Effect of adenosine and inosine on carbon tetrachloride-induced liver damage in rats.

Liver damage induced in rats by carbon tetrachloride (CCL4) was obvious macroscopically as well as microscopically in stained sections. Levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutamyl transpeptidase (gamma-GT) were also significantly raised. Adenosine and inosine effectively countered the damage when these were given before and during the period during which CCl4 produces the typical damage. The beneficial effect was seen in biochemical as well as pathological studies.

Effect of aspartate and glutamate on carbon tetrachloride induced liver damage in rats.

Liver necrosis was produced in rats by administering 3 doses of a mixture of carbon tetrachloride + olive oil, 2 ml/kg, ip. The liver damage was evidenced by the elevated levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutamyl transpeptidase (gamma-GT) and by histopathological observations of liver sections. Aspartate and glutamate administration (100 mg/kg, ip) significantly reduced these elevated levels of AST, ALT, and gamma-GT. Carbon tetrachloride induced liver necrosis was also found to be significantly reduced in aspartate and glutamate pretreated animals as observed macroscopically and histologically.

Effect of aspartate and glutamate on experimental myocardial infarction in rats.

Cardiac necrosis was produced in rats by administering isoproterenol sulphate (85 mg/kg, sc for 4 days). The myocardial damage was proved by observing the elevated levels of serum aspartate amino-transferase, lactate dehydrogenase and creatine phosphokinase and the changes were confirmed by histopathology of the tissue. Both aspartate and glutamate (100 mg/kg, ip) significantly reduced the elevated levels of these enzymes. The average degree of cardiac necrosis produced in these rats when observed macroscopically and histologically was also found to be significantly reduced on pretreatment with aspartate and glutamate.

Status of platelet functions in volunteers of various blood groups: effect of aspirin.

Platelet functions (platelet aggregation and adhesiveness) were studied in volunteers of different blood groups. The platelet aggregation time was found to be significantly (P less than 0.01) more in blood group O as compared A, B and AB blood groups. Similarly, platelet adhesive index was higher in A, B and AB blood groups when compared to that of blood group O. The administration of a single dose of aspirin (4 mg/kg, po) increased the platelet aggregation time and reduced the platelet adhesive index in all the blood groups.

Cardiovascular effects of a withanolide from Withania coagulans, dunal fruits.

A new withanolide, with a unique chemical structure similar to the aglycones of the cardiac glycosides, with mol. wt. 488 6, m. p. 260-261 degrees, isolated from the fruits of Withania coagulans, was screened for cardiovascular effects. At doses of 5 mg/kg body weight, the withanolide produced a moderate fall of blood pressure in dogs (34 +/- 2.1, mm Hg) which was blocked by atropine and not by mepyramine or propranolol. In rabbit Langendorff preparation and ECG studies, it produced myocardial depressant effects but in perfused frog heart it produced mild positive inotropic and chronotropic effects.

Enhanced platelet aggregation by oral contraceptives: effect of PG synthetase inhibitors.

Platelet aggregation time was significantly (P less than 0.01) decreased in female rabbits treated with oral contraceptive (a preparation containing low dose of estrogen) as also by injection of diethylstilbestrol (10 mg/kg), while in animals that received indomethacin (10 mg/kg) or aspirin (30 mg/kg) (PG synthetase inhibitors) along with oral contraceptives or diethylstilbestrol there was no significant alteration in platelet aggregation time. The increased synthesis of prostaglandins or some of the intermediary product like TXA2 might be responsible for this effect.

Effect of glucagon on arrhythmias induced by coronary artery occlusion and ouabain in dogs.

The effect of glucagon in arrhythmias induced by coronary artery occlusion and ouabain was studied in dogs. Intravenous administration of glucagon (50 microgram/kg) to 6 dogs with more than 70% ectopic activity after coronary artery occlusion, resulted in significant (P less than 0.01) decrease in ectopics and increase in heart rate. Infusion of glucagon (2.5 microgram/kg/min) for 30 min caused complete elimination of ectopic activity during infusion period. In another series of 7 experiments, glucagon failed to abolish the ouabain-induced ectopic beats. In fact the hormone itself caused a significant (P less tha 0.01) increase in ectopic activity and heart rate. However, in 7 dogs with complete heart block produced after ouabain conversion to normal sinus rhythm was observed after glucagon.

Effect of glucagon on the perfused rat hind-quarter vessles and on perfused coronary arteries of rabbit.

In rat hind-quarter perfusion experiments, glucagon (1 microgram) produced a significant vasodilation. On the other hand, in experiments with isolated perfused rabbit heart, glucagon (1 microgram) caused coronary vasoconstriction irrespective of whether noradrenaline was added to perfusion fluid or not. Glucagon had no effect on rate or force of contraction of heart.