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Left ventricular performance in the isolated heart of a dog was observed at normal temperatures (37.7 C) and under hypothermia (32.2 C) at comparable heart rates. The peak pressure of isovolumic contractions at the same ventricular end-diastolic pressures averaged 40% higher at the lower temperature. Diastolic pressure-volume relationships were similar at both temperatures. In studies in which the ventricle ejected fluid and performed work the hypothermic ventricle was capable of performing greater work at comparable heart rates, left ventricular end-diastolic pressures, and loading. When the ventricle was allowed to perform work by compressing air into a chamber of constant volume left ventricular oxygen consumption (Vo2) increased with the peak systolic pressure as the temperature was lowered. If the peak systolic pressure was maintained constant by increasing the volume of the air chamber as the temperature was lowered no consistent relationship could be shown between left ventricular Vo2 and the integral of systolic pressure in time which invariably increased with hypothermia.

In the isolated, blood-perfused heart of the dog, left ventricular developed pressure and developed mean wall stress were observed while the ventricle contracted at a constant, nearly isovolumic afterload and while end-diastolic pressure was raised to levels exceeding 100 mm Hg. Coronary perfusion pressure was maintained at the level of the peak systolic pressure. Dilatation of die mitral ring and consequent mitral regurgitation were avoided by left atrial plication. Normalized graphs of percent of peak developed pressure against end-diastolic pressure showed that developed pressure rose abruptly with diastolic pressure, peaked at a diastolic pressure of approximately 30 mm Hg, and declined 14.7% (±0.9 SE) at an end-diastolic pressure of 100 mm Hg. Likewise, developed mean wall stress rose abruptly with diastolic pressure, peaked at a higher diastolic pressure of approximately 50 mm Hg, and declined only 7.5% (±0.8 SE) from this peak at an end-diastolic pressure of 100 mm Hg. Similar findings were observed in hearts acutely depressed with propranolol. Electron micrographs showed sarcomere length to average 2.275fi and 2.300/A in ventricles fixed in diastole while subjected to pressures of 61 and 100 mm Hg, respectively, after potassium arrest, confirming the findings illustrated by the normalized graphs. These observations imply that in the isolated heart of the dog there is no loss of ventricular performance attributable to a descending limb of the Frank-Starling mechanism until the end-diastolic pressure exceeds 60 mm Hg and that this loss is minimal at diastolic pressures as high as 100 mm Hg. ADDITIONAL KEY WORDSsarcomere length supported heart propranolol Frank-Starling developed pressure descending limb isovolumic contraction mean wall stress ventricular circumference developed tension • It is generally accepted that the tension developed by striated muscle during the active state is a direct function of its resting length up to a point at which a further increase in resting length is accompanied by a decrease in developed tension. Recent observers have shown both for cardiac and skeletal muscle strips that an increase in resting length is accompanied by a decrease in developed tension when the sarcomere is stretched beyond 2.2/J L and the H band appears (1-4).In contrast to muscle strips, evidence for a descending limb of ventricular performance in the intact ventricle has been less consistent. Some observers have not been able to find a descending limb at left ventricular enddiastolic pressures far exceeding the physiological range (5-7). In addition, arguments have been presented which imply that the cardiovascular system can support the instability inherent* in a descending limb for only a very short period of time and that such a