With the use of a strain-gauge plethysmograph, the effect of a brief (0.3 sec) contraction of the forearm muscles on forearm blood flow has been studied in eight healthy adults. An increase in flow due to dilatation of the muscle vessels could be detected within a second after the completion of the contraction. This increase was proportional to the strength of the contraction. The blood flow was maximal immediately and decreased rapidly. A second contraction of the same magnitude made during the period of increased flow caused an additional increase in flow. The maximal increase in flow caused by a strong brief contraction was only about 25% of that recorded after strong repeated rhythmic contractions or a sustained contraction. Cervical sympathectomy did not change these findings, indicating the local nature of the response. Since breathing oxygen failed to reduce the dilatation for a given strength of contraction, it is unlikely that oxygen lack was the stimulus for vasodilatation. The oxygen saturation of blood that drained the muscles could not be determined accurately immediately after contraction because at this time, muscle venous blood was contaminated by venous blood from the skin. exercise-induced vasodilatation; local mechanism of vasodilatation; venous O2 saturation during muscle contraction; brachial arterial pressure during vasodilatation; speed of muscle vasodilatation Submitted on May 8, 1963

Although ethyl alcohol has a long medicinal history (1), its precise effects on the cardiovascular system have not been defined. Acute alcohol ingestion is known to result in triglyceride accumulation in the liver, which appears dependent upon an intact sympathetic nervous system (2). Evidence for stimulation of this system after ethanol ingestion has been advanced (3). Since sustained catecholamine infusion has been associated with lipid accumulation in the myocardium (4, 5), a study of the acute effects of ethanol on myocardial metabolism and function has been undertaken in animals considered nutritionally normal. The quantity given produced blood level concentrations usually associated with moderate intoxication. MethodsMongrel male dogs weighing 19 to 22 kg were anesthetized 18 hours postprandially with morphine sulfate, 3 mg per kg, and pentobarbital (Nembutal), 12 mg per kg, and studied without opening the chest. After insertion of an endotracheal tube, respiration was regulated with a Harvard respiratory pump, facilitating the maintenance of arterial oxygen saturation and pH in the normal range. Catheters were placed in the coronary sinus, pulmonary artery, aorta, and left ventricle for blood sampling and pressure determinations. Although initially the catheters were filled with dilute heparin, slow saline infusions or intermittent flushes were used during the experiment to maintain their patency. Since the level of arterial free fatty acids did not rise during the experiment, the earlier limited use of heparin did not appear to affect substrate concentrations.During the evaluation of cardiac performance in the intact animal in experiments of many hours duration, a direct measurement of contractility utilizing the forcevelocity relationship is not feasible, but less direct methods may be employed to characterize myocardial function. Thus, contractility change has been deduced from the relation of stroke output to left ventricular end-diastolic pressure (LVEDP) (6, 7).Sympathetic stimulation of isolated papillary muscle analyzed in terms of the force-velocity relationship has revealed an enhanced velocity of muscle shortening, representing a primary contractility increase (8). Sympathetic stimulation of the intact heart under conditions of controlled heart rate, before and after loading, has evoked an increase of stroke output as well as dp/dt maximum of left ventricular pressure as manifestations of primary contractility increments (9).A rise in LVEDP is normally associated with a corresponding stroke output increment (9), presumably a reflection of the rise in maximal isometric force without a velocity change that attends increased length of papillary muscle (8). The failure of stroke output to rise in this situation would appear to represent impaired muscle function (6,9,10) particularly when the duration of systole is prolonged or unchanged (6). In this present study the ventricular ejection rate was analyzed in terms of ventricular systolic duration and the maximal rate of rise of left ventricular pres...

Cardiac output was measured simultaneously with blood flow in hand and forearm in eight healthy subjects before and during body heating. The heating was carried out by immersing the feet and legs in water at 44 C. and wrapping the body with blankets. After 50 min of heating the oral temperature had risen to between 99.5 and 100.8 F. The cardiac output had increased by 1.9—4.5 (mean 3.3) liters/min, mainly because of an increase in heart rate. The blood flow through the fingers increased rapidly to reach maximal values soon after heating started, whereas the forearm blood flow, like the cardiac output, increased gradually throughout the heating period. Since the increase in limb blood flow is confined to the skin vessels and since there is no evidence that flow to the internal organs is increased, the total increase in skin flow amounts on the average to 1.8 liters/m2/min. Submitted on June 2, 1961

These findings are of practical importance for the correct interpretation of coronary arteriographies and in the field of coronary artery surgery.