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Biomedical subjects

L Rammer

Publications and source records attributed to L Rammer.

At least 37 records · Page 2Linked to original sources

Normal mitotic reactivity of fibroblasts and mesothelial cells in thrombocytopenic rat.

Mitotic reactivity following 48/80-induced mast-cell secretion was studied in the mesentery of rats made thrombocytopenic, 7 days following a single injection of melphalan. In spite of a low platelet count (7% of normal), the mitogenic reaction of the mesenteric fibroblasts and mesothelial cells was normal as judged by DNA-synthesis and mitotic index. The findings suggest that platelets and platelet-growth factors are not essential for the mast-cell-mediated mitogenic reaction of these two types of connective-tissue cells studied in vivo.

Animals↗

Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat.

Intravascular coagulation in the rat kidney was induced by intravenous infusion of thrombin for 1 hr. The proximal tubular free-flow (Pt) and stop-flow (Psf) pressures were measured by micropuncture. Some proximal tubules were obstructed with solid paraffin before infusion of thrombin. In certain rats saralasin or indomethacin was administered for 1 hr starting 30 min after the thrombin infusion, and the effect on the tubular pressures was studied. The deposition of fibrin in the glomeruli was examined by light and electron microscopy. Pt fell from 15 +/- 1 (SE) to 7 +/- 2 mm Hg (P less than 0.05) during the infusion of thrombin. After a brief period of increased pressure the Psf fell rapidly from 37 +/- 1 to 17 +/- 1 mm Hg (P less than 0.05). In the previously obstructed nephrons the pressure (Po) increased parallel to the increase in Psf but remained elevated after the infusion of thrombin, 54 +/- 2 mm Hg. The arterial blood pressure (Pa) increased from 119 +/- 2 to 138 +/- 3 mm Hg (P less than 0.05). Saralasin raised the Psf from 15 +/- 1 to 19 +/- 1 mm Hg (P less than 0.05) but had no effect on Pt, Po, or Pa. Indomethacin did not influence the pressures. Morphological examination revealed fibrin in all glomeruli of normal nephrons. In the previously obstructed nephrons the deposition of fibrin was almost totally prevented. The results suggest that glomerular filtration is important for deposition of fibrin in the kidney.

Animals↗

Effect of unilateral ureteral occlusion on fibrin deposition in the kidney and renal blood flow during intravascular coagulation in rat.

The effect of unilateral ureteral occlusion on fibrin deposition in the kidney and the interrelation of the fibrin deposition and the renal blood flow was studied in rat. Intravascular coagulation in the kidney was induced by infusion of thrombin and inhibition of fibrinolysis with tranexamic acid. The effects unilateral occlusion of the ureter for 1 and 24 h on fibrin deposition and renal blood flow were studied. Fibrin in the kidneys was quantitated by intravenous injection of 125I-labelled fibrinogen 24 h before the experiment. The renal blood flow was measured before and after infusion of thrombin by injection of 85Sr- and 141Ce-labelled microspheres into the left ventricle. After ureteral occlusion for 1 h the deposition of fibrin in the kidneys was unaffected. After 24 h substantially less fibrin deposition was found in the occluded than in the unoccluded kidney (0.3 +/- 0.2 and 5.7 +/- 1.6 mg, respectively; p less than 0.05). Before thrombin infusion the blood flow to the occluded kidney was less than that in the unoccluded kidney (2.1 +/- 0.8 and 3.7 +/- 1.2 ml/min, 100 g body weight, respectively; p less than 0.05). The blood flow after infusion of thrombin was equally reduced in both kidneys. The results contradict the hypothesis that vasoconstriction increases the amount of fibrin in the kidneys in thrombin-induced intravascular coagulation.

Animals↗

Fibrin deposition in the kidney and renal blood flow during intravascular coagulation in the rat: influence of the renin-angiotensin system.

1. Intravascular coagulation in the kidneys of rats was induced by intravenous infusion of thrombin and by inhibition of fibrinolysis with tranexamic acid under alpha-chloralose anaesthesia. The amount of fibrin in the kidneys was measured with radioactively labelled fibrinogen. Chronic saline loading and inhibition of angiotension II (ANG II) with saralasin reduced the fibrin deposition in the kidneys. Infusion of ANG II had the opposite effect. 2. Renal and aortic blood flows were measured by injection of radioactively labelled microspheres. After thrombin infusion the renal and aortic blood flows were reduced to about one-third of the pre-infusion values. Chronic saline loading diminished these changes, but saralasin had no effect. 3. Plasma renin activity (PRA), measured by radioimmunoassay, decreased by about 50% after thrombin infusion. 4. The reduction in PRA and the lack of effect of saralasin indicate that the renin-angiotensin system is not the mediator of the observed decrease in the renal blood flow. As saralasin reduced the amount of fibrin the mechanism regulating fibrin deposition appears to be independent of the mechanism that reduces the renal blood flow.

Angiotensin II↗

Primary fracture immobilization as a method to prevent post-traumatic pulmonary changes- an experimental model.

Post-traumatic pulmonary insufficiency or "respiratory distress syndrome" (RDS) is one of the most feared complications of severe trauma. The aetiology is probably multifactorial, and is obscure. Although modern treatment has reduced the mortality, there is no certain way of preventing the syndrome. The aim of the investigation was to develop an experimental model on anaesthetized pigs subjected to trauma and folllowed up for 3-4 days, still under anaesthesia, the repeated lung X-rays and post-mortem naked-eye and histological examination of lung tissue. 26 pigs were used. 12 (Group I) were subjected to missile trauma of a limb, with a fracture that was left without immobilization. 10 were treated similarly but with immobilization of the fracture (Group II). Four control animals were prepared and observed under anaesthesia but no trauma was inflicted (Group III). In Group I, all but two developed, 10-70 h after the injury, roentgen and morphological changes identical to those seen in patients with clinically documented RDS. No such changes were seen in the controls or in Group II. With our experimental model it seems possible to induce in experimental animals roentgen and morphological changes corresponding to RDS in man. The method provides new means of studying the mechanisms behind and the effects of different forms of treatment in RDS. The results also support the hypothesis that early immobilization of fractures is an important step in preventing RDS.

Animals↗

Protective effect of angiotensin II inhibition on acute renal failure after intravascular coagulation in the rat.

Infusion of thrombin and the fibrinolysis inhibitor tranexamic acid during ether anaesthesia in the rat gives rise to fibrin deposition in the renal glomeruli. This resulted in renal insufficiency as indicated by an increase in the serum urea nitrogen, reduction in the renal blood flow and patchy cortical necrosis in the kidneys. The plasma renin activity was elevated initially probably due to the ether anaesthesia. Infusion of the angiotensin II antagonist saralasin prevented the renal insufficiency if it was given during the thrombin infusion but not if it was given afterwards. The deposition of fibrin in the kidneys was also reduced. The results indicate that angiotensin II is involved in the pathogenesis of the renal injury.

Acute Kidney Injury↗

Effect of beta-adrenergic blockade by propranolol upon intravascular coagulation in the rat kidney.

Disseminated intravascular coagulation in rats was induced by intravenous infusion of thrombin for 30 min. The glomercular filtration rate was measured as the clearance of polyethylene glycol 1000. The fibrin deposition in organs was quantitated by a method using previous injection of 125I-labelled fibrinogen. Administration of the beta-adrenergic blocking agent, propranolol, prevented the decrease in glomerular filtration rate after infusion of thrombin. This result could be explained by an observed partial redistribution of the fibrin from the kidneys to the lungs.

Animals↗

Inhibitory effect of dextran 40 upon thrombin-induced fibrin deposition in rat lungs.

The effect of dextran 40 upon thrombin-induced fibrin deposition in rat lungs was studied. A quantitative method employing isotope-labelled fibrinogen was used to determine the amount of fibrin in the lungs. It was shown that pretreatment was dextran 40 suppressed the accumulation of fibrin in the lungs after injection of thrombin. This was not due to redistribution of the fibrin to other organs but appeared to be a result of decreased intravascular coagulation. It seemed unlikely that the finding could be explained by an effect of dextran upon fibrinolysis.

Animals↗

Insulin in post-mortem blood.

In 29 cases of sudden death the insulin concentration in blood from the right heart and the femoral vein was determined by a radioimmunological method. The concentrations in the femoral venous blood were below 60 muU/ml serum (mean 23 muU/ml), i.e. in the same order of magnitude as in living persons. In right heart blood the insulin values were about 10 times higher, probably due to post-mortal diffusion of insulin via the portal vein. In suspected hyperinsulinism the measurements should therefore be made on peripheral venous blood.

Adult↗

Protection against the impairment of renal function after intravascular coagulation in the rat kidney by increased ingestion of sodium chloride.

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.

Acute Kidney Injury↗