The comparative physiologist chooses from the broad spectrum of animal species those which best demonstrate the phenomenon he wishes to study. Accordingly, investigations into the physiology of asphyxia might logically start with those animals which have a special adaptation to breathholding during prolonged underwater dives. In this article we shall consider some inferences from the comparative physiology of diving by examining the cardiovascular responses to immersion of some aquatic species and comparing them with responses of some terrestrial animals, including man. Apnea, simple cessation of breathing during immersion, is characteristic of diving. It leads to progressively increasing tissue anoxia and hypercapnia, and eventually to asphyxial death. It will be seen that the associated circulatory and cardiac adjustments are so profound as to considerably extend the normal range of physiological responses. Historical Review

Radiotelemetry was used to study regional blood flow distribution in Alaska sled dogs during cross-country runs. Doppler ultrasonic flowmeter transducers were chronically implanted on the coronary, renal, and mesenteric arteries, terminal abdominal aorta, and ascending aorta or pulmonary artery, and a miniature blood pressure gauge was installed in the aorta or carotid artery. Flow and pressure data telemetered from dogs running on the trail were received and recorded remotely. The heart rate, 40 to 60/min in sleeping dogs, increased to 80 to 100/min when the dogs were ambulatory and to 100 to 150/min when the dogs were excited before a race. Heart rate accelerated to 300/min at the start of exercise and commonly remained at that level throughout prolonged runs. Aortic blood pressure averaged 130/90 mm Hg at rest, but the systolic pressure often exceeded 300 mm Hg when the dogs were running. A transient drop in mean pressure occurred at the onset of running, but mean pressure during sustained exercise was practically identical to that at rest. Flow in the terminal aorta increased 9 to 12 times and coronary flow 5 to 6 times, but mesenteric and renal flows were unchanged during violent, prolonged exercise. These findings contrast with diminished visceral flows recorded in exercising humans and suggest that compensatory redistribution of flow is not a significant reserve mechanism in these animals during exercise.

The effects of stimulating the carotid sinus nerves on the distribution of cardiac output and peripheral vasoactivity was studied in intact, unanesthetized dogs instrumented with ultrasonic or electromagnetic flow probes on the ascending aorta, mesenteric, renal, and iliac arteries, and miniature pressure gauges in the aorta. A radiofrequency pacemaker was used to stimulate the nerves in dogs at rest, during treadmill exercise, and after autonomic blockade. Thirtysecond periods of stimulation in the resting dog resulted in an average decrease in aortic pressure of 28%, cardiac output remained unchanged, total peripheral resistance fell 29%, mesenteric flow 12%, mesenteric vascular resistance 18%, renal flow 8%, and renal vascular resistance 22%. In the iliac bed flow increased by 90% while resistance declined by 62%. Heart rate decreased initially by 13%, and returned to control during stimulation. The bradycardia was determined to be predominantly due to vagal stimulation. During treadmill exercise carotid sinus nerve stimulation resulted in similar decreases in arterial pressure, mesenteric and renal resistance, and a further decrease in iliac resistance from exercise control values. Thus, electrical stimulation of the carotid sinus nerves in the conscious dog produced a differential pattern of peripheral vasodilatation, the most profound dilatation being observed in the hind-limb circulation. This release of sympathetic tone also occurred during stimulation in exercising animals when the muscular bed was already dilated on a metabolic basis. This investigation was supported by U. S. Public Health Service Grant HE-12373. ADDITIONALReceived May 13, 1970; accepted for publication July 30, 1970. similar significance in the intact, unanesthetized animal in which all control systems are intact and the additional effects of anesthesia are not present.To study the effects of the carotid sinus reflex, the carotid sinus nerves were electrically stimulated while arterial pressure, heart rate, cardiac output, and blood flow in the mesenteric, renal, and iliac beds were measured. These experiments were performed in normal conscious dogs at rest, after interruption of efferent loops through pharmacologic blockade, and also during treadmill exercise. This investigation was designed to demonstrate the extent of central neural control of the heart and peripheral circulations in the conscious animal, to examine the relative importance of changes in peripheral

The cytoarchitectural changes which take place in the walls of small arteries (about 1 mm. O.D.) during vasoconstriction and vasodilation have been studied. Vessels were fixed while in their functional state by immersion in liquid isopentane at -170 C. and prepared for microscopic examination by freeze substitution. The walls of control vessels were thin in relation to the diameter of lumina (WT:L 1:30), indicating that they are more distended than they appear in routinely fixed sections. Vessels dilated with ACH had even thinner walls (WT:L 1:40). Vasoconstriction, induced by local application of epinephrine, increased the wall thickness and reduced the size of the lumen (WT:L 1:2) but in no case was the lumen obliterated in arteries of this size. Although an increase in the WT:L ratio is commonly employed as evidence of vascular hypertrophy, normal vessels which are fixed and sectioned while in a functional state of vasoconstriction may exhibit similar gross characteristics. Constricted vessels are characterized by progressive deformation of the internal elastic lamina, crowding of endothelial cells, and distortion of smooth muscle cells and their nuclei, particularly in the region immediately adjacent to the lumen. During intense vasoconstriction, the wall tension appears to be supported only by the outer layers of the vessel.

No abstract

Control of the coronary circulation by the carotid sinus was studied in intact, unanesthetized dogs instrumented with Doppler ultrasonic flow probes on the left circumflex coronary artery, miniature pressure gauges in the aorta, and stimulating electrodes on the carotid sinus nerves. A radiofrequency pacemaker was used to stimulate the nerves in dogs at rest, during sleep, exercise, and after autonomic blockade. Thirty-second periods of stimulation in the resting conscious dog resulted in an average decrease in aortic pressure of 28%, an average decrease in mean coronary flow of 7%, while heart rate decreased by 13% at the beginning of stimulation and then returned to control levels. Mean and late diastolic coronary resistances decreased by an average of 22% from control. Similar results occurred with carotid sinus nerve stimulation during sleep and during treadmill exercise. Combined beta-receptor blockade with propranolol and atropine prevented the changes in heart rate with carotid sinus nerve stimulation but not the decrease in arterial pressure or the coronary dilatation. After alpha-receptor blockade with phenoxybenzamine or sympathetic blockade with guanethidine, coronary dilatation was not observed with carotid sinus nerve stimulation. Thus sympathetic constrictor tone is present in the resting conscious dog and the coronary dilatation observed with electrical stimulation of the carotid sinus nerves is due to a reduction in resting sympathetic constrictor tone. ADDITIONAL KEY WORDScoronary vasodilatation atropine alpha receptor carotid sinus reflex sympathetic blockade beta receptor baroreceptor exercise coronary blood flow• Although the general circulatory effects of activating the carotid sinus reflex have been well described, particularly in anesthetized preparations, the influence of this reflex on the coronary circulation has not been established. There is substantial evidence that coronary blood flow is regulated primarily by the metabolic requirements of the myocardium; though it is clear that the coronary vascular

Blood pressure was telemetered from transducers chronically implanted in the carotid arteries of two adult, wild, male giraffes captured and released near Kiboko, Kenya. Cerebral perfusion pressure ranged from 280/180 mm-Hg while the animal was lying with its head on the ground to 125/75 mm-Hg when it was standing erect; it varied between these levels during spontaneous activity such as walking, grazing, and running.

Medical student distress was examined in two consecutive first-year classes (N = 312) in September, before they interacted with the school regimen, and again in May before exams. Anxiety means were one SD above the normative mean for nonpatients at both times. The number of students reporting a significant level of depression doubled from September (N = 36) to May (N = 78). The correlation of distress in September and May was .40, indicating that for many students distress was enduring. A biopsychosocial model of initial distress explained more variance (36%) in the cross-validation sample than did any one variable alone. Distressed students had higher Type A scores. Also, anger held in was a risk factor for distress in students with a family history of cardiovascular disease (CVD). Students who hold anger in may experience prolonged stress which, coupled with a family history of CVD, could make them psychobiologically vulnerable to distress.