Myocardial Oxygen Tension during Left Ventricular Bypass

1988 ◽  
pp. 463-471 ◽  
Author(s):  
Yoshinori Mitamura ◽  
Takeo Matsumoto ◽  
Tomohisa Mikami
Keyword(s):  
Oxygen Tension ◽  
Left Ventricular

Cardiac performance as a function of intracellular oxygen tension in buffer-perfused hearts

2001 ◽  
Vol 281 (6) ◽  
pp. H2463-H2472 ◽  
Author(s):  
Kenneth A. Schenkman
Keyword(s):  
Oxygen Consumption ◽  
Guinea Pig ◽  
Oxygen Tension ◽  
Myocardial Oxygen Consumption ◽  
Arterial Oxygen Tension ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Arterial Oxygen ◽  
Adenosine Release ◽  
Lactate Release

Critical intracellular myocardial oxygen tension was determined by optical spectroscopic measurement of myoglobin oxygen saturation in crystalloid-perfused guinea pig hearts. Accurate end-point determinations of the maximally oxygenated and deoxygenated myoglobin were made. Hearts were subjected to a steady decrease in perfusate oxygen tension while left ventricular developed pressure, maximal left ventricular dP/d t, myocardial oxygen consumption, lactate release, and adenosine release were measured as indices of myocardial function. Intracellular myoglobin was found to be only 72% saturated under baseline conditions with an arterial oxygen tension of >600 mmHg at 37°C. Baseline intracellular oxygen tension was 6.3 mmHg. Myocardial oxygen consumption was decreased by 10% when the oxygen tension fell to 5.7 mmHg, and cardiac contraction decreased 10% when oxygen tension was 4.1 mmHg. Adenosine release and, finally, lactate release began to increase at sequentially lower oxygen tensions. The present results indicate that the buffer-perfused guinea pig heart at 37°C has an intracellular oxygen tension just above the threshold for impaired function.

Coronary physiology

1983 ◽  
Vol 63 (1) ◽  
pp. 1-205 ◽  
Author(s):  
E. O. Feigl
Keyword(s):  
Blood Flow ◽  
Metabolic Control ◽  
Coronary Blood Flow ◽  
Oxygen Tension ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Strenuous Exercise ◽  
Unexpected Finding ◽  
Coronary Vasoconstriction ◽  
Coronary Physiology

The major areas of normal coronary physiological research since Berne's 1964 review have been the measurement of ventricular transmural blood flow distribution with microspheres, the adenosine hypothesis of local metabolic control of coronary blood flow, and the autonomic control of coronary blood flow. There is an improved understanding of intramyocardial tissue pressure and extravascular compressive forces on coronary vessels. However, the unexpected finding of zero flow during a prolonged diastole with a coronary artery pressure of 40 mmHg (PZF) is a reminder that the physical forces, including vascular smooth muscle contraction, that determine coronary vascular resistance are incompletely understood. During normal circumstances, the left ventricular subendocardium probably receives more blood flow than the subepicardium does, but the difference is small. When the coronary circulation is compromised by stenosis or aortic valve lesions, the subendocardium is much more vulnerable to underperfusion than is the subepicardium. The coronary vasodilating effect of arterial hypoxia has been confirmed in many studies, but the role of tissue oxygen tension in local metabolic control of coronary blood flow during normoxia is unknown. The coronary vasodilating action of carbon dioxide has received renewed attention, but its role in local control is also unknown. The adenosine hypothesis has passed several critical tests, but despite much research the importance of adenosine in normal coronary regulation is not established. Local metabolic control of coronary blood flow probably involves more than just one factor, but a unified hypothesis has not been put forward. Sympathetic alpha-receptor-mediated coronary vasoconstriction has been demonstrated by nerve stimulation and during a carotid sinus baroreceptor reflex. Sympathetic coronary vasoconstriction is capable of competing with local metabolic control to lower coronary venous oxygen tension under experimental circumstances, but its importance during normal resting conditions is not established. Parasympathetic muscarinic coronary vasodilation has been shown by vagal nerve stimulation, but a role for it during normal blood flow regulation has yet to be demonstrated. There have been elegant descriptive studies of the coronary blood flow response during excitement and exercise, where coronary blood flow increases pari passu with myocardial metabolism; however, there are also data that indicate a concomitant sympathetic vasoconstrictor effect during strenuous exercise. Overall there has been encouraging progress in coronary physiology. Inevitably new knowledge has focused old questions and presented new ones.

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.

Myocardial oxygenation and adenosine release in isolated guinea pig hearts during changes in contractility

2005 ◽  
Vol 288 (5) ◽  
pp. H2062-H2067 ◽  
Author(s):  
J. Chiaka Ejike ◽  
Lorilee S. L. Arakaki ◽  
Daniel A. Beard ◽  
Wayne A. Ciesielski ◽  
Eric O. Feigl ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Oxygen Tension ◽  
Near Infrared ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Maximum Pressure ◽  
Epinephrine Infusion ◽  
Adenosine Concentration ◽  
Hypoxic Fraction ◽  
Perfused Hearts

Previous work from this laboratory using near-infrared optical spectroscopy of myoglobin has shown that ∼20% of the myocardium is hypoxic in buffer-perfused hearts that are perfused with fully oxygenated buffer at 37°C. The present study was undertaken to determine cardiac myoglobin saturation in buffer-perfused hearts when cardiac contractility was increased with epinephrine and decreased during cardiac arrest with KCl. Infusion of epinephrine to achieve a doubling of contractility, as measured by left ventricular maximum pressure change over time (dP/d t), resulted in a decrease in mean myoglobin saturation from 79% at baseline to 65% and a decrease in coronary venous oxygen tension from 155 mmHg at baseline to 85 mmHg. Cardiac arrest with KCl increased mean myoglobin saturation to 100% and coronary venous oxygen tension to 390 mmHg. A previously developed computer model of oxygen transport in the myocardium was used to calculate the probability distribution of intracellular oxygen tension and the hypoxic fraction of the myocardium with an oxygen tension below 0.5 mmHg. The hypoxic fraction of the myocardium was ∼15% at baseline, increased to ∼30% during epinephrine infusion, and fell to ∼0% during cardiac arrest. The coronary venous adenosine concentration changed in parallel with the hypoxic fraction of the myocardium during epinephrine and KCl. It is concluded that catecholamine stimulation of buffer-perfused hearts increases hypoxia in the myocardium and that the increase in venous adenosine concentration is a reflection of the larger hypoxic fraction of myocardium that is releasing adenosine.

Coronary vasomotor tonus in moderate hypothermia

1962 ◽  
Vol 203 (5) ◽  
pp. 825-828 ◽  
Author(s):  
Cecil E. Cross ◽  
P. Andre Rieben ◽  
Peter F. Salisbury
Keyword(s):  
Oxygen Tension ◽  
Coronary Vessels ◽  
Arterial Oxygen Tension ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Arterial Oxygen ◽  
Moderate Hypothermia ◽  
Right Heart ◽  
Blood Temperature

Coronary blood flow was measured in open-chest preparations with fixed cardiac output and bypassed right heart. Arterial oxygen tension (pO2), pH, and temperature were measured. The slope of regression lines between mean coronary driving pressure (aortic pressure minus left ventricular pressure) and coronary flow indicated directional changes of coronary vasomotor tonus. During periods of blood cooling in nonfailing hearts the coronary vessels dilated only when arterial oxygen tension was permitted to fall, but not when pO2 remained stable. In failing hearts moderate decreases of blood temperature and pO2 did not cause further decrements of coronary vasomotor tonus. It was concluded that blood temperature per se did not influence coronary vasomotor tonus.

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.

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Intracellular EDEMA does not adversely affect the ability to cryopreserve intact hearts

1993 ◽  
Vol 51 ◽  
pp. 278-279
Author(s):  
CL Hastings ◽  
RD Carlton ◽  
FG Lightfoot ◽  
AF Tryka
Keyword(s):  
Cell Injury ◽  
Median Sternotomy ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Hypoxic Cell ◽  
Free Wall ◽  
Sprague Dawley ◽  
Left Ventricular Free Wall ◽  
Sprague Dawley Rats

The earliest ultrastructural manifestation of hypoxic cell injury is the presence of intracellular edema. Does this intracellular edema affect the ability to cryopreserve intact myocardium? To answer this guestion, a model for anoxia induced intracellular edema (IE) was designed based on clinical intraoperative myocardial preservation protocol. The aortas of 250 gm male Sprague-Dawley rats were cannulated and a retrograde flush of Plegisol at 8°C was infused over 90 sec. The hearts were excised and placed in a 28°C bath of Lactated Ringers for 1 h. The left ventricular free wall was then sliced and the myocardium was slam frozen. Control rats (C) were anesthetized, the hearts approached by median sternotomy, and the left ventricular free wall frozen in situ immediately after slicing. The slam frozen samples were obtained utilizing the DDK PS1000, which was precooled to -185°C in liguid nitrogen. The tissue was in contact with the metal mirror for a dwell time of 20 sec, and stored in liguid nitrogen until freeze dry processing (Lightfoot, 1990).

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