William F. Hamilton

Relation Between Coronary Sinus Plasma Potassium and Cardiac Arrhythmia

Infusion of insulin glucose which reduces the level of potassium in the coronary sinus blood will prolong the life of dogs after coronary ligation.

Functional Cardiac Deterioration During Development of Hemorrhagic Circulatory Deficiency

A massive infusion test has been devised to evaluate the functional capacity of the heart. In five dogs extensive surgical procedures followed by episodes of arterial hypotension at 30 mm Hg and lasting 90 minutes caused severe cardiac incapacity, which was demonstrated by failure of rate of cardiac work to increase throughout the infusion together with a large rise in left atrial pressure. This incapacity was not evident in tests made immediately after the hypotensive episode. The damage became more and more severe in tests performed 90 and 150 minutes after the end of the hypotension even though mean arterial pressure was maintained at 100 mm Hg. Operated control dogs did not show cardiac deterioration in tests timed as above. The rate of cardiac work continued to increase throughout the infusion with a relatively small rise of left atrial pressure. In a series of five dogs, flow to the coronary arteries and to those supplying the head and forelimbs was maintained by normal blood pressure while the rest of the animal was made hypotensive for 90 minutes. The arterial pressure in the whole animal was then returned to an average level of 100 mm Hg. Tests made at intervals after the hypotension showed equivocal evidence of cardiac deterioration. In another series of four dogs, prepared as above, the partial hypotension lasted 150 minutes before the arterial pressure was returned to normal. Tests at intervals after hypotension showed cardiac damage in all the animals and severe damage in three. Evidence is presented indicating that the peripheral vascular bed had deteriorated functionally as a result of 150 minutes of partial hypotension.

Physical Effects of Increased Venous and Extrarenal Pressure on Renal Vascular Resistance

The oil perfused kidney preparation was used to determine the passive effects of increased venous and extrarenal pressure on renal vascular resistance. The dimensional tube factor of renal resistance varied inversely with the arteriovenous pressure gradient because this pressure difference also determined the pressure difference across the walls of the intrarenal vessels.

Study of Spontaneous Congestive Heart Failure in the Dog

Spontaneous cardiovascular disease has been found in dogs from the Savannah River Valley area, predominantly in the male house pet and hunting dog. The causes have been Dirofilariasis, chronic mitral valvular disease, and congenital cardiovascular defects. Cardiac stress in these dogs caused marked salt and water retention, increased blood volume, increased central venous and right heart pressures, and cardiac dilation and hypertrophy. These compensatory mechanisms were similar to those in man. Cardiac dilation was more pronounced in spontaneous failure than in experimental failure. Regression of cardiac dilation was very slow even after apparent compensation and clinical improvement. Plasma protein concentrations were decreased, but total extracellular protein mass was markedly increased. Sodium and potassium plasma concentrations were within normal range. Hyponatremia was occasionally observed in dogs as in man.20 Dirofilariasis was characterized by marked pulmonary hypertension, caused primarily by pulmonary vascular changes rather than mechanical blockage. There was massive hypertrophy of the right ventricular myocardium. Heartworm dogs in congestive failure have a similar range of right heart pressure to experimental pulmonic stenosis dogs in failure.21 Cage rest was of little therapeutic value in these dogs in congestive failure. Clinical response and physiological changes were remarkable with the use of saltabsorbing resin or digitalis compounds causing negative sodium balance. Digitalization of the dog required vigorous individual treatment controlled by clinical symptoms and P-R interval of the electrocardiogram. Acquired tolerance to digitalis required increased dosage levels every few months. The veterinary practitioner who recognizes the necessity of individual digitalization and the importance of detection and removal of thoracic fluid will be rewarded with improved clinical therapy of congestive heart failure. Experimental dogs during periods of severe cardiac stress can benefit from adequate digitalization. The similarity of biochemical and physiological changes in spontaneous heart disease, as it occurs in man and in dogs, affords an avenue for clinical research. This applicability to man is enhanced because the dog can be more comprehensively studied.

Acute Effects of Cardiac Glycosides on Aldosterone Secretion in Dogs with Hyperaldosteronism Secondary to Chronic Right Heart Failure

A marked elevation in the rate of aldosterone secretion was observed in eight dogs with experimental congestive heart failure secondary either to controlled progressive pulmonic stenosis or to combined tricuspid insufficiency and pulmonic stenosis, and in one dog with spontaneously occurring congestive heart failure. In the dogs with pulmonic stenosis, digitalization with digoxin resulted in improvement in cardiovascular function, and subsequent further constriction of the pulmonary artery again led to right ventricular failure; in each animal aldosterone output decreased within 90 minutes after digitalization, and increased markedly within one hour after further constriction of the pulmonary artery. In the dog with naturally occurring congestive heart failure, ouabain administration caused a similar striking hemodynamic improvement, and a marked reduction in aldosterone secretion was observed within 55 minutes after the glycoside was given. In the dogs with combined tricuspid insufficiency and pulmonic stenosis, no hemodynamic improvement occurred after digitalization; in these animals, the aldosterone secretion rate did not change significantly during the two-hour period following the digoxin injection. These data demonstrate that changes in the rate of aldosterone secretion in dogs with right heart failure were closely correlated with alterations in cardiovascular function; in these animals, hemodynamic improvement consistently led to decreased aldosterone production, and subsequent worsening of cardiovascular function resulted in increased aldosterone output.

Cardiovascular response to graded exercise in the sympathectomized-vagotomized dog.

Seven dogs who ran well on a motor-driven treadmill were completely sympathectomized (including adrenal denervation) and subjected to unilateral vagotomy below the recurrent laryngeal branch. After recovery and retraining, a terminal experiment was performed in which, after completing the vagotomy, direct Fick determinations of cardiac output and continuous recordings of mean arterial pressure, heart rate, and oxygen consumption were made at rest and during increasing exercise The results were compared with those described by Barger et al. ( Am. J. Physiol. 184: 613, 1956) for normal dogs running at smaller speeds and grades. The heart rate of the operated dogs increased from 117 to 134. Bargers normal dogs doubled their heart rate. The A-V oxygen difference increased with work slightly less than Bargers normal dogs but the scatter in both groups was wide, as was the case with the stroke volume. The resting cardiac output was nearly normal in the operated dogs but increased only 34% with exercise, as against 200–300% in Bargers normals. Oxygen consumption increased about twofold as against the expected normal of three- to sevenfold. Peripheral resistance in both groups went down about 40%. The blood pressure in the normal increased substantially while that in the operated dogs fell about 20% to an average of 60 mm Hg.

Intrathoracic Volume Changes in Relation to the Cardiopneumogram

The outflow of blood from the chest during the phases of the cardiac cycle is found to be nearly equaled by a phasic inflow. The net volume change exerts very small pressure changes in the intrathoracic (intrapulmonary) air. This is not due to the distensibility of the chest wall because when allowance is made for this factor and the intrathoracic blood volume change is calculated, it is found to be a very small fraction of the stroke volume.

Electrocardiographic changes during development of right ventricular hypertrophy in the dog

Abstract Dogs with surgically induced volume overload of the right ventricle were studied for progressive electrocardiographic changes over postoperative periods as long as 4.5 years. Right ventricular hypertrophy was evaluated at autopsy. Progressive electrocardiographic changes were observed in (1) an increasing ratio of R wave voltage to that of the total RS excursion in V 1 ; (2) RS configurations, which appeared progressively farther toward the left side of the chest in the V leads, and (3) the earliest vectors of depolarization, which shifted toward the sternum or left anterior quadrant of the chest. Possible diagnostic use of these findings is discussed.