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- Gerdin, Bengt, 1947-, et al.
(författare)
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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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Ingår i: International journal on tissue reactions. - 0250-0868. ; 7:5, s. 373-80
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Tidskriftsartikel (refereegranskat)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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- Grögaard, B, et al.
(författare)
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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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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 127:1, s. 17-25
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Tidskriftsartikel (refereegranskat)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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| 5. |
- McCann, E, et al.
(författare)
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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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Ingår i: International journal on tissue reactions. - 0250-0868. ; 8:3, s. 205-12
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Tidskriftsartikel (refereegranskat)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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- Olofsson, A M, et al.
(författare)
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Heparin-binding protein targeted to mitochondrial compartments protects endothelial cells from apoptosis
- 1999
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Ingår i: Journal of Clinical Investigation. - 0021-9738. ; 104:7, s. 885-894
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Tidskriftsartikel (refereegranskat)abstract
- Neutrophil-borne heparin-binding protein (HBP) is a multifunctional protein involved in the progression of inflammation. HBP is stored in neutrophil granules and released upon stimulation of the cells in proximity to endothelial cells. HBP affects endothelial cells in multiple ways; however, the molecular and cellular mechanisms underlying the interaction of HBP with these cells are unknown. Affinity isolation and enzymatic degradation demonstrated that HBP released from human neutrophils binds to endothelial cell-surface proteoglycans, such as syndecans and glypican. Flow cytometry indicated that a significant fraction of proteoglycan-bound HBP is taken up by the endothelial cells, and we used radiolabeled HBP to determine the internalization rate of surface-bound HBP. Confocal and electron microscopy revealed that internalized HBP is targeted to perinuclear compartments of endothelial cells, where it colocalizes with mitochondria. Western blotting of isolated mitochondria from HBP-treated endothelial cells showed that HBP is present in 2 forms - 28 and 22 kDa. Internalized HBP markedly reduced growth factor deprivation-induced caspase-3 activation and protected endothelial cells from apoptosis, suggesting that uptake and intracellular routing of exogenous HBP to mitochondria contributes to the sustained viability of endothelial cells in the context of locally activated neutrophils.
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| 7. |
- Schoenberg, M H, et al.
(författare)
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Hemorrhagic shock in the dog. I. Correlation between survival and severity of shock.
- 1985
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Ingår i: Research in experimental medicine. - 0300-9130 .- 1433-8580. ; 185:1, s. 21-33
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Tidskriftsartikel (refereegranskat)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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| 8. |
- Schoenberg, M H, et al.
(författare)
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Hemorrhagic shock in the dog. II. Studies on central hemodynamics and regional blood flow.
- 1985
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Ingår i: Research in experimental medicine. - 0300-9130 .- 1433-8580. ; 185:6, s. 469-82
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Tidskriftsartikel (refereegranskat)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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