Effects of halothane, enflurane, and isoflurane on coronary vascular tone, myocardial performance, and oxygen consumption during controlled changes in aortic and left atrial pressure. Studies on isolated working rat hearts in vitro.
The effects of equi-anesthetic concentrations of halothane (HAL, n = 11), enflurane (ENF, n = 11) and isoflurane (ISO, n = 10) on cardiac function were studied and compared with a control group (n = 12) in isolated paced rat hearts by means of an antegrade heart perfusion technique. Left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other, and aortic flow, coronary flow (CF), and po2 in venous coronary effluent were continuously recorded. Stroke volume (SV), myocardial oxygen consumption (MVO2), and myocardial oxygen extraction were calculated: 1) MAP was altered from 60 to 120 mmHg at a constant LAP (7.5 mmHg), and 2) LAP was varied from 4 to 12.5 mmHg at a constant MAP (80 mmHg). Left ventricular function curves (LVFC) were constructed and the maximal SV (SVmax) was obtained. The LAP needed to perform 75% of the maximal SV (LAP0.75) was estimated to assess the effect of the anesthetics on diastolic function. HAL ENF and ISO decreased SVmax significantly compared to control. This decrease was more pronounced for HAL (41%) compared to both ENF (26%) and ISO (26%). Accordingly, SV, at various levels of MAP, at a constant LAP, was significantly lower for HAL than for both ENF and ISO, while there was no significant difference between the latter two. None of the anesthetics shifted the LVFC to the right, i.e., did not affect diastolic properties. HAL induced the most pronounced decrease in MVO2, while there was no significant difference between ENF and ISO in this respect. Coronary flow (CF), at controlled perfusion pressures, decreased significantly with HAL but not with ENF or ISO compared to control. CF was significantly higher with ISO compared to both ENF and HAL. HAL and ISO, but not ENF, decreased myocardial oxygen extraction significantly compared to control and, thus, increased the myocardial oxygen supply-to-demand ratio.
Sahlman
L
L
Department of Anesthesia and Intensive Care, Sahlgren's Hospital, University of Gothenburg, Sweden.
Henriksson
B A
BA
Martner
J
J
Ricksten
S E
SE
D000818:Animals; D001011:Aorta / Q000502:physiology; D016275:Atrial Function; D001794:Blood Pressure; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004737:Enflurane / Q000494:pharmacology*; D006221:Halothane / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D007530:Isoflurane / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
D004737:Enflurane; D007530:Isoflurane; D006221:Halothane