EFFECT OF HYPOXIC AND CARBON MONOXIDE-INDUCED HYPOXIA ON REGIONAL MYOCARDIAL SEGMENT WORK AND O-2 CONSUMPTION

The purpose of this study was to investigate the potentially greater r esponses of regional myocardial work and O-2 consumption to hypoxic hy poxia than to CO-induced hypoxia. Twenty open-chest anesthetized dogs were studied under control and four hypoxic conditions, hypoxic hypoxi a induced with either 8% O-2 (SaO(2) = 56%) or 6% O-2 (SaO(2) = 40%) g as mixtures, or CO-induced hypoxia produced by a 1% CO gas mixture for either 7 min (SaO(2) = 67%; SaCO = 30%) or 20 min (SaO(2) = 40%; SaCO = 56%). Ultrasonic crystals and a force gauge were utilized to measur e myocardial shortening and force. Regional myocardial segment work wa s calculated by integrating myocardial segment shortening multiplied b y its corresponding force. Radioactive microspheres were used to measu re regional coronary blood flow during each condition. Transmural biop sies were utilized to measure arterial and venous O-2 saturation with a four-wavelength microspectrophotometric method. Regional O-2 extract ion and consumption were calculated. Regional coronary blood flow (77 +/- 38 ml/min per 100 g, control) increased with severe hypoxic hypoxi a (293 +/- 206) and CO-induced hypoxia (150 +/- 128). Regional myocard ial O-2 extraction was decreased with both hypoxic and CO hypoxia. Reg ional myocardial O-2 consumption was maintained even with severe hypox ic and CO hypoxia. Regional myocardial segment work/min increased from 343 +/- 205 g() mm/min with increasing levels of hypoxic hypoxia (56 4 +/- 677) and decreased with increasing levels of CO hypoxia (169 +/- 111). Regional segment work increased with increasing levels of hypox ic hypoxia and decreased with increasing CO hypoxia. The differential effects on segment work caused by the two types of hypoxia may be due to direct metabolic or autonomic differences.