Recovery of Microvascular Po2 in Rats with Chronic Heart Failure

Abstract

0181 Chronic heart failure (CHF) impairs muscle O2 delivery (Qo2) and thus reduces microvascular O2 pressures (Po2m: determined by the Qo2-to-O2 utilization ratio), which may impair the recovery of high-energy phosphates following exercise. PURPOSE: Because CHF preferentially impairs Qo2 to slow-twitch muscles (Musch & Terrell, Am. J. Physiol. 262: H411-419, 1992), we hypothesized that recovery Po2m kinetics would be slowed to a greater extent in soleus (SOL: ∼84% type I fibers) than peroneal (PER: ∼14% type I) muscles of CHF rats. METHODS:Po2m dynamics were determined in SOL and PER muscles of control (CON: n = 6; left ventricular enddiastolic pressure, LVEDP: 3±1 mmHg), moderate CHF (MOD: n = 7; LVEDP: 10±2 mmHg) and severe CHF (SEV: n = 4; LVEDP: 28±4 mmHg) CHF following cessation of electrical stimulation (180s; 1 Hz). RESULTS: In PER, neither the recovery Po2m values nor their recovery kinetics (mean response time, MRT; CON: 66.8±8.0, MOD: 72.4±11.8, SEV: 69.1±9.5s) were altered by CHF. In marked contrast, SOL Po2m was reduced significantly in the SEV group (∼6 Torr) and Po2m recovery kinetics were slowed progressively with increased severity of CHF (MRT, CON: 45.1±5.3, MOD: 63.2±9.4, SEV: 82.6±12.3s; P<0.05 CON vs SEV). CONCLUSION: These data indicate that CHF slows Po2m recovery and thus lowers capillary O2 driving pressure in slow-twitch SOL, but not fast-twitch PER muscle with SEV CHF. These results may explain, in part, the slowed recovery kinetics (phosphocreatine and Vo V2) and fatigue following muscular work in CHF patients. Supported by: NIH HL-50306, HL-67619, AG-19228