It has been known that exercise causes an increase in the coronary blood flow in animals. The present work has been carried out to study the effect of exercise on coronary blood flow and myocardial oxygen consumption of the human heart in vivo. The results indicate that the heart responds to the increased load of exercise with a rise in coronary blood flow. Since the arteriovenous coronary oxygen difference shows little change, the increase in oxygen consumption of the heart muscle is primarily the result of an increased coronary blood flow. As the cardiac work rises more than the myocardial oxygen consumption, the left ventricular efficiency increases. The response of the failing heart muscle to acute increases in load produced by exercise does not differ from that of the normal heart or of the isolated heart. C ATHETERIZATION of the coronary sinus in man in conjunction with the nitrous oxide method has made it possible to determine coronary blood flow and myocardial oxygen consumption in man.1'2 Until now, the method has been used to follow the behavior of human heart muscle of resting individuals only.3 A study of the coronary circulation and myocardial oxygen consumption during exercise would appear to be of interest, because exercise constitutes a temporary increase in load to which the heart must adjust itself by coronary circulatory and metabolic changes. The alterations in the coronary circulation and myocardial oxygen consumption are of particular importance since it is during in-

Compression of the neck of the sitting subject caused increase in urinary sodium output without change in glomerular filtration (creatinine clearance) or apparent cardiac output (electrokymograph). The possible existence of an intracranial mechanism sensitive to alterations in volume of extracellular fluid and regulating the volume of extracellular fluid is suggested. P REVIOUS studies from this laboratory,',' have indicated: (a) that under comparable conditions the urinary excretion of sodium, like that of chloride' and of water,4 is less in the sitting than in the recumbent position, and (b) that compression of the neck of the sitting subject may cause increase in sodium excretion. Since renal clearances were not measured, the previous work provided no evidence concerning the relative importance of alterations in filtration and in reabsorption.The purposes of the present communication are to extend the previous observations, particularly in relation to: (a) investigations of glomerular filtration and cardiac output, (b) studies of the excretion of chloride and of potassium, as well as of sodium and water, and (c) measurements during congestion of the head under different circumstances (induced by tilting the body or by compression of the neck of the recumbent subject). It is hoped that such observations may furnish information concerning some of the mechanisms regulating sodium excretion under physiologic conditions, in order that these mechanisms may later be investigated in patients with circulatory disorders. METHODS The subjects were normal males, aged 22 to 30. Various attempts were made to maintain

Removal of small amounts of blood from sitting subjects caused reduction of sodium excretion without alterations in creatinine clearance, or in apparent cardiac output (electrokymographic method). This reduction could be prevented by compression of the neck. The experiments support the concept of an homeostatic central mechanism which regulates the volume of extracellular fluid by altering sodium excretion. If such a mechanism exists it is apparently activated by changes in the volume of body fluids rather than by changes in cardiac output.P REVIOUS studies'-3 have shown that compression of the neck causes increased urinary excretion of sodium in the sitting position, but has little or no effect in the recumbent position. Marked decline in urinary sodium, which ordinarily occurs in the sitting as compared to the recumbent position, can be partially although not completely prevented by compression of the neck. The data were interpreted as indicating the probable existence of some central mechanism concerned in the regulation of electrolyte excretion, apparently set into operation by alterations in the volume of fluid in the cranial cavity or by some closely related factor. The present study is the first of a number aimed at further elucidating the nature of the mechanism. METHODSGeneral Plan of Experiments. Normal healthy young men were bled, and measurements of electrolyte excretion and glomerular filtration rate were made. The symptoms were observed, and blood pressure and pulse rate were measured before and after bleedings. Observations of the effect of bleeding on the apparent cardiac output (electrokymographic method) were also made.In the beginning, there was some doubt as to how much blood needed to be removed in order to produce alterations in the excretion of sodium. Hence a series of preliminary experiments was done, and it was found that the amount of bleeding needed to produce changes varies markedly with posture ( fig.

No abstract

A patient is presented with an arteriosclerotic abdominal aneurysm that ruptured into the inferior vena cava. Clinically, the picture was that of a peripheral arteriovenous communication with heart failure of the "high-output" type. Intestinal bleeding occurred as a result of venous engorgement and hemorrhagic colitis.ANEURYSM of the abdominal aorta is a rare finding. abdominal tenderness to deep palpation with some abdominal distention, and was expelling large amounts of gas both by mouth and by rectum. At this time it was thought that the patient had diverticulitis with partial intestinal obstruction. He was hospitalized and x-ray studies were made. These revealed numerous distended loops of small bowel. There was a moderate amount of gas within the colon, with a distended loop in the left upper quadrant. There was a rounded area of calcified density in the right upper quadrant which suggested a gallstone. No fluid level was seen. No other masses or soft tissue shadows were visible. X-ray findings were thought to be compatible with intestinal obstruction. He was treated with penicillin, streptomycin, and sulfathalidine. He improved on this regime but continued to have some lower abdominal cramping. On the third hospital day he was discovered to have an abdominal mass about the size of an orange. This was situated a little more to the right of the midline than to the left. During the next few hours the mass increased in size and a continuous murmur over it was noted. The next morning an associated continuous thrill was found over the mass. It was thought at this time that the mass represented aneurysmal dilatation with an arteriovenous communication, most likely between the aorta and the inferior vena cava. The blood pressure was 140/40 and there was a typical Corrigan pulse.Four days later bleeding from the rectum occurred but this promptly subsided following the administration of morphine. During the remaining six weeks of his life there was constant severe anorexia, and, after taking food, nausea would become evident. In addition, he developed progressive right-sided heart failure which responded poorly to digitalis and mercury. All the typical signs of a high cardiac output were present during this time. The loud continuous murmur and the pronounced thrill continued to be present over the abdominal mass. He became progressively more edematous in spite of therapy, and it finally became necessary to make puncture holes in his legs to allow the fluid to drain. This procedure was associated with a 30 pound weight loss. However, he continued to lose strength as the result of starvation.