In the past thirty years, numerous observations have been made on the hemodynamic effects of arteriovenous fistulae. Arteriovenous fistulae of variable size and location have been studied in patients as well as in animals. Such studies have consisted a) in observing the effect of suddenly opening and closing a fistula in acute experiments, b) in studying the effects of suddenly closing and opening a fistula in an animal or a patient who had had such a fistula for a relatively long time, and c) in recording the effect of complete surgical eradication of a long-standing fistula. While some agreement has been reached on many points, there persists some controversy about most of them (1). It is now generally agreed that an acute as well as a chronic arteriovenous fistula increases the cardiac output (1-8). However, Lewis and Drury (9) came to the conclusion that the cardiac output is not increased unless the arteriovenous shunt is very large. Van Loo and Heringman (10) concluded that acute arteriovenous fistulae increase the cardiac output although the flow of blood in certain vascular areas outside the fistula circuit is decreased. The venous pressure is definitely increased near the site of the arteriovenous communication, but most investigators have found that the increment of venous pressure decreases rapidly as the pressure is measured further down the venous bed toward the right atrium, and in the venae cavae and right atrium the pressure is elevated little or not at all I This work was made possible by a grant-in-aid from the New York Heart Association, the Sidney A. Legendre Gift, and the Charles A. Frueauff Gift. It was presented at the Annual Meeting of the American Physiological Society in New York City in 1952.2Fellow of the New York Heart Association. (3, 4, 11). However, one group of workers (12) has reported more striking increases of right atrial pressure in dogs with an arteriovenous fistula. The blood volume seems to be increased by an arteriovenous fistula of a certain size and duration (3, 13) although some observers (4) suggest that this increase in blood volume occurs only in the presence of an incipient or frank cardiac failure.Since the magnitude of the effects of an arteriovenous fistula would seem a priori to depend upon the volume of blood shunted through the abnormal pathway, it is rather surprising that in no study has any attempt been made to measure simultaneously the rate of flow through the fistula and the other functions of interest such as cardiac output, arterial and venous pressures. The present study was undertaken in an attempt to determine the acute cardiovascular adjustments to arteriovenous fistulae of different sizes, by recording simultaneously and continuously the flow of blood through the fistula, the flow of blood into the systemic circulation exclusive of the arteriovenous fistula circuit, the mean arterial blood pressure and the mean central venous pressure. METHODSFifteen dogs weighing between 13 and 28 kilograms were anesthetized by the intravenous infusion of 100 m...

The effect of electrically induced auricular and ventricular tachycardia of various rates was studied in the anesthetized dog. When, the control heart ranging between 140 and 190 per minute, atrial tachycardia of a rate only slightly higher than the control rate was induced, a very temporary initial decrease in arterial blood pressure, cardiac output and coronary blood flow occurred, then all three parameters essentially returned to control level. With atrial tachycardia of a higher rate, blood pressure, cardiac output and coronary flow fell more markedly, then blood pressure and cardiac output rose to or toward control level, remaining below control level with higher rates of tachycardia, whereas the coronary flow rose to or above control level and only exceptionally remained below control level. Ventricular tachycardia had essentially the same effects as atrial tachycardia, but a ventricular tachycardia of a given rate had the same quantitative effect as an atrial tachycardia of a higher rate.A LTHOUGH there has been a great deal of work on the effect of changes in heart rate on the coronary circulation, most of it has been done on artificial preparations such as the isolated heart or the heart-lung preparation. Since under average cardiovascular conditions, more coronary flow occurs during diastole than during systole, it would be expected that, within certain Limits, an increase in heart rate per se would tend to decrease the amount of coronary flow per minute, and a decrease in heart rate would tend to increase it. This was proved to be correct by Anrep and Hiiusler 1 who found that an increase iu heart rate decreased the coronary flow in the heart-lung preparation in which a coronary artery was perfused under constant pressure. However, these authors also found that if the heart rate was so high that each beat became very weak, the decrease in coronary flow, due to the relatively greater shortening of diastole than of systole, might be offset by the decrease in the restriction of flow due to systole, and that the coronary flow might remain unchanged or even increase instead of decreasing as the heart rate increased. On the other hand, in experiments by Anrep and King 2 on the denervated heartlung preparation, and by Anrep and Segall 3 on the innervated heart-lung preparation, changes in heart rate within wide limits were found to have no effect on the coronary flow. Different results were later reported by Hausner, Essex, Herrick and Mann,4 who obseryed that an increase in coronary flow resulted from an increase in heart rate in the denervated heart-lung preparation. Wegria and Keating 5 reported that an increase in heart rate in the anesthetized dog produced a very temporary decrease in coronary flow followed by a rise above control level within wide ranges of tachycardia. More recently, Laurent, Bolene-Williams, Williams and Katz 0 studied the effect of heart rate on the coronary circulation in a preparation in which the output of the right ventricle consisted only 624

1. The effect of adenosine on left ventricular contractility and developed tension was studied in the anaesthetized intact dog. Normal and propranolol-treated animals were used. Adenosine was infused through a catheter into one of the two main branches of the left coronary artery, usually the circumflex branch. The rate of infusion was 150 x 10(-9)M/min. The infusion was maintained during 50 min.2. In both series of animals, no change was observed in the heart rate, aortic pressure, left ventricular end-diastolic pressure, time from onset of left ventricular contraction to peak dP/dt, peak dP/dt and left ventricular tension-time index. It is concluded that a regional increase in adenosine concentration in the left ventricular wall has no inotropic effect when the adrenergic mechanisms are normal or depressed.3. The myocardial blood flow response to adenosine was determined at the 10th, 30th and 50th min of the infusion by the radioactive inert gas method. At the 10th min of the infusion, the myocardial blood flow averaged three times the control value in both series of dogs. Thereafter, the flow response remained stable in the normal dogs but declined at the 50th min of the infusion in the propranolol-treated animals. It is suggested that autoregulation of the coronary circulation in response to overperfusion of the myocardium at constant cardiac work may be enhanced at the lower myocardial oxygen requirements of the propranolol-treated dogs while, in the normal animals, it was insufficient to overcome the potent coronary dilator action of adenosine.

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