Evaluation of two different oxygen inspiratory fractions on the hemodynamic effects of No-nitro-L-arginine methyl ester in anesthetized dogs

The effect of two different oxygen inspiratory fractions (FiO2 = 21 percent and 100 percent) on the hemodynamic responses induced by N(omega)-nitro-L-arginine methyl ester (L-NAME) was investigated in anesthetized dogs. L-NAME (0.01-10.0 mg/kg), but not D-NAME, induced dose-dependent changes in the hemodynamic parameters of the animals. At the highest dose, L-NAME increased mean arterial blood pressure in both room air (from 86.2 +/- 3.2 to 125.1 +/- 7.8 mmHg) and pure oxygen (from 100.0 +/- 7.5 to 139.0 +/- 3.2 mmHg) ventilated animals. L-NAME also increased systemic and pulmonary vascular resistances. These effects were accompanied by a decrease in cardiac output and bradycardia (37 percent and 31 percent decreases for pure oxygen and room air, respectively). However, there were no significant differences in the responses to L-NAME between the dogs ventilated with FiO2 = 21 percent and those ventilated with FiO2 = 100 percent. L-NAME did not modify blood gas analyses, despite the expected difference in PO2 levels between the two experimental groups of animals (3 times higher in the animals ventilated with pure oxygen). These results indicate that nitric oxide release accounts for the maintenance of hemodynamic function in the anesthetized dog, and that L-NAME-induced effects are not affected by hyperoxemia.

Alterations in rat carbohydrate metabolism induced by canatoxin as a probable consequence of primary hypoxia

Canatoxin, a protein displaying lipoxygenase-activating properties isolated from Canavalia ensiformis seeds, induces hypoxia and hyperglycemia in male rats. Liver glycogen, blood glucose and lactate levesls were measured in male and female rats after canatoxin (50 mU, iv) injection. Increased levels of serum glutamic oxaloacetic transaminase activity were used as an indicator of hepatic injury. There was no sex-related difference observable during canatoxin-induced hypoxia but male and female rats did whow different patterns of metabolic change and hepatic injury after toxin observed in male rats while female rats showed only hypoglycemia and glycogenolysis. Pretreatment of male rats with either glucose, diazepam or hexamethonium abolished both the hypoxia and hepatic injury and the metabolic alterations produced by toxin injection. The results suggest that the metabolic alterations and hepatic injury detected after canatoxin injection may be a consequence of primary hypoxia