Lennart Rammer

Insulin in post-mortem blood

SummaryIn 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 μU/ml serum (mean 23 μU/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.ZusammenfassungIn 29 Fällen von plötzlichem Tod wurden die Insulinkonzentrationen mit einer radioimmunologischen Methode gemessen im Blut von der rechten Herzkammer und von der Femoralvene. Die Todesursachen waren Herzkrankheit in 20 Fällen, Lungenembolie in 3, Gehirnblutung in 2, Erhängung oder Erdrosselung in 2, traumatische Aortaruptur in 1 Fall und Vergiftung mit Desimpramine in 1 Fall. Die Konzentrationen im Femoralvenenblut waren unter 60 μU/ml im Serum (Mittelwert 23 μU/ml): das ist die gleiche Größe wie bei lebenden Personen. Im rechten Herzkammerblut waren die Insulinkonzentrationen ungefähr 10mal höher, wahrscheinlich von postmortaler Diffusion des Insulin verursacht via der Portalvene. In verdächtigem Hyperinsulinismus müssen die Messungen deshalb an peripherem Venenblut vorgenommen werden.

Delayed fibrin elimination from the lungs of burned rats with endogenous inhibition of the fibrinolytic system

Abstract The elimination of fibrin from the lungs of burned rats with endogenous inhibition of the fibrinolytic system was studied after intravenous injection of thrombin. The fibrin content of the lungs was quantified, using labelled fibrinogen and albumin. It was found that in burned rats the elimination of fibrin from the lungs was delayed. The lungs of these rats showed micro-atelectases which were more numerous than in rats without fibrinolysis inhibition.

Effect of anticoagulation upon nephron obstruction in experimental acute ischaemic renal failure. A morphological study

Ischaemic‐reperfusion injury as a model of acute renal failure (ARF) results in increased macromolecular permeability, tubular obstruction, and renal oedema. To investigate the role for coagulation in this model, anticoagulated and saline‐pretreated rats were subjected to 60 min unilateral renal artery occlusion (RAO). After 15 min of reflow, specimens were collected for electron and light microscopic examination. Morphometry was employed to study podocyte changes and Bowmans space dilatation as measures of increased permeability and tubular obstruction, respectively. After 15 min of reflow, Bowmans space increased significantly and the podocytes were markedly widened and flattened. Rats pretreated with heparin or warfarin showed less widening of Bowmans space than saline‐treated rats, whereas no significant difference was seen regarding the podocyte changes. In saline‐treated rats, fibrin‐positive material was seen in the tubules but not in the urine sediments collected after 90 min of reflow, either due to fibrinolysis or poor urinary elimination. The results suggest that anticoagulation does not preclude the glomerular sieving of macromolecules, but seems to reduce tubular obstruction, probably by preventing conversion of filtered fibrinogen into fibrin.

Protective effect on postischemic renal edema by anticoagulation.

The effect of anticoagulation upon renal edema and plasma protein accumulation in acute ischemic renal damage was studied. Rats were subjected to unilateral renal artery occlusion for 60 min and 15 min of reflow. The kidney weight and the content of 125-I-fibrinogen and 131-I-albumin, injected 24 h priorly, were measured and the renal morphology studied. Groups of rats were pretreated with a heparin analogue with low anticoagulant effect, standard heparin, warfarin or saline. A marked increase in fibrinogen and albumin content and of the weight of the damaged kidney was noted. Heparin and warfarin both significantly attenuated these changes, whereas the heparin analogue did not. Microscopically, fibrin-positive material was seen in the peritubular capillaries, vasa recta and in the tubules of rats pretreated with saline or the heparin analogue, but not in rats pretreated with heparin or warfarin. The results support the hypothesis that fibrin deposition in the kidney is of importance for the development of renal edema in this model of ischemic renal damage.

Postmortem Vertebral Angiography in Cases of Traumatic Subarachnoid Hemorrhage

A case of traumatic subarachnoid hemorrhage caused by vertebral rupture was diagnosed by postmortem vertebral angiography. Lumbar spinal puncture is recommended as a screening method. The value of roentgenological examination prior to autopsy, especially in forensic medicine, is discussed.

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.

Renal Function in Burned Rats with Reference to the Effect of Intravascular Coagulation

The importance of the coagulation process in the renal functional changes was studied following a standardized, sublethal third degree thermal injury in rats covering 14% of the body surface. Immediately post-burn, the glomerular filtration rate, measured as clearance of PEG 1000, decreased to about one-third of the pre-burn value, which gradually was regained within 24 hours. No decrease in the TmPAH/GFR ratio, indicating impairment of the tubular secretory capacity, was found. The serum urea nitrogen level was moderately elevated 24 hours after the burn, but at later intervals normal values were found. Anticoagulation with heparin or fibrinolysis inhibition with tranexamic acid did not influence the results of the GFR, TmPAH or serum urea nitrogen measurements and therefore no causative connection was found between a coagulation process and the renal functional changes in this trauma model.

Reduction of Renal Edema by Heparin in Postischemic Renal Damage

Rats were subjected to unilateral renal artery clamping for 60 min and contralateral nephrectomy. 125I-labelled fibrinogen and 131I-labelled albumin were injected intravenously 24 h before the experiment. A significant increase in the fibrinogen and albumin content and weight was found already 5 and 15 min after reflow. Rats given heparin (2,000 IU/kg body weight) 5 min before clamping and killed 15 min after reflow showed significantly smaller increases in these values than rats given saline. Morphological studies showed fibrin deposition in Bowmans space, tubules and peritubular capillaries. The results indicate that fibrin deposition occurs and is of importance in the development of renal edema in this type of renal damage.

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.

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.