Cardiac output and its distribution through capillaries and A‐V shunts in diving seals

Abstract

Regional blood flow and cardiac output were determined by distribution of radioactive microspheres injected via catheter into the left ventricle during experimental diving and recovery in juvenile spotted seals (Phoca vitulina largha) and grey seals (Halichoerus grypus). Cardiac output was 9.7 L/min before diving, declined 90% during submersion and increased to 12.1 L/min after 40 s of recovery. Left ventricular myocardial perfusion declined from 179 +/- 24 (21) to 25 +/- 2 (6) ml/min . 100 g at 2 min submersion, and measured 23 +/- 3 (8) after 10 min of submersion. Cerebral cortical flow was reduced from a pre-dive value of 115 +/- 3 (15) to 40 +/- 5 (3) and 49 +/- 6 (3) at 2 and 5 min of diving, respectively, but increased to 253 +/- 14 (4) ml/min . 100 g at 10 min along with elevated PCO2 (84 torr) and lowered pH (7.10) in arterial blood. It remained at that level in recovery. Brain stem perfusion after 10 min submersion was still identical with control, but increased to 275% of control in recovery. Adrenal flow decreased to 34 and 27% of control at 2 and 5 min of diving, respectively. Recovery flow after 10 min of diving was 200% of control. Liver, kidney, fat, skin, and stomach were ischemic throughout the dive. Recovery flow increased slowly in these tissues. Skeletal muscle (M. psoas) was perfused at a low rate. (3 ml/min . 100 g) pre-dive and was ischemic during diving. Recovery muscle perfusion was variable at different sites (from 5 to 105 ml/min . 100 g). Pre-dive pulmonary capillary perfusion was 58 +/- 8 (9) ml/min . 100 g, decreased to 7 +/- 0 (3) ml/min . 100 g min of submersion, and had increased to 50% of pre-dive value after 40 s of recovery from a 10 min dive. Conclusions are: (1) previous information from implanted flow transducers was confirmed, (2) detailed data for discrete tissues elaborate the concept of selective redistribution of cardiac output in diving seals, (3) non-uniform reperfusion contributes to the maintenance of arterial pressure during recovery, and (4) substantial A-V shunting of cardiac output took place in the first 2-5 min of the dive, when total capillary/nutritive flow was low. Late in the dive, however, CO was routed through systemic capillaries mainly in the cerebral circulation and less than 15% through A-V shunts.

What triggers the aerobic dive limit? Patterns of muscle oxygen depletion during dives of emperor penguins

“…MBF values at rest in dogs (Hutter et al, 1999;Pendergast et al, 1985), seals (Blix et al, 1983;Zapol et al, 1979), pigs (Armstrong et al, 1987), sheep (Hales, 1973), horses (Armstrong et al, 1992) and humans (Stevens et al, 1971) are reported between 25 and 250mlkg -1 musclemin -1 . In small birds such as ducks and guinea fowl (Numida meleagris), MBF at rest is greater, 200-450mlkg -1 musclemin -1 (Ellerby and Marsh, 2006;Grubb, 1981;Jones et al, 1979).…”

“…) (Blix et al, 1983;Zapol et al, 1979 . In addition, even for dives of similar duration, there is a large range of end-of-dive air sac O 2 fractions, blood Hb saturations and muscle Mb saturations.…”

Evaluating cardiac physiology through echocardiography in bottlenose dolphins: using stroke volume and cardiac output to estimate systolic left ventricular function during rest and following exercise

“…This results in a physiological conflict as exercise causes increased O 2 demand, while breath-hold diving results in O 2 limitation (Ponganis, 2011). Few studies have measured CO in live marine mammals, and most of these have been made in pinnipeds (Blix et al, 1983(Blix et al, , 1976Elsner et al, 1964;Murdaugh et al, 1966;Ponganis et al, 1991Ponganis et al, , 1990Sinnett et al, 1978;Zapol et al, 1979;Sommer et al, 1968). Although it has been recognized that stress significantly affects physiological responses and probably affects any extrapolations to normal cardiac function, only three of these studies were performed in unrestrained and/or free-swimming animals (Elsner et al, 1964;Ponganis et al, 1991Ponganis et al, , 1990.…”

A study on change in ejection fraction during simulated diving in humans

“…Bradycardia and associated arrhythmias including supraventricular tachycardia have been reported with breathhold immersion of the face in water. [8] Myocardial contractility is an important factor that contributes to efficient cardiac pumping activity or in other words the stroke volume. It has also been shown in the previous studies that there is increase in parasympathetic activity to the heart during breath-hold immersion of the face in water, due to stimulation of trigeminal nerve endings on the face.…”