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| 2. |
- Eriksson, M, et al.
(author)
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Angiotensin converting enzyme dependent and non-dependent effects of a fibrinogen-derived pentapeptide on microvascular permeability in rat skin.
- 1983
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In: Upsala Journal of Medical Sciences. - 0300-9734 .- 2000-1967. ; 88:2, s. 95-101
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Journal article (peer-reviewed)abstract
- A permeability-increasing pentapeptide, termed peptide 6A, derived from plasmin-degraded human fibrinogen and known to potentiate the increase in microvascular permeability caused by bradykinin was investigated concerning its angiotensin converting enzyme (A.C.E.) related effects. When applied to a rat skin model together with a specific inhibitor of this enzyme, peptide 6A showed a potentiated effect after 30 min. but not after 5 min. The same was also true for bradykinin. These findings suggest that the degradation rate of these peptides is decreased with resulting prolongation of the period of leakage, when the action of A.C.E. is opposed. It is deduced that peptide 6A may act as a partial antagonist of this enzyme in the rat skin model. Addition of peptide 6A to a mixture of bradykinin together with inhibitors of the enzymes degrading bradykinin before application to the rat skin, significantly augmented the extravasation of 125I-albumin. These findings are consistent with data indicating that peptide 6A is a prostacyclin-releaser able to induce vasodilation. This effect of peptide 6A on the microcirculation seems to be separate from its angiotensin converting enzyme-related effects.
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| 3. |
- Gerdin, Bengt, 1947-, et al.
(author)
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Deposition and clearance of fibrin in the rat lung following acute haemorrhage.
- 1979
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In: Circulatory shock. - 0092-6213. ; 6:4, s. 357-64
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Journal article (peer-reviewed)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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| 4. |
- Gerdin, Bengt, 1947-, et al.
(author)
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Inhibitory effect of the flavonoid O-(beta-hydroxyethyl)-rutoside on increased microvascular permeability induced by various agents in rat skin.
- 1983
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In: International journal of microcirculation, clinical and experimental. - 0167-6865. ; 2:1, s. 39-46
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Journal article (peer-reviewed)abstract
- Flavonoids are used clinically in conditions with inflammatory oedema. The effects of a clinically employed flavonoid preparation, O-(beta-hydroxyethyl)-rutoside, in this paper abbreviated 'HR', were studied in a rat skin model designed to evaluate the leakage of 125I-labelled human serum albumin after intracutaneous injection of substances increasing microvascular permeability. Intravenous injection of 25-500 mg HR/kg body weight (b.w.) 30 min before administration of permeability-increasing agents gave a dose-related attenuation of the permeability increase due to histamine, bradykinin and fibrin degradation products. The maximum inhibitory effect of HR was observed at 250 mg/kg b.w.. Treatment with the beta 2-receptor agonist terbutaline also reduced the increased permeability. This effect of HR and terbutaline included reduction of oedema due to formaldehyde, citrate and dextran 70. The effect of terbutaline was counteracted by the beta-receptor blocker propanolol. The effect of HR on blood flow in the skin, determined as clearance of 133Xe, was not considered important as an explanation for its inhibition of microvascular permeability.
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| 5. |
- Gerdin, Bengt, 1947-, et al.
(author)
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Permeability-increasing ability of PAF-acether in rat skin.
- 1985
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In: Inflammation. - 0360-3997 .- 1573-2576. ; 9:1, s. 107-12
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Journal article (peer-reviewed)abstract
- Platelet-activating factor (PAF-acether), a phospholipid compound with effects on several cells, e.g., platelets and polymorphonuclear leukocytes (PMNs), was examined for its effect on microvascular permeability in rat skin. It was found to increase microvascular permeability, measured as exudation of [125I]human serum albumin, in amounts exceeding 1 pmol, and was more than 1000 times as potent as histamine. The effect was independent of cell infiltration, as no accumulation of PMNs, measured as the amount of myeloperoxidase in the skin, occurred and as the response was unaltered in animals rendered neutropenic due to treatment with an antiserum against PMNs.
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| 6. |
- Gerdin, Bengt, 1947-, et al.
(author)
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Pulmonary insufficiency in the rat after intravascular coagulation and inhibition of fibrinolysis. II. Investigations on oedema formation and morphology.
- 1982
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In: European Surgical Research. - 0014-312X .- 1421-9921. ; 14:4, s. 252-61
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Journal article (peer-reviewed)abstract
- Solute and fluid compartments in the lungs were investigated following thrombin-induced intravascular coagulation in rats treated with the fibrinolysis inhibitor, Trans-4-(amino-methyl) cyclohexanecarboxalic acid. The lung weight was increased to almost three times normal due to accumulation of extravascular water with albumin and chloride concentrations similar to those in plasma. The blood content and dry weight were doubled. Microscopic sections were characterized by widespread fibrin-rich microemboli, thickened alveolar walls, distension of peribronchiolar and perivascular spaces with fluid, dilated lymph vessels and protein-rich alveolar oedema. An increased microvascular permeability to protein explains the findings. When the dose of thrombin was decreased to a point where no pulmonary oedema developed, supplementary infusion of low molecular weight fibrinogen degradation products induced oedema formation as verified microscopically.
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| 7. |
- Gerdin, Bengt, 1947-
(author)
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Use of 125I-labeled human serum albumin for quantitation of microvascular permeability in rat skin : reevaluation of an old method for studies on substances with an enhancing effect on microvascular permeability.
- 1981
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In: Journal of pharmacological methods. - 0160-5402. ; 6:3, s. 167-75
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Journal article (peer-reviewed)abstract
- A method of determining the leakage of 125I-labeled human serum albumin in the plasma into a standardized area of rat skin to study the effects of intracutaneous application of vasoactive substances on microvascular permeability, was reevaluated. The effect is expressed as a quotient (Q) between the amount of labeled albumin in the test area and that in an area injected with buffer. This calculation is simple and as reliable as more complicated expressions of activity. Within a limited dose range, linear/log dose-response curves can be obtained after application of histamine or bradykinin. Locally injected 125I-labeled human serum albumin is eliminated very slowly from rat skin and determination of the amount of radiolabeled albumin in skin after an intravenous injection therefore represents leakage from the vascular compartments. The potentialities and advantages of this method in pharmacological studies are stressed.
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| 8. |
- 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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| 9. |
- 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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| 10. |
- 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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