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Pressure-induced homeometric autoregulation (HAR) has been demonstrated by many investigators in the mammalian ventricle; In isolated cardiac muscle, however, several investigators have reported the opposite effect (anti-HAR); namely, that the first beat after a transition from isotonic to isometric contraction is the most forceful, with a decline over several beats to a steady state. In the present study we find that trabeculae from the canine right ventricle demonstrate either HAR or anti-HAR, depending on the rate of stimulation, the calcium level, and the temperature. Higher calcium, higher temperature, and lower rate of stimulation produce either less HAR or more anti-HAR. When only temperature and rate of stimulation are varied, in each muscle there is a unique rate for each temperature above which HAR occurs and below which anti-HAR occurs.

Myoglobin levels were assayed in each urine specimen voided during 12 hours before and 48 hours after routine cardiac catheterisation in 146 patients using an indirect haemagglutination method detecting concentrations in excess of 0.015 mg/ml. Myoglobinuria was found in only one patient before but in 39 patients after cardiac catheterisation (27%), either in the first (34 patients) or the second (5 patients) post-catheterisation urine sample. Once detected, myoglobin was present in all subsequent urine specimens for the next 3 to 22 hours (mean 11.8 hours). The mean amount excreted +/- SE was 14.0 +/- 1.6 mg (range 2.6 to 30 mg) excluding the one patient with myoglobinuria before catheterisation. This patient, who had severe aortic stenosis and atherosclerotic heart disease, excreted 130 mg myoglobin. Patients with myoglobinuria required longer screening time to complete the procedures undertaken than those in whom myoglobin was not detected--15.6 +/- 1.4 and 11.1 +/- 0.6 minutes, respectively (mean +/- SE:P less than 0.01). We conclude that myoglobinuria is not uncommon after cardiac catheterisation, and that though the myoglobin detected may be released from skeletal muscle, it could be partly or wholly of cardiac origin and indicate transient, and presumably reversible, myocardial injury.

We studied myoglobin excretion in 33 patients admitted to the coronary care unit with a provisional diagnosis of acute myocardial infarction. Sixteen proved to have definite and uncomplicated acute myocardial infarction and 17 possible infarction, using WHO criteria. For 5 days after admission, aliquots of every urine specimen voided by each patient were analysedfor myoglobin using an immunochemical method able to detect a minimum urinary myoglobin concentration of 0-02 mg/ml. Myoglobinuria was detected in 14 of the 16 patients with definite infarction but was not found in any of the 1 7 patients with possible infarction. There were 3 patterns of myoglobin excretion. In 8 of the 14 patients it was excreted in one episode starting 10 to 40 hours after the onset of chest pain and lasting for 5 to 45 hours. In 3 of the remaining patients it was excreted over a much longer period (mean 83 hours) and in the final 3 patients myoglobinuria occurred in 2 or 3 intermittent episodes with periods of between 10 and 20 hours during which it was not detected. Total myoglobin excretion, which varied between 2 and 100 mg (mean 51 mg), did not correlate with peak serum enzyme levels. We concluded that in the appropriate clinical setting, the finding of myoglobinuria provides additional evidence for a diagnosis of acute myocardial infarction. The variable myoglobin excretion pattern suggests that in seemingly uncomplicated myocardial infarction there is considerable variation between patients in the pattern of evolution of the infarction process. This may be relevant to the assessment of measures directed towards limiting infarct size.