Hsueh-Hwa Wang

An experimental study of the immediate hemodynamic adjustments to acute arteriovenous fistulae of various sizes.

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

Experimental coronary arterial occlusion and release: Effects on enzymes, electrocardiograms, myocardial contractility and reactive hyperemia

After less than 1 hour of coronary arterial occlusion, the myocardium suffers irreversible changes as revealed by electron microscopy. Yet, the earliest clinical laboratory indexes of myocardial infarction--elevated serum enzyme levels and significant Q waves on the electrocardiogram--are not detected until at least 6 hours after coronary occlusion. To study the early period after coronary occlusion in the dog, occlusion of the left anterior descending coronary artery for 1 to 3 hours was followed by release, and coronary sinus and venous enzyme levels, the electrocardiogram and myocardial contractility from the infarcted area, and reactive hyperemia were monitored. Coronary sinus enzyme levels rose within 15 minutes after release of occlusion in half of the experiments with 1 to 1 1/2 hours and in all of those with 2 to 3 hours of occlusion, and this rise preceded the rise in venous levels by only 10 to 20 minutes. Significant Q waves appeared 15 to 30 minutes after release of occlusion as the serum enzymes were increasing. Thus, clinically, the delayed appearance of increased serum enzymes and significant electrocardiographic Q waves is probably largely due to a lack of circulation in the infarcted area rather than to prolonged survival time. Also, the venous enzyme level reflects the coronary sinus level minutes later. The presence of viable myocardium in the infarcted area was suggested by elevation of the S-T segment upon reclamping, and by residual myocardial contractility and retained capacity for reactive hyperemia. These findings occurred in some experiments even in the presence of a significant Q wave.

Effects of Changes in Coronary Blood pH on the Heart

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), Na2CO3 or NaHCO3. 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 Na2CO3 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. NaHCO3 infusion caused changes similar to those induced by DMO but of smaller magnitude. It was suggested that the direct effects of DMO and NaHCO3 are attributable to intracellular acidosis, whereas those of THAM and Na2CO3 are attributable to intracellular alkalosis.

The effect of atrial and ventricular tachycardia on cardiac output, coronary blood flow and mean arterial blood pressure.

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.

Effects of synthetic parathyroid hormone on hemodynamics and regional blood flows.

In pentobarbital anesthetized dogs, synthetic bovine parathyroid hormone, containing the amino terminal 34 amino acids (bPTH-(1-34] in doses of 0.1-0.8 microgram/kg i.v. caused dose-related decrease in arterial blood pressure, increase in cardiac output and prominent reduction of total peripheral resistance. Marked increase of coeliac, coronary and renal blood flows and decrease of vascular resistances in these beds occurred. Mesenteric and iliac blood flows usually decreased. Changes in mesenteric resistance were minimal while iliac resistance increased substantially. The increase of renal blood flow was still obvious 10-20 min or longer after arterial blood pressure had returned to control levels. Mesenteric and iliac vasoconstriction were attributable to reflex increase in sympathetic activity since some decrease in resistances in these beds were seen in response to bPTH-(1-34) after ganglionic blockade. Renal vasodilation was not related to a prostaglandin mechanism as similar dilation occurred after prostaglandin synthesis inhibition with indomethacin. In summary, bPTH-(1-34) has prominant effects on the circulation, and does not affect all vascular beds similarly. The exact mechanism of the vasodilating action of bPTH remains to be elucidated.

A Study of the Usefulness and Limitations of Electrical Countershock, Cardiac Massage, Epinephrine and Procaine in Cardiac Resuscitation from Ventricular Fibrillation

The efficacy of electrical countershock, cardiac massage, epinephrine and procaine in stopping ventricular fibrillation and restoring a competent ventricular contraction was studied in anesthetized dogs. It was found that countershock is a reliable means of stopping fibrillation. However, it must be preceded by cardiac massage if not applied promptly after the initiation of fibrillation. Epinephrine helps restore a competent ventricular contraction once fibrillation has been stopped by countershock but it increases the incidence of recurrence of fibrillation. The doses of procaine which constitute a reliable means of stopping fibrillation depress the rhythmicity of the heart to such an extent that the cessation of fibrillation is followed by prolonged periods of cardiac standstill.

An Experimental Study on Intercoronary Reflexes

There is no evidence in the anesthetized dog that occlusion of one of the three coronary arteries leads to vasoconstriction in the vascular areas irrigated by the other two arteries. On the contrary, occlusion of one coronary artery appears to lead to a decrease in the resistance of the two adjacent vascular beds in most experiments. The mechanisms and the implications of this effect are discussed.

Effect of Acute Experimental Aortic Stenosis on Coronary Circulation

Acute experimental aortic stenosis was produced by a special instrument in dogs anesthetized with morphine and chloralose. The effect of aortic stenosis was compared to aortic constriction distal to the coronary ostia in 45 matched runs in 12 dogs. In 10 pairs of matched runs in eight dogs, coronary oxygen A-V difference was measured. The runs were matched as to duration, heart rate, and rise in left intraventricular systolic pressure. With the increase in left intraventricular systolic pressure, the mean arterial blood pressure did not change significantly, and the left ventricular output either remained the same or decreased only slightly. The coronary sinus outflow increased in all runs of aortic stenosis as well as in aortic constriction. The coronary oxygen A-V difference tended to increase in aortic stenosis and to decrease in aortic constriction. The rise in coronary blood flow in aortic stenosis was due to vasodilatation alone, since the perfusion pressure remained the same and there was an increase in extravascular compression; in aortic constriction, the increased coronary blood flow was best explained by increased coronary perfusion pressure.

Isolating the Total Coronary Artery Inflow for Administering Pharmacologic Agents New Method Without Coronary Dissection.

Summary In anesthetized open-chest dogs, a relatively simple method is described for isolating total coronary artery inflow without coronary dissection by using a specially designed double lumen cannula. The small lumen is used for injecting pharmacologic agents into the coronary artery inflow; the large lumen permits direct measurement of left ventricular output. The method can be modified for studying the aortic arch receptors.

Effects of Intravenous and Intracoronary tham on Coronary Blood Flow

Dogs weighing 17 to 24 kg were given 1 mg/kg of morphine sulfate intramuscularly and anesthetized 30 minutes later with 100 mg/kg of chlorolose intravenously. Under artificial ventilation, the left chest was opened and the heart suspended in a pericardial cradle. The method for isolating the total coronary artery inflow and measurement of left ventricular output was previously described (Blumenthal et al. 1963). A diagram is shown in Fig. 1. Briefly, a specially designed double-lumen cannula was passed retrograde from the descending thoracic aorta into the left ventricle. The aorta was tied around the cannula proximal to the origin of the brachiocephalic artery. Coronary ostea were located in the isolated segment of the aorta between the ligature and the aortic valve. The coronary arteries were perfused by blood entering the isolated segment around the outside of the cannula during systole. The capacity of this isolated segment, 3 to 7 ml, was more than adequate for perfusion of the coronary artery during the entire cardiac cycle. A small inner tube of the cannula ended in this isolated segment and injections through this tube mixed only with the total coronary artery inflow. The left ventricular output was directed through the large lumen of the cannula, a Hufnagel valve, a Shipley-Wilson rotameter and then returned into