The changes in plasma levels of arginine-vasopressin (AVP) and oxytocin (OXT) of rabbits by intraventricular administration of various drugs and their effects on the release of both hormones from the isolated posterior pituitary of rats were examined. An intraventricular injection of hypertonic saline, carbachol, angiotensin II, prostaglandin E2 or histamine to a rabbit increased the concentrations of plasma AVP and OXT, whereas serotonin decreased their plasma levels. Noradrenaline increased the concentration of OXT, but not that of AVP. Dopamine did not significantly affect the plasma level of either hormone. The release of AVP and OXT from the posterior pituitary fragments of rats was stimulated by changing the osmolality of the perfusion medium in vitro. Perfusion with medium containing dopamine suppressed the release of both hormones. However, the other bioactive amines and the drugs mentioned above did not affect the release of AVP and OXT.

Angiotensin II↗

PubMedDate not supplied

Biorhythm of arginine- vasopressin in the paraventricular, supraoptic and suprachiasmatic nuclei of rats.

The diurnal variations in content of arginine-vasopressin in the supraoptic nucleus, the paraventricular nucleus and the suprachiasmatic nucleus of rats were determined using radioimmunoassay. In the supraoptic nucleus and the paraventricular nucleus the arginine-vasopressin level was relatively constant during the light phase (the inactive phase). When it became dark, the level of arginine-vasopressin lowered during the early and middle dark phase and then increased to the highest level during the late dark phase. In the suprachiasmatic nucleus the level was stable during the light phase, while in the early and the late dark phase it was significantly higher than that in the middle dark phase.

Animals↗

PubMedDate not supplied

Congenital intrahepatic arteriovenous fistulae in a young beagle dog.

Congenital intrahepatic arteriovenous fistulae, a rare hepatic vascular anomaly, in an 8-mo-old female beagle dog was investigated. The animal showed anorexia, repeated vomiting, hemorrhagic diarrhea, and jaundice for approximately 2 wk. There was mild to severe increase of serum alkaline phosphatase, glutamic-oxalacetic transaminase, glutamic pyruvic transaminase, total cholesterol, total bilirubin, and gamma-glutamyl transpeptidase. Macroscopically, the main abdominal organs showed hemorrhagic edema together with bloody ascites. Other characteristic findings were severe hepatic atrophy (right medial, quadrate, left medial, and lateral lobes) with multiple vascular cysts and compensatory hypertrophy of the other lobes. The cystic vessels seemed to extend from the proper hepatic arteries and their branches but were indistinguishable from the portal vein. Histopathologically, the atrophied hepatic lobes were characterized by wide, fibrous septa containing severe hyperplasia and anastomosis of the arteriolae and venulae and proliferation of bile ducts.

Animals↗

PubMedDate not supplied

A new mechanism of serum creatine phosphokinase elevation in strangulated small bowel obstruction: an experimental rat model.

An experimental rat model was used to investigate the mechanisms of serum creatine phosphokinase (CPK) elevation in strangulated small bowel obstruction. Two models were used: a strangulated ileus model with the bowel lumen and blood flow obstructed simultaneously, and a control ileus model with only the bowel lumen occluded. The experiments demonstrated that CPK was released into the blood when the mesenteric blood flow was restored, and that CPK was released into the intestinal lumen in the strangulated ileus model but not the control ileus model. CPK activity in the mucosal layer of the strangulated ileus model was significantly decreased compared with that in the control ileus model. Purified CPK injected into the intestinal lumen was absorbed by the healthy intestine. These results suggest a new mechanism of serum CPK elevation in strangulated small bowel obstruction in which serum CPK is elevated with a significant decrease in mucosal CPK. Strangulated bowel content including mucosal CPK may be reabsorbed by the healthy distal intestine when bowel obstruction is incomplete.

Animals↗