Why the study?
Does inferior vena cava occlusion alter left ventricular end-systolic pressure-volume relations in intact canine hearts?
Does inferior vena cava occlusion alter left ventricular end-systolic pressure-volume relations in intact canine hearts?
A sudden decrease in venous return induces a decrease in afferent vagal nerve activity and increases efferent cardiac sympathetic nerve activity, resulting in enhanced myocardial contractility.
Vagal reflexes may confound Emax during IVCO in canines; leaves open applicability to clinical PV-loop assessments.
The effect of inferior vena cava occlusion (IVCO) on end-systolic pressure-volume relations (ESPVR) of the left ventricle was studied in intact canine hearts. In 12 anesthetized open-chest dogs, left ventricular (LV) pressure and volume were measured simultaneously using a microtip catheter and a conductance catheter, respectively. ESPVR was constructed from LV pressure-volume loops during IVCO (10 sec) and subsequent IVCO release under 5 conditions: control, after righ or left cardiac sympathetic nerve (CSN) stimulation, bilateral vagotomy (VAT), and both VAT and bilateral CSN resection. Emax in IVCO release was significantly greater than that in IVCO in the control state. Following right or left CSN stimulation, Emax was increased increased in both IVCO and IVCO release, with the same hysteretic change in Emax. With VAT, however, no hysteretic change was observed because Emax was the same in IVCO and IVCO release. After VAT and CSN resection, Emax was decreased in both IVCO and IVCO release, and again no hysteretic change was observed. These data imply that a sudden decrease in venous return into the heart induces a decrease in afferent vagal nerve activity, and thus increases efferent CSN activity, resulting in enhanced myocardial contractility.
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Miyahara et al. (1996) studied this question.
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