SAH). Thirty-six patients operated for aneurysmal SAH were evaluated retrospectively; 24 received haemodilutive therapy and 12 patients, as a control group, received no additional therapy. There was a 'spontaneous' drop in haematocrit by 22% in both groups, and a corresponding drop in haemoglobin by 23% in the treatment group and 19% in the non-haemodiluted group, during the first 4 days after the SAH. After the initial decrease the haematocrit remained stable between 0.28 and 0.33 until day 14 in both groups. The haemodilutive group had only a minor lower haematocrit level during days 8-12 as the additional fluid resulted in increased renal excretion. This minor difference was, however, significant (p < 0.02).
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| 4. |
- Ekelund, A, et al.
(författare)
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Transcranial cerebral oximetry related to transcranial Doppler after aneurysmal subarachnoid haemorrhage
- 1998
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Ingår i: Acta Neurochirurgica. - : Springer Science and Business Media LLC. - 0001-6268 .- 0942-0940. ; 140:10, s. 1029-1036
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Tidskriftsartikel (refereegranskat)abstract
- Noninvasive methods for detecting cerebral artery vasospasm, still a serious complication following aneurysmal subarachnoid haemorrhage, are of vital interest. Up-to-date transcranial Doppler ultrasound (TCD) has proved to be sensitive in detecting vasospasm in the middle cerebral artery, but has less accuracy for other cerebral arteries. Transcranial cerebral oximetry (TCCO) is a new non-invasive technique which may increase the reliability for detecting cerebral ischaemia. The purpose of the present study was to evaluate a putative correlation between TCCO and TCD. We examined the two hemispheres in 14 patients with the aim of evaluating a proposed correlation between TCD and TCCO. Analysis of all absolute values (maximum TCD mFV and minimum TCCO saturation, respectively) in all series indicate a correlation between TCCO and TCD, p < 0.01, r = -0.62. All patients with TCD mean flow velocity > 120 cm/s also presented TCCO saturation < 60%. Conversely, all patients with normal TCCO saturation (> or = 63%) presented normal or moderately increased TCD velocities. In clinical neurosurgical practice it is of great interest if a true correlation between TCD and TCCO exists. The present results support the assumption that TCCO may enhance the reliability for detecting cerebral ischaemia after aneurysmal subarachnoid haemorrhage.
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| 5. |
- Roijer, Anders, et al.
(författare)
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Cardiac changes in stroke patients and controls evaluated with transoesophageal echocardiography
- 1997
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Ingår i: Scandinavian Cardiovascular Journal. - : Informa UK Limited. - 1651-2006 .- 1401-7431. ; 31:6, s. 329-337
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Tidskriftsartikel (refereegranskat)abstract
- In stroke patients several cardiac changes associated with embolism can be detected with transoesophageal echocardiography. Potential major cardiac embolic sources (e.g. atrial fibrillation, thrombi of left ventricle/atrium, vegetation, myxoma, dilated cardiomyopathy) have a causal relationship to embolism. Other changes with no certain causal relationship are regarded as potential minor cardiac embolic sources (e.g. atrial septal aneurysm, patent foramen ovale, mitral annular calcification, mitral valve prolapse, protruding atheroma of the aorta). We compared the prevalences of major and minor potential cardiac embolic sources in a stroke population with that in controls. One hundred and twenty-one patients with first-ever stroke were compared with 68 randomly selected controls. All subjects underwent magnetic resonance imaging of the brain, carotid ultrasound and transthoracic/transoesophageal echocardiography. The patients were slightly older (mean age 70.7 +/- 10.3 years) than the controls (65.5 +/- 15.5 years) (p < 0.05). Potential major cardiac embolic sources were found in 27% of the patients and in 4% of the controls (p < 0.001). The most common major potential embolic source was atrial fibrillation, detected in 22/121 patients. Fifteen of these also had spontaneous echocontrast in the left atrium. Eleven left atrial thrombi were found (four of these patients had atrial fibrillation and seven had sinus rhythm). A history of heart disease was more common in patients with a potential major cardiac embolic source or a carotid artery stenosis (77%) than in those patients without (44%) (p < 0.01). After excluding subjects with a major potential cardiac embolic source and/or carotid artery stenosis, no differences in the prevalence of minor potential cardiac embolic sources were found between patients (55%) and control subjects (47%) (p = NS). Even when subjects without a major potential cardiac embolic source or a carotid artery stenosis were categorized into three age groups (35-54, 55-74 and > 74 years) the prevalence of potential minor cardiac embolic sources did not differ between patients and controls. To conclude, major potential cardiac embolic sources are more common in an older population with first-ever stroke than in a comparable control group. However, potential minor cardiac embolic sources did not differ in prevalence in the patients compared with controls. Certain changes (e.g. atrial septal aneurysm) might have a potential embolic role in younger stroke patients but in our study no difference was found between older stroke patients and controls.
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| 6. |
- Ekelund, Ulf
(författare)
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Effects of angiotensin-converting enzyme inhibition on arterial, venous and capillary functions in cat skeletal muscle in vivo
- 1996
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 158:1, s. 29-37
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to analyse quantitatively, on a cat gastrocnemius muscle preparation in vivo, the effects of local angiotensin-converting enzyme (ACE) inhibition by enalaprilat on total regional vascular resistance (tone) and its distribution to the large-bore arterial resistance vessels (> 25 microns), the small arterioles (< 25 microns) and the veins. Associated effects on capillary pressure and fluid exchange were also studied. Close-arterial infusion of enalaprilat (0.05-0.20 mg kg muscle tissue min-1) elicited a moderate dilator response in all three consecutive sections of the muscle vascular bed, an increase in capillary pressure and transcapillary fluid filtration. This dilation could be abolished by the selective bradykinin B2-receptor antagonist Hoe 140 (2 mg kg-1 min-1, i.a.), indicating that the dilator mechanism of ACE inhibition was an increased local concentration of bradykinin, and hardly at all a decreased concentration of angiotensin (AT) II. The generalized dilator response to ACE inhibition along the vascular bed suggested a relatively uniform distribution of ACE from artery to vein and this was further supported by the finding that a close-arterial infusion of AT I (0.04-0.32 microgram kg-1 min-1), which was vasoactive only after conversion to AT II by local ACE, elicited a generalized constrictor response in all three vascular sections. In contrast, infused AT II (0.01-0.16 microgram kg-1 min-1) constricted almost selectively the large-bore arterial vessels. The specific angiotensin AT1-receptor antagonist losartan (2 mg kg-1 min-1, i.a.) abolished the constrictor response to AT II but did not affect vascular tone under control conditions, indicating that AT II is not involved in the initiation of basal vascular tone in muscle. These results, taken together, indicate that under basal conditions vascular ACE contributes to the local control of vascular tone in skeletal muscle by degrading the endogenous dilator bradykinin, and not by converting AT I into vasoconstrictor AT II.
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| 7. |
- Ekelund, Ulf, et al.
(författare)
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Endogenous nitric oxide as a physiological regulator of vascular tone in cat skeletal muscle during haemorrhage
- 1996
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 157:4, s. 471-479
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Tidskriftsartikel (refereegranskat)abstract
- The problem whether endogenous nitric oxide (NO) may serve as a true physiological regulator of vascular tone in vivo was approached by testing its role during graded acute haemorrhage with the aid of the nitric oxide synthase (NOS) inhibitor L-NAME. The study was performed on the vascular bed of cat skeletal muscle with a technique permitting quantitative recordings of vascular resistance in the whole vascular bed (RT) and in its consecutive sections, the proximal arterial resistance ('feeder') vessels (> 25 microns; Ra,prox), the small arterioles (< 25 microns) and the veins. NO blockade by close-arterial L-NAME infusion in the control situation increased RT from 16.3 to 33.0 PRU (+102%), because of a selective increase in Ra,prox by 16.7 PRU. A 35% blood loss per se raised RT from 13.6 to 21.7 PRU. Superimposed NO blockade in this state caused a much stronger vasoconstriction than in the control situation, increasing RT to 60.9 PRU (+181%) and Ra,prox by 40.5 PRU, which indicated an approximately 2.4-fold increase (P < 0.001) in the NO dilator influence in the Ra,prox section above control. The effect was independent of autonomic nerves. The increased NO dilator influence during haemorrhage most likely was caused by an increased production of endothelium-derived nitric oxide (EDNO), The constrictor response to L-NAME was graded in relation to the blood loss (17.5 vs. 35%). The results indicate that EDNO functions as a physiological regulator of vascular tone in the arterial 'feeder' vessels during haemorrhage, serving to counterbalance to a significant extent the concomitant adrenergic constriction, and thereby preventing critical reduction of blood flow and untoward heterogeneous flow distribution within the tissue.
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| 8. |
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| 9. |
- Dahm, Peter
(författare)
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Nitric oxide in experimental sepsis
- 1998
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Nitric oxide (NO) is important in the control of blood pressure and organ perfusion. In septic shock, NO produced by inducible NO-synthase (NOS) has been claimed to mediate pathological vasodilation and cell injury, while NO produced by constitutive NOS may be protective in counteracting hypoperfusion and organ injury. This thesis comprises studies on the effects of inhaled NO on pulmonary function in a porcine model of unresuscitated Gram-negative septic shock and acute lung injury (ALI). In this model and in normal pigs, we also investigated the effects of non-selective NOS inhibition on global and regional haemodynamics and oxygen extraction. NO inhalation: Inhaled NO (57 and 60 ppm) selectively attenuated pulmonary vasoconstriction without direct effects on the systemic circulation. Early NO inhalation preserved gas exchange by reducing venous admixture and alveolar dead space, but had no effects on respiratory mechanics. The effects on pulmonary haemodynamics and gas exchange were repeatable. Inhaled NO may mitigate endotoxic lung injury by reducing leukocyte sequestration in the pulmonary microvasculature. NOS inhibition: In both normal and endotoxic pigs, the pulmonary vasculature was more sensitive to the vasoconstricting effects of NOS inhibition than the systemic. In normal pigs, this pulmonary vasoconstriction was enhanced by prior stimulation with acetylcholine. The enhancement may be related to an associated release of a vasoconstricting prostanoid. In endotoxic shock, NOS inhibition caused several animals, with extreme pulmonary hypertension, to die before the end of the observation time. In spite of the fatal overall effects, hepatic perfusion was unharmed by NOS inhibition. The capacity to increase oxygen extraction, in response to the decrease in oxygen delivery, was preserved. In hypodynamic shock, compensatory mechanisms other than NO may be more important in the regulation of hepatic blood flow.
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| 10. |
- Ekbäck, Gustav, et al.
(författare)
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Perioperative autotransfusion and functional coagulation analysis in total hip replacement
- 1995
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 39:3, s. 390-395
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Tidskriftsartikel (refereegranskat)abstract
- Functional coagulation analyses like Sonoclot and thromboelastography have not been evaluated during perioperative autotransfusion. We have prospectively studied three different transfusion regimes in 45 patients undergoing total hip arthroplasty. Blood losses were replaced either with heterologous erythrocyte concentrate (group I), intra- and postoperative autotransfusion of blood salvaged with cellsaver technique (group II) or predonated autologous erythrocyte concentrates together with salvaged blood (group III). Routine and functional coagulation analyses with a Sonoclot were performed preoperatively, 6 hours postoperatively (6 h), day 1–5 and 10. An early postoperative hypo- and late postoperadve hypercoagulative phase could be detected with Sonoclot signs of platelet function and fibrin deposition in all groups. Sonoclot coagulation analyses better correlated to both blood loss and dextran dosage than APTT and platelet count in the routine coagulation analyses. Functional coagulation analysis has a potential use in individualizing plasmasubstitution and thromboprophylaxis regimes during autotransfusion in THR.
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