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
The effects of localized acidosis and alkalosis on coronary blood flow, myocardial contractile force, and heart rate were studied in anesthetized, open-chest dogs. Acidosis of the coronary vascular bed was induced by infusion of 5,5-dimethyl-2, 4-oxazolidinedion (DMO) into the total coronary artery inflow, and alkalosis by infusion of tris hydroxymethyl aminomethane (THAM), Na 2 CO 3 or NaHCO 3 . DMO infusion caused an initial slight increase of coronary blood flow, followed by a decrease. The decrease was accompanied by and attributed to a moderate to marked decrease of myocardial contractile force and bradycardia. THAM and Na 2 CO 3 infusion caused a marked increase of coronary blood flow, associated with a decrease of coronary oxygen A-V difference, indicating coronary vasodilation. A slight to moderate increase of myocardial contractile force but little or no change in heart rate was noted. NaHCO 3 infusion caused changes similar to those induced by DMO but of smaller magnitude. It was suggested that the direct effects of DMO and NaHCO 3 are attributable to intracellular acidosis, whereas those of THAM and Na 2 CO 3 are attributable to intracellular alkalosis.
Efferent vagal stimulation in the anesthetized dog with constant ventricular rate caused either no change in coronary sinus outflow and cardiac work, or a decrease in coronary sinus outflow associated with a greater decrease in cardiac work. When the decreases were observed they could best be explained by a negative inotropic effect of vagal stimulation on ventricular muscle, rather than by a direct vasomotor effect of vagal stimulation on the coronary bed. Critical review of apparent divergent results previously reported regarding the effect of vagal stimulation on coronary flow reveals that they are not inconsistent with the above hypothesis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.