Increased Outflow Resistance Research Articles

Action of eserine, hexamethonium and atropine on outflow resistance of monkey eyes indicating that eserine releases acetylcholine besides protecting it.

Eserine injected into the anterior chamber of monkeys in deep barbiturate anaesthesia decreases outflow resistance. The effect is obtained even after previous ganglionic block by hexamethonium and is then still counteracted by atropine. This indicates the presence of acetylcholine not released by nervous tone. Systemic hexamethonium itself increases outflow resistance, as does atropine, but atropine has no effect after hexamethonium. This argues against the spontaneous release of appreciable amounts of acetylcholine after ganglionic block. The action of eserine on outflow resistance therefore seems to be dual, to release acetylcholine and not only to protect it.

Ventricular Response to Increased Outflow Resistance in Absence of Elevated Intraventricular End-Diastolic Pressure

In the isolated, supported, canine heart preparation, the response of the left ventricle to augmented outflow resistance was compared under conditions in which ventricular end-diastolic pressure and volume were increased and in which the pressure and volume remained virtually constant. The compensatory changes were much greater when end-diastolic pressure and volume were increased, even if these alterations in pressure and volume subsequently returned to or toward control levels. Immediately after resistance was augmented, peak ventricular power and stroke work diminished to less than control values. Within a very few beats, however, both of these parameters rose to exceed control levels. However, definite adaptive changes were also observed under conditions in which ventricular dimensions and pressures did not change appreciably, even temporarily. After a similar initial reduction in peak power and work after resistance was increased, peak power rose progressively to a value still significantly below control, while stroke work attained control levels by the end of a mean interval of 32 seconds of increased resistance. The intrinsic adaptation of the ventricle to increased resistance per se undoubtedly contributes to the total compensatory response, even under conditions in which diastolic stretch of the ventricle plays a major role.

Arterial inflow into the mesenteric and hepatic vascular circuits during hemorrhagic shock.

Mesenteric artery and hepatic artery flows were studied in dogs during a standardized hemorrhagic shock procedure. Both flows decreased in response to hemorrhage, with development of greater vascular resistance in the hepatic artery circulation. Toward the end of the hypotensive period vascular resistance in the mesenteric artery often entered a declining phase, correlated with an increase in portal venous pressure, but hepatic artery resistance increased somewhat further. On transfusion, mesenteric artery flow increased rapidly, often exceeding the control values. Portal pressure doubled, and mesenteric resistance decreased to values less than control for about 30 minutes. This may represent a phase of pooling and trapping of blood in the capillaries and venules of the mesenteric circulation favored by reduced inflow resistance, and increased outflow resistance. This was followed by a phase of increased mesenteric resistance which often persisted until the demise of the animal, although it decreased in some animals during the terminal stage. Following transfusion, hepatic artery flow increased more gradually than mesenteric artery flow and reached a peak about 1 1/2 hours post-transfusion, at a time when flow in the mesenteric artery was markedly reduced and its resistance was maximal. The mechanism of this reciprocity of flow and resistance is discussed and its relevance to the interpretation of the hepatic artery flow changes in shock is considered.