Autoregulation of cardiac output is overcome by adrenergic stimulation in the anaconda heart

Wang

2020

Self Cite

In the 1950s, Arthur C. Guyton removed the heart from its pedestal in cardiovascular physiology by arguing that cardiac output is primarily regulated by the peripheral vasculature. This is counterintuitive, as modulating heart rate would appear to be the most obvious means of regulating cardiac output. In this Review, we visit recent and classic advances in comparative physiology in light of this concept. Although most vertebrates increase heart rate when oxygen demands rise (e.g. during activity or warming), experimental evidence suggests that this tachycardia is neither necessary nor sufficient to drive a change in cardiac output (i.e. systemic blood flow, Q̇sys) under most circumstances. Instead, Q̇sys is determined by the interplay between vascular conductance (resistance) and capacitance (which is mainly determined by the venous circulation), with a limited and variable contribution from heart function (myocardial inotropy). This pattern prevails across vertebrates; however, we also highlight the unique adaptations that have evolved in certain vertebrate groups to regulate venous return during diving bradycardia (i.e. inferior caval sphincters in diving mammals and atrial smooth muscle in turtles). Going forward, future investigation of cardiovascular responses to altered metabolic rate should pay equal consideration to the factors influencing venous return and cardiac filling as to the factors dictating cardiac function and heart rate.

Section: The Regulation Of Cardiac Functionmentioning

confidence: 93%

Section: The Regulation Of Cardiac Functionmentioning

confidence: 99%

What determines systemic blood flow in vertebrates?

Wang

2020

Self Cite

“…Because input and output pressures were controlled in tandem, input pressure was calculated as the average of right and left atrial input pressures and output pressure was calculated as the average of pulmonary artery and right aortic pressures (Farrell et al, 1994;Joyce et al, 2017). Total cardiac output was defined as the sum of pulmonary and right aortic blood flow and normalised to body mass.…”

Section: In Situ Perfused Heartsmentioning

confidence: 99%

Contraction of atrial smooth muscle reduces cardiac output in perfused turtle hearts

Axelsson

Wang

2019

Self Cite

Unusual undulations in resting tension (tonus waves) were described in isolated atria from freshwater turtles more than a century ago. These tonus waves were soon after married with the histological demonstration of a rich layer of smooth muscle on the luminal side of the atrial wall. Research thereafter waned and the functional significance of this smooth muscle has remained obscure. Here, we provide evidence that contraction of the smooth muscle in the atria may be able to change cardiac output in turtle hearts. In in situ perfused hearts of the red-eared slider turtle (Trachemys scripta elegans), we demonstrated that activation of smooth muscle contraction with histamine (100 nmol kg −1 bolus injected into perfusate) reduced cardiac output by decreasing stroke volume (>50% decrease in both parameters). Conversely, inhibition of smooth muscle contraction with wortmannin (10 µmol l −1 perfusion) approximately doubled baseline stroke volume and cardiac output. We suggest that atrial smooth muscle provides a unique mechanism to control cardiac filling that could be involved in the regulation of stroke volume during diving.

“…In their study, the decrease in filling time presumably reduced cardiac preload (e.g. Altimiras and Axelsson, 2004), which, in the absence of pronounced inotropic effects (see Joyce et al, 2017a), was likely responsible for the decrease in V S . However, in the intact circulatory system of the anesthetized alligators, adrenaline also exerts direct effects on vascular capacitance.…”

Section: Resultsmentioning

confidence: 86%

Contribution of active atrial contraction to cardiac output in anesthetized American alligators (Alligator mississippiensis)

Crossley

Elsey

et al. 2018

Self Cite

Ventricular filling may occur directly from the venous circulation during early diastole or via atrial contraction in late diastole. The contribution of atrial contraction to ventricular filling is typically small in mammals (10-40%), but has been suggested to predominate in reptiles. We investigated the importance of atrial contraction in filling of the ventricle in American alligators (Alligator mississippiensis) by bypassing both atria (with the use of ligatures to prevent atrial filling) and measuring the resultant effects on cardiac output in anesthetized animals. Atrial ligation had no significant effects on total systemic blood flow before or after adrenaline injection. Unexpectedly, pulmonary flow was increased following atrial ligation prior to adrenaline treatment, but was unaffected after it. These findings suggest that the atria are non-essential (i.e. redundant) for ventricular filling in alligators, at least under anesthesia, but may serve as important volume reservoirs.