We studied gastric and intestinal function by gastric intubation/intestinal perfusion in six healthy male volunteers to evaluate optimal use of a 6% glucose-electrolyte (GES) solution. Gastric volume, residual volume, emptying rate, and secretion were measured for an initial 763 +/- 19 ml gastric load of GES and at the beginning and end of four additional gastric loads (2.2 ml.kg-1; approximately 180 ml) given at 10-min intervals. The relatively high gastric (713 +/- 58 ml) and residual (507 +/- 26 ml) volumes maintained a high gastric emptying rate (19.5 +/- 1.4 ml.min-1). Composition of the GES emptied into the duodenum was also measured in this first experiment. In a second experiment, this modified solution was infused (triple lumen tube) into the duodenum at a rate equal to gastric emptying rate, or at 38 or 77% greater rates. Absorption of water (11.3-12.9 ml.h-1.cm-1) and glucose 4.3-5.6 mmol.h-1.cm-1) were similar at all perfusion rates during the second experiment. We conclude that duodenojejunal segmental absorption rates of water and glucose produced by a rapid, sustained gastric emptying rate cannot be increased by delivering a greater load of glucose and water by intestinal perfusion.
Endothelin-1 has been appreciated in animals and humans as a potential target for inhibition in patients with acutely decompensated congestive heart failure (CHF), as well as patients with a chronic low-output state. There has been intense interest in determining the effects of endothelin-1 on the cardiovascular system. Elevated plasma levels of endothelin-1 in patients with CHF portend a poorer prognosis than similar patients without elevated levels. Endothelin-1 levels correlate inversely with maximum oxygen consumption, and inhibition of the myocardial endothelin pathway in rats with CHF improves survival. An association between endothelin-1 and the development of CHF has recently been supported. Selectively inhibiting the endothelin A receptors in dogs with CHF produced hemodynamic improvement. Similarly, in rabbits, a structural advantage was demonstrated. Benefits in cardiac remodeling have been demonstrated in several models of CHF by nonselectively antagonizing endothelin receptors. In human trials using nonselective endothelin-1 inhibitors, researchers have demonstrated hemodynamic benefit and improvement in cardiac function in patients with decompensated CHF. Inhibition of endothelin-1 in patients with CHF appears to have potential therapeutic value, and ongoing clinical trials will further investigate the safety, efficacy, and role of this new potential therapeutic target for the treatment of CHF.
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