| 1. |
- Gerdin, Bengt, 1947-, et al.
(author)
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Selective tissue accumulation of manganese and its effect on regional blood flow and haemodynamics after intravenous infusion of its chloride salt in the rat.
- 1985
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In: International journal on tissue reactions. - 0250-0868. ; 7:5, s. 373-80
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Journal article (peer-reviewed)abstract
- Manganese chloride (MnCl2), with or without the addition of trace amounts of 54Mn2+, was administered as a 7-min i.v. infusion in rats. Tissue accumulation of 54Mn2+ was determined 0-15 min after the infusion, and cardiac output, regional blood flows and vascular resistances were measured 5 and 60 min after the infusion by the microsphere technique. The plasma half-life of 54Mn2+ was found to be 4.7 min. Mn2+ accumulated in several organs, the highest relative concentrations being seen in the liver, duodenum, jejunum, kidney and heart, and intermediate concentrations in the ileum, colon, stomach and spleen. There was no uptake in the lung, skeletal muscle or brain. During the infusion of 180 mumol/kg b.w. of Mn2+, the arterial blood pressure fell from a mean of 123 +/- 5 mm Hg to a minimum of 85 +/- 7 mm Hg, and thereafter returned to normal. Five minutes after termination of the infusion, there was a decrease in cardiac output and minute work but not in total peripheral resistance, a finding interpreted as a negative inotropic effect of Mn2+. At this time blood flow was decreased in the stomach, ileum, colon, spleen and skin, and increased in duodenum, jejunum and liver. The blood flows were normalized 60 min after termination of the infusion in all organs except the liver and heart. The effects are probably due to the calcium-antagonistic properties of Mn2+ and the tissue accumulation is most probably a result of intracellular accumulation through calcium channels. The relation between tissue accumulation and tissue selectivity of blood-flow alterations is unexplained.
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| 2. |
- Grögaard, B, et al.
(author)
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Effect of carotid artery occlusion and ganglionic blockade on regional blood flows and intestinal damage after haemorrhagic hypotension in the rat.
- 1986
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In: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 127:1, s. 17-25
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Journal article (peer-reviewed)abstract
- The effects of cerebral ischaemia by carotid artery occlusion and of a ganglionic blocking agent (Arfonad) on cardiac output and regional blood flows were studied after 15 min of haemorrhagic hypotension (mean arterial pressure 50 mmHg) in the rat. The microsphere technique was used for blood flow determinations. Animals subjected to haemorrhagic hypotension and simultaneous carotid artery occlusion (group BC) exhibited a stronger immediate vasoconstrictor response than animals subjected to haemorrhagic hypotension only (group B) and more blood had to be withdrawn to achieve stable hypotension at 50 mmHg (2.6 +/- 0.1 vs. 2.2 +/- 0.4 ml per 100 g body weight (body wt); P less than 0.05). However, group B showed the same decrease in cardiac output as group BC, but the blood flows of the kidneys, spleen, intestine, liver and skin were less deranged at the end of the hypotensive period. Groups B and BC exhibited similar intestinal ischaemic mucosal damage, measured as leakage of [125I]albumin. When induction of haemorrhagic hypotension was combined with ganglionic blockade administration (Arfonad) and carotid artery occlusion (group ABC), significantly less blood had to be withdrawn than in groups BC (1.6 +/- 0.2 vs. 2.6 +/- 0.1 ml per 100 g body wt; P less than 0.05). The blood flows of the kidneys, small intestine, liver, spleen and skin were less compromised in group ABC. In addition, group BC had more profound metabolic acidosis and were more haemoconcentrated than group ABC; moreover, group BC, tended to be hypoglycaemic and showed intestinal mucosal damage, whereas neither of these effects occurred in group ABC.(ABSTRACT TRUNCATED AT 250 WORDS)
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| 3. |
- McCann, E, et al.
(author)
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Selective actions of calcium antagonistic drugs on the haemodynamics and regional organ blood flow in rats.
- 1986
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In: International journal on tissue reactions. - 0250-0868. ; 8:3, s. 205-12
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Journal article (peer-reviewed)abstract
- Six substances, all of which influence calcium utilization by smooth muscle, namely nimodipine (50 micrograms/kg), flunarizine (1 mg/kg), verapamil (0.2 mg/kg), lidoflazine (1 mg/kg), magnesium (600 mumol Mg++/kg), and manganese (180 mumol Mn++/kg), were given intravenously to rats and their effects on regional blood flows and on cardiac output were determined by the radioactive microsphere technique. All compounds caused a temporary fall in mean arterial blood pressure. Cardiac output was decreased by manganese, and minute work by nimodipine, manganese and lidoflazine. Nimodipine increased blood flow in the liver, skeletal muscle and heart and decreased that in the stomach, ileum, colon, kidney, spleen and skin; manganese increased flow in the duodenum, jejunum, liver and myocardium and decreased that in the stomach, ileum, colon, spleen and skin; flunarizine increased flow in the liver, heart and brain; and magnesium increased flow in the liver, spleen and brain. Lidoflazine and verapamil, although leading to haemodynamic alterations, had no selective effect on organ blood flow. Selective actions by calcium effector drugs can provide information on mechanisms of calcium flux in various types of vascular smooth muscle, and show that it is possible to tailor combinations of anti-calcium agents with optimal effects on a given organ.
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| 4. |
- Schoenberg, M H, et al.
(author)
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Hemorrhagic shock in the dog. I. Correlation between survival and severity of shock.
- 1985
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In: Research in experimental medicine. - 0300-9130 .- 1433-8580. ; 185:1, s. 21-33
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Journal article (peer-reviewed)abstract
- A prerequisite elucidating the pathomechanism of hemorrhagic shock are reproducible experimental models, leading to a predictable outcome. Two concepts have been reported to be a good predictor for the outcome both employing a fixed hypotension level: total oxygen deficit and shed blood volume uptake. To correlate these two models we subjected 31 dogs to a standardized hemorrhagic shock procedure. Besides determination of acid-base status, hematocrit, mean arterial pressure, and cardiac output, these two parameters were measured continuously. Seventeen dogs survived the shock procedure, 14 died within 24 h. During shock, neither oxygen deficit nor any other parameter mentioned above correlated with the final outcome of the shock state. The only significant difference between surviving and non-surviving animals during this period was the amount of uptake. The non-surviving dogs exhibited a higher uptake volume, indicating an incipient collapse of the microcirculation. Terminating the duration of hypotension at an uptake volume of 5% of the maximum shed blood, all animals survived, while after an uptake volume of 15% about 50% of the dogs died. Using uptake volumes of various degrees in a hemorrhagic shock model as the endpoint of the hypotensive stress, it seems possible to produce reliable survival rates.
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| 5. |
- Schoenberg, M H, et al.
(author)
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Hemorrhagic shock in the dog. II. Studies on central hemodynamics and regional blood flow.
- 1985
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In: Research in experimental medicine. - 0300-9130 .- 1433-8580. ; 185:6, s. 469-82
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Journal article (peer-reviewed)abstract
- Oxygen consumption, hemodynamics, and regional blood flow (with the radioactive microspheres technique) were determined in 12 anesthetized dogs subjected to hemorrhagic shock. The animals were kept in hypotension at 40 mmHg, until 15% of the maximum shed blood had been infused to keep arterial pressure stable, whereafter all the shed blood was retransfused. Cardiac output (CO) decreased to 33% and 25% of preshock values in survivors (S) and nonsurvivors (NS), respectively, and after retransfusion it was significantly higher in S. After retransfusion, NS showed a higher arterial pCO2 than S adding a respiratory component to the metabolic acidosis that occurred during and after hemorrhage. Blood flow to the brain was not impeded during shock, but as CO decreased the fraction delivered to the brain was increased 2.6-3.3-fold. Myocardial blood flow decreased to about 28% of preshock values immediately after hemorrhage, and increased to about 54% at the end of hemorrhage. After retransfusion S had a higher myocardial flow than NS. The flow to the gut paralleled the decrease in CO during hemorrhage and immediately after retransfusion NS exhibited an overperfusion in ileum and colon compared to the preshock values. Kidney blood flow fell progressively during the course of hypotension, similarly in S and NS. After retransfusion it was normalized in S but not in NS. The preshock flow to pancreas was significantly higher in S than in NS, but during and after shock the blood flow did not differ between S and NS.
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| 6. |
- Grøgaard, B, et al.
(author)
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Delayed hypoperfusion after incomplete forebrain ischemia in the rat. The role of polymorphonuclear leukocytes.
- 1989
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In: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 9:4, s. 500-5
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Journal article (peer-reviewed)abstract
- The role of polymorphonuclear leukocytes (PMNLs) in postischemic delayed hypoperfusion in the rat brain was investigated. Cerebral ischemia was accomplished by reversible bilateral occlusion of the common carotid arteries for 15 min combined with bleeding to an MABP of 50 mm Hg. The animals of one group were depleted of their circulating. PMNLs by intraperitoneal injections of an antineutrophil serum (ANS) prior to the experiment. All animals included in this group had fewer than 0.2 x 10(9) circulating PMNLs/L at the start of the experiments. In another group ANS was injected intravenously for 5 min starting 2 min after the ischemic insult. After 4 min of recirculation, the number of circulating PMNLs in this group was below 10% of the normal. Control animals were injected with the same amount of normal sheep serum or were not treated at all. Sixty minutes after termination of ischemia, the local blood flow in previously ischemic cerebral structures was 40-50% of the normal as measured with the [14C]iodoantipyrine technique. In animals treated with ANS prior to the ischemic insult, the postischemic blood flow in the frontal, sensorimotor, and parietal cortex as well as caudoputamen and thalamus was significantly higher than that in non-ANS-treated animals. Treatment with ANS immediately after the ischemic period caused no improvement of the local CBF. It is concluded that PMNLs are involved in the cerebral postischemic flow derangements seen in this model. Their effects seem to be exerted during ischemia or immediately upon reinstitution of blood flow.
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| 7. |
- Grøgaard, B, et al.
(author)
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Forebrain ischemia in the rat. Relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery.
- 1986
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In: Stroke. - 0039-2499 .- 1524-4628. ; 17:5, s. 1010-5
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Journal article (peer-reviewed)abstract
- The relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery was studied in a rat model giving reversible subtotal forebrain ischemia. Ischemia was induced by bilateral carotid artery clamping and controlled hemorrhage to a mean arterial pressure of 50 mm Hg in animals artificially ventilated under 70% N2O. After variable lengths of time, the clamps were removed and the drawn blood was reinfused. In some animals, the ganglion blocker Arfonad was given (group A+) on induction of ischemia to facilitate hypotension. There was a strict dose-response relationship between duration of ischemia and mortality. Mortality was higher among animals not given Arfonad (group A-; 37% after 10 min of ischemia and 100% after 13 min) than in group A+ (about 20% after 12-13 min of ischemia, 50% after 15 min and 80% after 19 min). In group A+ more than half of the animals died later than 24 h after ischemia. All of them were hyperexcitable and 12% died during witnessed epileptic fits. Group A- animals regularly died within the first 24 h, with no indication of central nervous system involvement. Less blood had to be drawn to attain hypotension (mean arterial pressure 50 mm Hg) in group A+ (1.5 +/- 0.3 ml/100 g b.w.) than in group A- (2.5 +/- 0.2 ml/100 g b.w.). Group A+ also had less "washout" acidosis 5 min after reinfusion of the shed blood than group A- (15 min of ischemia: pH 7.24 +/- 0.07 v 6.96 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
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| 8. |
- Grøgaard, B, et al.
(author)
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Inability of flunarizine, lidoflazine or magnesium to counteract delayed hypoperfusion after forebrain ischaemia in the rat.
- 1988
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In: Acta Neurochirurgica. - 0001-6268 .- 0942-0940. ; 95:3-4, s. 136-42
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Journal article (peer-reviewed)abstract
- Local cerebral blood flow (lCBF) was measured autoradiographically 60 min after 15 min of forebrain ischaemia in rats treated with flunarizine (0.1 mg/kg b.w.), lidoflazine (1.0 mg/kg b.w.) or Mg2+ (600 mumol/kg b.w.) before or at the end of the ischaemic period. Incomplete forebrain ischaemia was produced by a combination of common carotid artery occlusion and bleeding to a mean arterial blood pressure of 50 mmHg. During ischaemia lCBFs in cortical areas were less than 1% of preischaemic values. Neither flunarizine, lidoflazine nor Mg2+ influenced lCBF during ischaemia. Sixty minutes after the start of recirculation lCBFs were decreased to between 40 and 60% of the values found in control animals. None of the instituted treatments improved postischaemic cerebral blood flow. The results do not lend support to the view that calcium plays an essential role in the pathogenesis of delayed postischaemic hypoperfusion in the brain in this model.
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| 9. |
- Schürer, L, et al.
(author)
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Is postischaemic water accumulation related to delayed postischaemic hypoperfusion in rat brain?
- 1988
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In: Acta Neurochirurgica. - 0001-6268 .- 0942-0940. ; 94:3-4, s. 150-4
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Journal article (peer-reviewed)abstract
- The effect of reversible cerebral ischaemia on brain oedema development was studied with a gravimetric method. Cerebral blood flow changes after ischaemia were correlated with alterations in brain specific gravity. Forebrain ischaemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The specific gravity of different brain structures was determined in a Percoll column up to 24 h after ischaemia. In addition, regional cerebral blood flow was measured by 14C-iodoantipyrine autoradiography. Cerebral ischaemia resulted in reduction of cerebral blood flow to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischaemia blood flows were still reduced to 30-50% of the control level indicative of delayed postischaemic hypoperfusion. Specific gravity in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischaemia, and was still significantly reduced at 1 h, while it was normal again 6 hrs later. Regression analysis between regional cerebral blood flows and the corresponding specific gravities were made at various time points, but no significant correlations could be established. Other mechanisms, like vasoconstriction, rheologic or metabolic factors may be causative for the delayed postischaemic hypoperfusion.
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| 10. |
- Smith, S M, et al.
(author)
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Role of neutrophils in hemorrhagic shock-induced gastric mucosal injury in the rat
- 1987
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In: Gastroenterology. - 0016-5085 .- 1528-0012. ; 93:3, s. 466-471
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Journal article (peer-reviewed)abstract
- Gastric mucosal clearance of 51Cr-labeled red blood cells (51Cr-RBC) was measured in rats during a 30-min control period, a 30-min ischemic period (hemorrhage to 27 mmHg arterial pressure), and a 60-min reperfusion period (reinfusion of shed blood). In untreated (control) rats, a dramatic rise in the leakage of 51Cr-labeled red blood cells into the gastric lumen was observed during the reperfusion period. Treatment with neutrophil antiserum attenuated 51Cr-labeled red blood cell flux into the gastric lumen. Using the radioactive microsphere technique, neutrophil-depleted animals were shown to have higher blood flows in the ischemic period than the untreated rats. Bleeding of untreated rats to a mean arterial pressure of 40 mmHg resulted in blood flows that were not different from those in antiserum-treated rats bled to 27 mmHg and leakage of 51Cr-labeled red blood cells similar to that measured in antiserum-treated rats. The results of this study indicate that neutrophils play an important role in hemorrhagic shock-induced gastric bleeding.
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