Oxygen exchange in the isolated, arrested guinea pig heart: theoretical and experimental observations

Abstract

A model of oxygen transport in perfused myocardial tissue is presented. Steady-state conditions are assumed in order to mimic the metabolic rate of the arrested heart. The model incorporates Michaelis-Menten dependence of mitochondrial oxygen consumption, oxymyoglobin saturation and oxyhemoglobin saturation on oxygen partial pressure (PO2). The transport equations model both the advective supply of oxygen via the coronary circulation and the diffusive exchange of oxygen between tissues and environment across the epicardial and endocardial surfaces. The left ventricle is approximated by an axisymmetric prolate spheroid and the transport equations solved numerically using finite element techniques. Solution yields the PO2 profile across the heart wall. Integration of this profile yields the simulated rate of metabolic oxygen uptake determined according to the Fick principle. Correction for the diffusive flux of oxygen across the surfaces yields the simulated true metabolic rate of oxygen consumption. Simulated values of oxygen uptake are compared with those measured experimentally according to the Fick principle, using saline-perfused, Langendorff-circulated, K(+)-arrested, guinea pig hearts. Four perfusion variables were manipulated: arterial PO2, environmental PO2, coronary flow and perfusion pressure. In each case agreement between simulated and experimentally determined rates of oxygen consumption gives confidence that the model adequately describes the advective and diffusive transport of oxygen in the isolated, arrested, saline-perfused heart.

Dietary pre‐exposure of rats to fish oil does not enhance myocardial efficiency of isolated working hearts or their left ventricular trabeculae

“…However, we consider that the delivery of O 2 to the myocardium in our study was adequate given that: (1) the downstream P O 2 was well above the normal physiological venous P O 2 at all afterloads (Fig. 1C), (2) an increase in downstream P O 2 was observed at high afterloads, thereby ruling out oxygen starvation at all submaximal workloads, and (3) there was clearly coronary vascular reserve present, as shown by administration of 5 μM adenosine (Mawson et al 1994;Krams et al 2004) (Fig. 1D).…”

“…C ), (2) an increase in downstream was observed at high afterloads, thereby ruling out oxygen starvation at all submaximal workloads, and (3) there was clearly coronary vascular reserve present, as shown by administration of 5 μ m adenosine (Mawson et al . ; Krams et al . ) (Fig.…”

Extracellular Ca2+ is obligatory for ouabain‐induced potentiation of cardiac basal energy expenditure

“…Hearts were mounted in a Langendorff perfusion apparatus and perfused, at constant flow, as described previously 20 . The glass chamber enclosing the heart was flushed continuously with a stream of humidified gas (5% CO 2 in room air) in order to standardize the rate of exchange of oxygen across the epicardial surface 21 . A water‐filled latex balloon (Hugo‐Sachs Elektronik, March‐Hugstetten, Germany) was placed in the left ventricle for measurement of left ventricular pressure ( P LV ).…”

SPECIES‐INDEPENDENT METABOLIC RESPONSE TO AN INCREASE OF [Ca2+]i IN QUIESCENT CARDIAC MUSCLE

“…These values decreased with extracellular Na + concentration to 17.3 ± 2.0 and 14.4 ± 6.6 kPa for guinea‐pig ( n = 5) and rat ( n = 3), respectively, when [Na + ] o was reduced to 3 mmol/L. Furthermore, there was no indication of hypoxia‐induced vasodilation of the coronary vasculature, such as occurs in the KCl‐arrested heart when arterial P o 2 is reduced below 150 mmHg 9 . In fact, there was no effect of either increasing [K + ] o or reducing [Na + ] o on coronary vascular flow in the hearts of either species.…”