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Biomedical subjects

N Krarup

Publications and source records attributed to N Krarup.

32 records · Page 2Linked to original sources

Imitation of glucagon effects on splanchnic hemodynamics and liver function by N6,2'-O-dibutyryl 3',5'-cyclic AMP (DBcAMP) in cats.

Fasting cats anesthetized with chloralose were used for the experiments. DBcAMP infused at a rate of 340 nmol/kg/min increased the gastrointestinal and intrahepatic portal conductances whereas the hepatic arterial conductance was decreased. The hemodynamic responses to portal and systemic venous administration of DBcAMP were identical. In half of the experiments DBcAMP increased the splanchnic ethanol elimination rate and oxygen consumption and in all experiments there was a decrease in the plasma clearance and extraction ratio of Indocyanine Green. No change in bile flow was observed. DBcAMP infused at a rate of 85 nmol/kg/min was without significant effects on either splanchnic hemodynamics or liver metabolism. DBcAMP infused at a rate of 850 nmol/kg/min accentuated the decrease in hepatic arterial conductanc- but was found to decrease the splanchnic ethanol elimination rate and oxygen cownsumption. Infusion of cAMP, AMP and adenosine at a rate of 340 nmol/kg/min were without measurable effects. Based on these results it is concluded that like the metabolic effects also the vascular effects of glucagon are caused by stimulation of specific glucagon receptors which results in an intracellular release of cAMP.

Animals↗

Effects of histamine, vasopressin, and angiotensin II on hepatosplanchnic hemodynamics, liver function, and hepatic metabolism in cats.

Continuous i.v. infusions of histamine (5 mug/kg - min), vasopressin (10 mU/kg -min), or angiotensin II (0.5 mug/kg - min) were given to fasting cats. Hepatic arterial flow was decreased 30% by histamine, increased 30% by vasopressin, and not significantly affected by angiotensin, whereas portal venous flow was increased 25% by histamine, decreased 40% by vasopressin, and not significantly affected by angiotensin. The hepatic arterial conductance was decreased about 25% by histamine and angiotensin, and not significantly affected by vasopressin. The gastrointestinal conductance was decreased about 40% by vasopressin and angiotensin, and increased 25% by histamine. The conductance in the intrahepatic low pressure vessels was not affected by histamine and vasopressin, but decreased 25% during the infusion of angiotensin. These hemodynamic effects, however, were not accompanied by changes in the liver function or hepatic metabolism as judged from the splanchnic elimination of ethanol, the hepatic uptake and excretion of ICG, the hepatic oxygen consumption, and lactate and ketone production. This indicates that the functional capacity of the liver and thereby the number of sinusoids perfused is not markedly influenced by these drugs. Vasopressin caused a decrease in the oxygen consumption and an increase in the lactate production in the prehepatic splanchnic area, which may be due to a redistribution of the gastrointestinal blood flow.

Angiotensin II↗