Reduced oxygen availability (hypoxia) is a potent stressor during embryonic development, altering the trajectory of trait maturation and organismal phenotype. We previously documented that chronic embryonic hypoxia has a lasting impact on the metabolic response to feeding in juvenile snapping turtles (Chelydra serpentina). Turtles exposed to hypoxia as embryos [10% O 2 (H10)] exhibited an earlier and increased peak postprandial oxygen consumption rate, compared with control turtles [21% O 2 (N21)]. In the current study, we measured central blood flow patterns to determine whether the elevated postprandial metabolic response in H10 turtles is linked to lasting impacts on convective transport. Five years after hatching, turtles were instrumented to quantify systemic ( _ Q sys ) and pulmonary ( _ Q pul ) blood flows and heart rate ( f H ) before and after a ∼5% body mass meal. In adult N21 and H10 turtles, f H was increased significantly by feeding. Although total stroke volume (V S,tot ) remained at fasted values, this tachycardia contributed to an elevation in total cardiac output ( _ Q tot ). However, there was a postprandial reduction in a net left-right (L-R) shunt in N21 snapping turtles only. Relative to N21 turtles, H10 animals exhibited higher _ Q sys due to increased blood flow through the right systemic outflow vessels of the heart. This effect of hypoxic embryonic development, reducing a net L-R cardiac shunt, may support the increased postprandial metabolic rate we previously reported in H10 turtles, and is further demonstration of adult reptile cardiovascular physiology being programmed by embryonic hypoxia.
Reptiles have the capacity to differentially perfuse the systemic and pulmonary vascular circuits via autonomic regulation of the heart and the vascular trees. While this aptitude is widely recognized, the role of 'shunting' as a homeostatic mechanism to match convective transport with tissue demand remains unknown. In crocodilians, it has been hypothesized that a pulmonary vascular bypass of systemic venous blooda right-to-left (R-L) shuntserves to deliver CO 2 -rich blood with protons needed for gastric acid secretion during digestion. This hypothesis is partially based on the unique crocodilian vascular anatomy where a left aorta (LAo) arises from the right ventricle, and appears to preferentially supply the gastrointestinal system, whereas the right aorta emerges from the left ventricle. Recent theoretical considerations imply that a R-L shunt would have minuscule effects on P CO2 , but direct measurements of blood gases in both the right and left aortae or both the right and left atria in fed animals have not been conducted. For this reason, we measured blood parameters including P O2 , P CO2 , pH e and [HCO 3 − ] in the right and left aortae and atria following ingestion of a gavage-fed standardized meal (5% body mass). Blood samples were taken at 3, 6, 12, 24, 36 and 48 h into the digestive period to encompass the period of maximal gastric acid secretion. At no point did P CO2 or pH differ between the left and right aortae, whereas P O2 was significantly lower in the left aorta at several time points during digestion. Our findings do not support the hypothesis that a R-L shunt serves to deliver CO 2 for the gastrointestinal system after feeding in crocodilians.
American alligators (Alligator mississippiensis) deposit eggs in a mound nest, potentially subjecting embryos to daily variations in temperature. Whilst adult crocodilian cardiovascular responses to changes in temperature have been investigated, similar studies in alligator embryos are limited. We investigated cardiovascular function of embryonic alligators during heating and cooling as well as at different temperatures. We measured arterial blood pressure (P) and heart rate (f) in response to cooling (30-26 °C), heating (26-36 °C), followed by a reciprocal cooling event (36-26 °C) and assessed the cardiac baroreflex at 30 and 36 °C. Embryonic f increased during heating events and decreased during cooling events, while embryos were hypotensive at 26 and 36 °C, although P did not differ between heating or cooling events. There was a clear temperature-dependent heart rate hysteresis at a given embryo's temperature, depending on whether embryos were cooling or heating. Cardiovascular regulation through the cardiac limb of the baroreflex was not affected by temperature, despite previous studies suggesting that vagal tone is present at both low and high temperatures.
Studies of animals native to high altitude can provide valuable insight into physiological mechanisms and evolution of performance in challenging environments. We investigated how mechanisms controlling cardiovascular function may have evolved in deer mice (
Peromyscus maniculatus
) native to high altitude. High-altitude deer mice and low-altitude white-footed mice (
P. leucopus
) were bred in captivity at sea level, and first-generation lab progeny were raised to adulthood and acclimated to normoxia or hypoxia. We then used pharmacological agents to examine the capacity for adrenergic receptor stimulation to modulate heart rate (
f
H
) and mean arterial pressure (
P
mean
) in anaesthetized mice, and used cardiac pressure-volume catheters to evaluate the contractility of the left ventricle. We found that highlanders had a consistently greater capacity to increase
f
H
via pharmacological stimulation of β
1
-adrenergic receptors than lowlanders. Also, whereas hypoxia acclimation reduced the capacity for increasing
P
mean
in response to α-adrenergic stimulation in lowlanders, highlanders exhibited no plasticity in this capacity. These differences in highlanders may help augment cardiac output during locomotion or cold stress, and may preserve their capacity for α-mediated vasoconstriction to more effectively redistribute blood flow to active tissues. Highlanders did not exhibit any differences in some measures of cardiac contractility (maximum pressure derivative, d
P
/dt
max
, or end-systolic elastance, E
es
), but ejection fraction was highest in highlanders after hypoxia acclimation. Overall, our results suggest that evolved changes in sensitivity to adrenergic stimulation of cardiovascular function may help deer mice cope with the cold and hypoxic conditions at high altitude.
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