Due to the marked effects of hemorrhage on cardiac output and splanchnic hemodynamics, the circulatory actions of vasopressin may differ during bleeding as opposed to stable conditions. We evaluated this hypothesis in conscious rats with portal hypertension due to chronic portal vein stenosis, by comparing the effects of a vasopressin infusion (0.02 IU per kg per min) to those of a control saline infusion, during and after a hypotensive hemorrhage (25 ml per kg). We also studied unbled portal hypertensive rats receiving an identical infusion of vasopressin or saline. During and after hemorrhage, vasopressin induced significant changes in systemic hemodynamics but had no effect on portal pressure, portal tributary blood flow and nonhepatic splanchnic arteriolar resistance. In unbled animals, by contrast, vasopressin decreased portal pressure and portal tributary blood flow and increased nonhepatic splanchnic arteriolar resistance. Our data further indicate that hemorrhage alone caused an early vasoconstriction in the portal tributaries and a delayed vasoconstriction in the nonsplanchnic vascular bed while vasopressin during hemorrhage induced an early and sustained vasoconstriction in the nonsplanchnic vascular bed as well as in the portal tributaries. The results show that, during and after severe bleeding, vasopressin exerts little influence on portal hemodynamics. Although these data do not allow firm conclusions concerning the therapeutic efficacy of vasopressin in bleeding esophageal varices, they demonstrate that the splanchnic actions of vasoactive substances cannot be readily extrapolated from stable conditions to hemorrhage.

Animals↗

PubMedDate not supplied

[Effects of cadmium chloride on the hypophyso-testicular axis of the golden hamster a study of the atenhypophysis with immunofluorescence technique (author's transl)(proceedings)].

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Animals↗

PubMedDate not supplied

[A case of oncocytic adenoma of the pituitary gland with galactorrhea and hyperprolactinemia].

A tumor of hypophysis, with suprasellar expansion, was removed surgically in a 68 years old woman with panhypopituitarism and galactorrhea. Light and electron microscopy studies have shown an oncocytoma. One year after pituitary ablation and cobaltherapy, the patient had normal pituitary functions and galactorrhea had disappeared. Since the prolactin cells were outside the adenoma and the prolactin secretion became normal after surgery, we can assume that galactorrhea was presumably due to the compression of the pituitary stalk by oncocytoma.

Adenoma↗

PubMedDate not supplied

[Effect of the development of portosystemic shunts in the maintenance of portal hypertension in rats].

We studied the role of portosystemic shunt development in the maintenance of portal hypertension in a prehepatic portal hypertension rat model. A first group was studied two days after partial portal vein ligation. When portosystemic shunts were negligible; the second group was studied 3 weeks after the partial portal vein ligation, when large portosystemic shunts were present. Portal pressure was significantly higher in the first group than in the second group (19.9 +/- 0.8 mmHg (mean +/- 1 SD) and 12.8 +/- 2.3 mmHg, respectively; p less than 0.001). When compared with sham operated rats: a) portal tributary blood flow (measured with the radioactive microspheres method) was decreased in the first group (- 34 p. 100; p less than 0.01) and increased in the second group (+ 32 p. 100; p less than 0.02); b) portal system vascular resistance was markedly increased in the first group (+ 269 p. 100; p less than 0.001) and did not significantly change in the second group (+ 30 p. 100). These results suggest that portosystemic shunt development decreases portal pressure but not to normal value because portal tributary blood flow is increased. Moreover the increase in portal system vascular resistance and in portal tributary blood flow play different roles in the maintenance of portal hypertension depending on the stage of evolution of portal hypertension.

Acute Disease↗