Digoxin produced mesenteric vasoconstriction in dogs with proximal superior mesenteric artery stenosis, an effect that was completely reversed by glucagon administration.
Does intravenous digoxin induce mesenteric vasoconstriction in the presence of proximal mesenteric artery stenosis, and is it reversible by glucagon?
In a canine model, intravenous digoxin induced mesenteric vasoconstriction even in the presence of severe arterial stenosis, an effect that was completely reversed by glucagon.
Previous studies have been shown that intravenous cardiac glycosides produce mesenteric vasoconstriction (MVC). The possibility that this might critically compromise blood flow in patients with mesenteric vascular disease was suggested. To evaluate whether MVC occurs with intravenous cardiac glycosides in the presence of proximal mesenteric artery stenosis, blood flow in the superior mesenteric artery (SMA) of thirteen dogs was measured with a Doppler flowmeter. The SMA was constricted and pressures were measured in the aorta, SMA, and superior mesenteric vein. Superior mesenteric vascular resistance (SMVR) was calculated by dividing the pressure difference between the SMA and superior mesenteric vein by the total blood flow to the superior mesenteric vasculature and was reported as mm Hg/cc-min. Blood flow was measured simultaneously by a drop rate meter in the vein of a surgically isolated intestinal segment supplied by a single arterial arcade. Venous outflow pressure from this segment was also monitored, which allowed calculation of isolated gut segment resistance (IGSR) in mm Hg/cc-min per 100 g gut. Stenosis of the SMA produced pressure gradients of 10 to 75 mm Hg and decreased resting blood flow by as much as 82%. Digoxin produced an increase in both SMVR and IGSR throughout the 30 to 120 minute period of the study in thirteen dogs despite the presence of severe grades of SMA stenosis. There was no relationship between the degree of proximal SMA stenosis and the magnitude of resistance change due to digoxin. To determine if this MVC was reversible, glucagon was administered to eleven dogs 30 to 60 minutes after digoxin and completely overcame the constriction. Thus, digoxin produced MVC in the presence of proximal SMA stenosis. This MVC was pharmacologically reversible. These data suggest that intravenous digoxin might contribute to intestinal ischemia in patients with preexisting vascular disease.
Levinsky et al. (Tue,) conducted a other in proximal mesenteric artery stenosis (n=13). Digoxin was evaluated on Superior mesenteric vascular resistance (SMVR) and isolated gut segment resistance (IGSR). Digoxin produced mesenteric vasoconstriction in dogs with proximal superior mesenteric artery stenosis, an effect that was completely reversed by glucagon administration.
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