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Central venous oxygen saturation (CVSO2) was measured in 31 patients with myocardial infarction. CVSO2 correlated well with the patients' clinical course. In those patients not in heart failure, mean + SEM for CVSO2 was 70 + 1%. When heart failure was present, CVSO2 averaged 56 + 1%. When both heart failure and shock were present, CVSO2 averaged 43 + 1%. In nine patients, serial determinations of arterial oxygen saturation and CVSO2 were made. In 22 of 26 instances, either a fall in CVSO2, was accompanied by an increase in the arteriovenous oxygen saturation difference or an increase in CVSO2 was accompanied by a decrease in arteriovenous oxygen saturation difference. Serial measurements of CVSO2 appear to be a useful method of monitoring changes in myocardial function in patients with myocardial infarction.Additional Indexing Words: Mixed venous oxygen saturation Central venous pressure MEASUREMENT of cardiac output and intracardiac pressures is used to assess myocardial function in the catheterization laboratory.

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The release of norepinephrine from the heart of anesthetized open-chest dogs has been determined both after the intravenous administration of guanethidine (15 mg/kg) and after reserpine (3 mg/kg) by measuring the plasma norepinephrine concentration with the fluorometric method (THI) in bloods obtained simultaneously from the coronary sinus and femoral artery. In four dogs following the administration of guanethidine, norepinephrine release into the coronary sinus blood occurred and persisted for two to three hours. This release of norepinephrine was accompanied by and adrenergic response of similar duration. The norepinephrine content of atrial appendage was reduced by 24% of control at four hours in these dogs and to extremely low levels in three other dogs 24 hours after guanethidine administration. Thus, the reduction of the tissue content of norepinephrine continued after measurable release of norepinephrine into the coronary sinus blood had ceased. In four dogs following reserpine administration the adrenergic response was consistently smaller, and detectable release of norepinephrine into the coronary sinus blood was found transiently only in one dog. However, the norepinephrine content of atrial appendage was reduced by an average of 65% of control values at four hours. These findings suggest a difference in the mechanism of norepinephrine depletion in the period immediately after administration of guanethidine and reserpine.

SUMMARYThe mechanism by which magnesium affects digitalis-induced arrhythmias was studied in dogs with and without beta-receptor blockade. Digoxin was infused at a rate of 2.5,ug/kg/min until ventricular tachycardia developed, then half the animals were given MgSO4, the other half saline. In animals given MgSO4, sinus rhythm was immediately re-established; in animals given saline, ventricular tachycardia persisted. In animals with beta-receptor blockade, MgSO4 was as effective in abolishing ventricular tachycardia as in those without beta-receptor blockade. We found no evidence that magnesium re-activated digoxin-inhibited (Na+, K+)-ATPase, altered myocardial or microsomal digoxin binding, or acted via the autonomic nervous system. Magnesium's direct effect on calcium and potassium fluxes across the myocardial cell membrane may be the mechanism of its antiarrhythmic action in digitalis-toxic arrhythmias.MAGNESIUM has been shown to be effective in the treatment of cardiac arrhythmias brought on by digitalis in man and experimental animals.1-4 The mechanism by which magnesium affects digitalistoxic arrhythmias has not been clearly demonstrated. Seller and coworkers3' 5 suggested that magnesium reverses digitalis-induced inhibition of membranebound sodium, potassium, adenosine triphosphatase (Na+, K+ )-ATPase, thought to be the " digitalis receptor" involved in both the arrhythmogenic and inotropic effects of digitalis.6`9 Magnesium-deficiency is associated with increased myocardial digoxin uptake;10 hypermagnesemia might, therefore, decrease digitalis uptake by the heart. Magnesium decreases potassium efflux and intracellular calcium"' and might thereby offset the toxicity of digitalis. In addition, by interfering with the effects of calcium, magnesium causes autonomic blockade12 which might influence digitalis-toxic arrhythmias.The present investigation was, therefore, designed to determine magnesium's mechanism of action in arrhythmias induced by digitalis toxicity. Our studies demonstrate no evidence of magnesium reactivation of digoxin-inhibited (Nal, K+)-ATPase, or displacement of digoxin from the heart, or of change in