Guenther F. Brobmann

Intrauterine transfusion and fetal death: Relationship of intraperitoneal pressure to umbilical vein blood flow

Abstract In this report, the hypothesis is advanced that fetal intraperitoneal transfusion may elevate intraperitoneal pressure above that in the umbilical vein and produce fetal death by anoxia. Three experiments are described in which dye-containing fluid was infused intraperitoneally into fetal baboons. Umbilical vein pressure was measured directly at 14.5 mm. Hg. Infusion of 23 and 25 ml. fluid was required to elevate the intraperitoneal pressure above 15 mm. Hg in 2 fetuses. At that pressure, umbilical flow ceased. In the third fetus 65 ml. was required to elevate intraperitoneal pressure to 13 mm. Hg. At that pressure umbilical flow ceased. In the latter fetus, the infusion was continued and the fetus died. On the basis of three experiments, the hypothesis is confirmed. It is recommended that fetal intraperitoneal pressure be monitored during human intrauterine fetal transfusion.

Effects of ouabain on splanchnic hemodynamics in the rhesus monkey

Abstract : When the effects of ouabain on splanchnic hemodynamics of the anesthetized monkey are evaluated, the major events were found to be a decrease in mesenteric blood flow and an increase in mesenteric vascular resistance. Implications of these findings are that use of cardiac glycosides may be contraindicated in clinical states characterized by low blood flow to the splanchnic region. (Author)

Altered Vascular Responsiveness: Initial Hypotensive Mechanism of Thiazide Diuretics

Conclusion In order to separate electrolyte and intravascular volume mechanisms of the thiazide diuretics from hemodynamic, local vascular, and neural factors mongrel dogs were studied before and 20 min after chlorothiazide (25 mg/kg, iv). Dose-response relationships of the mean arterial pressure curve following single bolus injections of norepinephrine and angiotensin were also obtained before and after chlorothiazide. Serum electrolytes, hematocrit, and plasma protein concentrations remained unchanged. Arterial pressure did not change, whereas cardiac output fell (p < .001). At each dose level the integrated pressure response to both pressor agents became significantly attenuated. These data indicate that the major immediate effect of the thiazide is local alteration in vascular responsiveness. Later, with natriuresis, electrolytic, volume, and possibly neural factors also participate. The authors gratefully acknowledge the fine technical assistance of Mr. Alan Chang and Mrs. Janice Pfeffer and the secretarial work of Mrs. Irene Smith.

Intestinal Vascular Responses to Gut Pressure and Acetylcholine in vitro

Active and passive elevation of intraluminal pressure in the denervated gut was studied to determine the effect on blood flow. In an in vitro preparation of canine intestinal segments, the vessels wer

Effects of Distension and Acetylcholine on Intestinal Blood Flow in vivo

In vivo canine gut segments perfused by branches of the superior mesenteric artery were subjected to increased intraluminal pressure to observe the effects upon arterial inflow, measured with an electromagnetic blood flowmeter, and venous effluent collected by a cannula. Inflation of the intestinal segment with air simultaneously reduced both inflow and outflow. Intra-arterial infusion of acetylcholine increased blood flow, even with intraluminal pressure maintained at 40 mm Hg. Mechanical distension of the gut impedes blood flow, but this effect can be overridden by a vasodilator. These findings correspond to results observed in similar experiments on in vitro gut segments.

Comparison of Early Hemodynamic Phenomena in Three Forms of Shock in Dogs

Summary Response patterns of arterial pressure, cardiac output, venous return, and total peripheral resistance were determined in 3 lethal shock states. Hemorrhagic shock decreased pressure and flows most profoundly and most persistently but increased resistance. Endotoxic shock caused an initial transient decrease in pressure and flows, followed by a later depression of these measurements and also decreased total peripheral resistance. Cardiogenic shock gradually decreased pressure and flows and did not change resistance. The concept of a single early circulatory derangement as the primary cause of irreversibility in shock is not supported by our findings.