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We investigated neurogenic, non-neurogenic, and structural contributions to vascular resistance in hindquarters in five groups of guinea pigs after heart failure produced by (1) constriction of the pulmonary artery (RHF), (2) constriction of the ascending aorta (LHFA), and (3) constriction of the descending thoracic aorta (LHFD); (4) after left ventricular hypertrophy produced by mild constriction of the ascending aorta (LVH); and (5) after sham surgery. Pressure-flow curves were used to assess vascular resistance in the isolated, perfused hindquarters. In RHF and LHFA, vascular resistance tended to increase and for different reasons. In the LHFA group, sympathectomy produced the greatest vasodilation. Therefore, neurogenic influences predominated. The high neurogenic tone may have been related to reduced arterial pulse pressure (P < 0.05) and reflexes arising in arterial baroreceptors. In contrast, the LHFD group had increased arterial pressure and pulse pressure (P < 0.05) and normal neurogenic vasoconstriction. However, non-neurogenic vasoconstriction was increased probably as a result of increased vascular responsiveness to constrictor stimuli. In the RHF group, papaverine produced the greatest vasodilation (P < 0.05). Therefore, non-neurogenic influences predominated. This was attributed to both increased vascular responsiveness and to altered humoral stimuli. Similar maximal vasodilation indicated that structural factors contributed equally to vascular resistance in all the groups. These results indicate differences in the regulation of vascular resistance in anesthetized, guinea pig models of right and left heart failure.

Differences in the regulation of vascular resistance in guinea pigs with right and left heart failure.