David E. Donald

Comparison of aortic and carotid baroreflexes in the dog

1. Experiments with vascularly isolated, blood‐perfused aortic arch and carotid sinus preparations in sixteen dogs have provided evidence which suggests that, in the reflex regulation of normal arterial blood pressure, the aortic and carotid baroreflexes are not equivalent.

Estimation of Coronary Blood Flow by Washout of Diffusible Indicators

In 13 canine hearts, 158 disappearance curves for 133Xe and antipyrine-1125I, given by intra-arterial slug injection, were recorded at a wide range of perfusion rates. Flow rates (ml/100 g/min) calculated from these curves by a variety of methods were compared with measured flow rates (Fa) per weight of perfused tissue. Perfusion of isolated, supported hearts and of anterior descending coronary arteries in open-chest dogs provided similar data. The semilogarithmic slope of curves from apex or whole heart decreased with time, particularly at high flow rates. There was a small, consistent difference in shape between antipyrine and xenon curves, suggesting that radioactivity in fat contributed somewhat to this tailing. Estimation of flow rate from the steepest semilog slope yielded an average value of 1.1 Fa for all rates; estimation from slope at 30% of peak radioactivity gave 0.9Fa. The curves were closely described by a two-exponential equation which gave flow estimates of 0.95Fa when collimation limited the observations to the heart apex, and lower values when the whole heart was observed. Peak height/area methods gave values of approximately 0.75Fa in spite of various compensations for the impossibility of recording the curve until radioactivity = 0.

Change in liver blood flow and blood content in dogs during direct and reflex alteration of hepatic sympathetic nerve activity.

SUMMARY A mean decrease of 60% in liver blood volume was recorded by a plethysmographic technique during electrical stimulation of the hepatic nerves in anesthetized, vagotomized dogs. A decrease in pressure in the vascularly isolated carotid sinus to 40 mm Hg, from a mean control of 144 mm Hg, decreased liver blood volume by a mean of 16%; arterial blood pressure increased by a mean of 77 mm Hg. Carotid sinus hypotension was accompanied by respective mean increases of 16% and 1.4% in hepatic arterial and portal venous blood flows, and of 45% and 22% in arterial and portal resistances. Increase in sinus pressure to 240 mm Hg increased liver blood volume by a mean of 20%; arterial blood pressure decreased by 90 mm Hg. Sinus hypertension was accompanied by respective mean decreases of 10% and 1.5% in hepatic arterial and portal venous blood flows, and of 44% and 18% in arterial and portal resistances. Interruption of afferent vagal traffic from cardiopulmonary receptors was maximally effective in decreasing liver blood volume at a carotid sinus pressure of 40 mm Hg and was ineffective at carotid sinus pressures greater than 160 mm Hg. Combined withdrawal of carotid and cardiopulmonary vasomotor inhibition decreased liver blood volume by 42%; of this 37% was due to the cardiopulmonary and 63% to the carotid baroreflex. The study showed the canine liver to function as a blood reservoir by active mobilization of a portion of its blood volume.

Cardiovascular Reflexes from Stretch of Pulmonary Vein-Atrial Junctions in the Dog

The reflex cardiovascular response to stretch of left pulmonary vein-atrial junctions was studied in anesthetized dogs in which both aortic nerves were cut and the carotid sinuses were isolated vascularly. After thoracotomy, the root of the left lung was tied and a small Silastic balloon (1.5-cm long), attached to a nylon catheter, was inserted into each of the three left pulmonary veins and tied so that its tip lay at the junction of the vein with the left atrium. In six dogs, heart rate response to balloon distension of 2.0 ml was studied over a range of initial heart rates (75 to 240 beats/min) achieved by varying the carotid sinus pressure. On distension of the balloons, slowing occurred if the initial heart rate was > 140 to 150 beats/min and acceleration if it were less. In eight dogs, aortic blood pressure and cardiac output measured before, during, and after balloon distension (0.25 to 2.0 ml) demonstrated a hyperbolic relationship between balloon volume and decrease in calculated systemic vascular resistance. All responses were abolished by vagotomy. The reflex vasodilatation was sustained and caused by decreased adrenergic activity; the reflex bradycardia or tachycardia was due to interplay of vagal and sympathetic cardiac efferents.

PULMONARY VASCULAR CHANGES IN A DOG AFTER AORTOPULMONARY ANASTOMOSIS FOR FOUR YEARS

When dogs are subjected to an anastomosis between a large systemic artery and one of the pulmonary arteries, the subsequent progress of events is related to the diameter of the fistula. If this is large, exceeding about 5 mm., there is usually a rapid onset of fatal cardiac failure, as in the animal described by Ekstrom et al. (1951-52) and in 16 of the 21 dogs reported on by Muller et al. (1953) who anastomosed the aorta with a pulmonary artery. When the communication is small, usually 3 mm. or less in diameter, as it frequently is when the subclavian artery is employed in the anastomosis, the animals survive with a normal or only slightly raised blood pressure in the pulmonary artery, and vascular changes do not occur in the small pulmonary arteries. In a third group where the diameter of the fistula is intermediate in size, the animals survive with pulmonary hypertension, and vascular changes occur (Muller et al., 1953; Ferguson and Varco, 1955). The structural changes described are usually medial hypertrophy and intimal fibrosis, histological features characteristic of an early grade of hypertensive pulmonary vascular disease in the human lung (grades 1 to 3 on the basis of the criteria of Heath and Edwards, 1958). The severe structural changes characterized by generalized and complex local forms of vascular dilatation, which are pathognomonic of the late stages of hypertensive pulmonary vascular disease associated with congenital cardiac septal defects in man (grades 4 to 6), do not appear to have been reported in dogs with artificial aorto-pulmonary anastomosis and generalized pulmonary hypertension. However, vascular changes comparable to these, confined to the left upper lobe, in dogs subjected to an endto-end anastomosis between the left subclavian artery and the pulmonary artery to this lobe have been reported by Dammann et al. (1957). In these animals there was pulmonary hypertension only in the restricted area of lung served by the anastomosis, while the blood pressure in the main pulmonary artery was normal, so that the hmodynamic conditions cannot be considered as analogous to those found in human disease. Hence up to the present it has not really been established that the complete progression of structural changes seen in human hypertensive pulmonary vascular disease can be experimentally produced in the dog exposed to comparable physiological conditions. In fact the frequency of the severe lesions in man, in contrast to the rarity of them in dogs, suggests that a factor of time in addition to elevation of blood pressure in the pulmonary artery is necessary for their development. The purpose of this communication is to demonstrate that higher grades of hypertensive pulmonary vascular disease can occur after the experimental production of an aorto-pulmonary anastomosis and generalized pulmonary hypertension. The presence of severe pulmonary vascular changes in one of three dogs subjected to this procedure is reported. The additional etiological factor is discussed later. The relation between the histological appearance of the pulmonary arteries of these dogs and that of the pulmonary arteries in man in patent ductus arteriosus is also discussed, bearing in mind that the hemodynamic abnormalities were acquired in the experimental animals but have been present from birth in human disease.

The Effect of Cortisone on Experimentally Produced Myocardial Infarcts

Administration of a moderately large or large dose of cortisone to dogs having acute myocardial infarctions inhibited slightly the rate of removal of necrotic muscle fibers in these animals as compared with untreated animals. Delay was appreciable at four and six days after production of the infarct in animals receiving 2.5 mg. of cortisone per kilogram of body weight and at 4, 6, 12 and 21 days in animals receiving 10 mg. per kilogram. At all other periods up to essentially complete healing of the infarcts as defined at 60 days, no appreciable differences existed between treated and untreated animals.