Number and distribution of capillaries as determinants of myocardial oxygen tension

1964 ◽  
Vol 207 (3) ◽  
pp. 653-660 ◽  
Author(s):  
Wayne W. Myers ◽  
Carl R. Honig
Keyword(s):  
Oxygen Tension ◽  
Left Ventricular ◽  
Red Cells ◽  
Tissue Oxygen ◽  
Blood Content ◽  
Left Ventricular Apex ◽  
Plasma Skimming ◽  
Oxygen Tensions ◽  
Open Capillaries ◽  
Transmural Gradient

Blood content per gram of tissue was measured in various regions of the myocardium of the dog, by use of I131-labeled albumin and Cr51O4-labeled red cells. The ratio of I131 to Cr51O4 distributions was uniform, indicating that plasma skimming does not increase O2 delivery to the inner layers. Gradients in blood content were observed from epicardium to endocardium, and in the base-apex dimension of the heart. Both the transmural gradient and the amount of blood per gram of tissue were greatest at the left ventricular apex. In this region the deeper layers contained 1.5 times as much blood as superficial ones. The data permitted estimates of the number of open capillaries, and of intercapillary distances. These estimates indicate that only a fraction of the available capillaries are perfused at rest. Mean tissue oxygen tensions were computed for various conditions of flow, capillarity, and metabolism by use of the Kety modification of the Krogh equation. Results are discussed in relation to the regulation of tissue PO2.

Nonuniform distribution of blood flow and gradients of oxygen tension within the heart

1964 ◽  
Vol 207 (3) ◽  
pp. 661-668 ◽  
Author(s):  
Edward S. Kirk ◽  
Carl R. Honig
Keyword(s):  
Blood Flow ◽  
Pressure Gradient ◽  
Oxygen Tension ◽  
Cardiac Cycle ◽  
Myocardial Tissue ◽  
Local Blood Flow ◽  
Tissue Pressure ◽  
Oxygen Tensions ◽  
Sufficient Magnitude ◽  
Transmural Gradient

Myocardial tissue pressure increases from epicardium to endocardium, and in the deeper layers exceeds ventricular blood pressure during one-third of the cardiac cycle (21). The effect of this tissue pressure gradient on local blood flow was studied using the depot clearance technique. Blood flow was found to be at least 25% lower in the deep regions as compared with superficial ones. With total coronary inflow held constant, vagal arrest of the heart removed the tissue pressure gradient, and simultaneously redistributed flow from superficial to deeper layers. We conclude that the gradient in tissue pressure, and hence in the extravascular component of coronary resistance, is at least in part, the cause of the nonhomogeneous blood flow across the wall. By use of the oxygen cathode, a gradient of oxygen tensions was observed which paralleled the blood flow gradient; mean oxygen tension in the subepicardium averaged twice that in the subendocardium. The gradient in oxygen tension appears to be of sufficient magnitude to determine a transmural gradient in aerobic metabolism.

Hypoxic reperfusion of the ischemic heart and oxygen radical generation

2006 ◽  
Vol 290 (1) ◽  
pp. H341-H347 ◽  
Author(s):  
Mark G. Angelos ◽  
Vijay K. Kutala ◽  
Carlos A. Torres ◽  
Guanglong He ◽  
Jason D. Stoner ◽  
...  
Keyword(s):  
Oxygen Tension ◽  
Left Ventricular ◽  
Oxygen Radical ◽  
Oxidase Inhibitor ◽  
Tissue Oxygen Tension ◽  
Lv Function ◽  
Resonance Spectroscopy ◽  
Tissue Oxygen ◽  
Xanthine Oxidase Inhibitor ◽  
Ros Burst

Postischemic myocardial contractile dysfunction is in part mediated by the burst of reactive oxygen species (ROS), which occurs with the reintroduction of oxygen. We hypothesized that tissue oxygen tension modulates this ROS burst at reperfusion. After 20 min of global ischemia, isolated rat hearts were reperfused with temperature-controlled (37.4°C) Krebs-Henseleit buffer saturated with one of three different O2 concentrations (95, 20, or 2%) for the first 5 min of reperfusion and then changed to 95% O2. Additional hearts were loaded with 1) allopurinol (1 mM), a xanthine oxidase inhibitor, 2) diphenyleneiodonium (DPI; 1 μM), an NAD(P)H oxidase inhibitor, or 3) Tiron (10 mM), a superoxide scavenger, and were then reperfused with either 95 or 2% O2 for the first 5 min. ROS production and tissue oxygen tension were quantitated using electron paramagnetic resonance spectroscopy. Tissue oxygen tension was significantly higher in the 95% O2 group. However, the largest radical burst occurred in the 2% O2 reperfusion group ( P < 0.001). Recovery of left ventricular (LV) contractile function and aconitase activity during reperfusion were inversely related to the burst of radical production and were significantly higher in hearts initially reperfused with 95% O2 ( P < 0.001). Allopurinol, DPI, and Tiron reduced the burst of radical formation in the 2% O2 reperfusion groups ( P < 0.05). Hypoxic reperfusion generates an increased ROS burst originating from multiple pathways. Recovery of LV function during reperfusion is inversely related to this oxygen radical burst, highlighting the importance of myocardial oxygen tension during initial reperfusion.

scholarly journals Oxygen dependent mitochondrial formate production and the reverse Pasteur effect

2020 ◽  
Author(s):  
Johannes Meiser ◽  
Alexei Vazquez
Keyword(s):  
Mathematical Model ◽  
Experimental Evidence ◽  
Oxygen Tension ◽  
Mammalian Cells ◽  
Oxygen Availability ◽  
Sweet Spot ◽  
Tissue Oxygen ◽  
Pasteur Effect ◽  
Oxygen Tensions ◽  
Formate Production

AbstractThe Pasteur effect dictates that oxygen induces respiration and represses fermentation. However, we have shown that oxygen stimulates mitochondrial formate production and excess formate production induces glycolysis in mammalian cells. Our observations suggest the hypothesis that increased respiration induces an increase, rather than a decrease, of fermentation, the reverse Pasteur effect. Using a mathematical model we show that, in the absence of mitochondrial formate production, we should always observe the Pasteur effect, a reduction in fermentation with increasing respiration. However, in cells with active mitochondrial formate production, the rate of fermentation first increases with increasing the rate of respiration, indicating a metabolic sweet spot at moderate oxygen availability that is within the range of tissue oxygen tensions. We provide experimental evidence for the manifestation of the reverse Pasteur effect at such oxygen tension.

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