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Effect of beta-adrenergic blockade by propranolol upon intravascular coagulation in the rat kidney
Insights
Propranolol, a beta-adrenergic blocking agent, protected against kidney damage in rats with disseminated intravascular coagulation. This protection was linked to a shift in fibrin deposition from kidneys to lungs.
Area of Science:
- Physiology
- Pharmacology
- Pathology
Background:
- Disseminated intravascular coagulation (DIC) is a severe condition characterized by widespread fibrin deposition.
- Kidney function impairment is a critical complication of DIC.
Purpose of the Study:
- To investigate the effect of propranolol on glomerular filtration rate (GFR) in a rat model of DIC.
- To explore the role of fibrin redistribution in the protective effects of propranolol.
Main Methods:
- DIC was induced in rats via intravenous thrombin infusion.
- Glomerular filtration rate was assessed using polyethylene glycol 1000 clearance.
- Fibrin deposition was quantified using 125I-labelled fibrinogen.
Main Results:
- Thrombin infusion significantly decreased GFR in rats.
- Propranolol administration prevented the thrombin-induced decrease in GFR.
- Fibrin deposition was partially redistributed from kidneys to lungs in propranolol-treated rats.
Conclusions:
- Propranolol exhibits a protective effect on renal function during DIC in rats.
- The protective mechanism may involve altering fibrin distribution away from the kidneys.
Abstract:
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.