Mechanisms responsible for changes in abdominal vascular volume during sympathetic nerve stimulation in anaesthetized dogs

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Abstract

This study was designed to determine the extent to which the decrease in volume of blood in the abdominal circulation in response to sympathetic stimulation was due to a passive effect of decreasing flow rather than an active constriction of the capacitance vessels. In dogs anaesthetized with α chloralose (100 mg kg-1 I.V.) the abdominal circulation was vascularly isolated and perfused either at constant flow or at constant pressure, and drained at constant pressure from the inferior vena cava. Changes in volume were determined by integration of the differences between inflow and outflow. Supramaximal stimulation of both splanchnic (sympathetic) nerves at 1 Hz decreased abdominal volume during constant pressure perfusion (active and passive components) by 3.04 ± 0.58 ml kg-1 and at constant flow (active responses only) by 2.30 ± 0.49 ml kg -1 (means ± S.E.M.). The responses at 8 Hz were respectively 9.52 ± 0.91 and 5.09 ± 0.49 ml kg-1. The proportion of the responses calculated to be passive at 1 and 8 Hz was 23 ± 6.3 and 45 ± 5.1%, respectively. These responses were almost identical to those induced by changing inflow by increasing the pump speed. Following ligation of the splenic pedicle, the responses during both constant pressure and constant flow were reduced by similar amounts, indicating that only the active response was affected. After ligation of the splenic pedicle, the proportion of the response calculated to be passive at 1 and 8 Hz increased to 44 ± 8.0 and 62 ± 3.7%, respectively. These results indicate the importance of passive volume changes in affecting abdominal volume, particularly following ligation of the splenic circulation.

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Noble, B. J., Drinkhill, M. J., Myers, D. S., & Hainsworth, R. (1997). Mechanisms responsible for changes in abdominal vascular volume during sympathetic nerve stimulation in anaesthetized dogs. Experimental Physiology, 82(5), 925–934. https://doi.org/10.1113/expphysiol.1997.sp004073

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