Hypoxia And The Circulation

Just one of a series of volumes on differing aspects of hypoxia, this authoritative text focuses on cutting-edge research at the interface of hypoxia and biomedicine. Hypoxia – or lack of oxygen – is a constant threat to the human body and its vital organs, one that can take its toll in a number of situations. There are many situations in which the threat is heightened in health and disease, but mechanisms have evolved to lessen its detrimental effects. The International Hypoxia Symposia was founded to enable scientists, clinicians, physiologists, immunologists, mountaineers and other interested individuals to share their experiences of the situations associated with the lack of oxygen and the adaptations that allow us to survive.

This e-book will review special features of the cerebral circulation and how they contribute to the physiology of the brain. It describes structural and functional properties of the cerebral circulation that are unique to the brain, an organ with high metabolic demands and the need for tight water and ion homeostasis. Autoregulation is pronounced in the brain, with myogenic, metabolic and neurogenic mechanisms contributing to maintain relatively constant blood flow during both increases and decreases in pressure. In addition, unlike peripheral organs where the majority of vascular resistance resides in small arteries and arterioles, large extracranial and intracranial arteries contribute significantly to vascular resistance in the brain. The prominent role of large arteries in cerebrovascular resistance helps maintain blood flow and protect downstream vessels during changes in perfusion pressure. The cerebral endothelium is also unique in that its barrier properties are in some way more like epithelium than endothelium in the periphery. The cerebral endothelium, known as the blood-brain barrier, has specialized tight junctions that do not allow ions to pass freely and has very low hydraulic conductivity and transcellular transport. This special configuration modifies Starling's forces in the brain microcirculation such that ions retained in the vascular lumen oppose water movement due to hydrostatic pressure. Tight water regulation is necessary in the brain because it has limited capacity for expansion within the skull. Increased intracranial pressure due to vasogenic edema can cause severe neurologic complications and death.

This presentation describes various aspects of the regulation of tissue oxygenation, including the roles of the circulatory system, respiratory system, and blood, the carrier of oxygen within these components of the cardiorespiratory system. The respiratory system takes oxygen from the atmosphere and transports it by diffusion from the air in the alveoli to the blood flowing through the pulmonary capillaries. The cardiovascular system then moves the oxygenated blood from the heart to the microcirculation of the various organs by convection, where oxygen is released from hemoglobin in the red blood cells and moves to the parenchymal cells of each tissue by diffusion. Oxygen that has diffused into cells is then utilized in the mitochondria to produce adenosine triphosphate (ATP), the energy currency of all cells. The mitochondria are able to produce ATP until the oxygen tension or PO2 on the cell surface falls to a critical level of about 4–5 mm Hg. Thus, in order to meet the energetic needs of cells, it is important to maintain a continuous supply of oxygen to the mitochondria at or above the critical PO2 . In order to accomplish this desired outcome, the cardiorespiratory system, including the blood, must be capable of regulation to ensure survival of all tissues under a wide range of circumstances. The purpose of this presentation is to provide basic information about the operation and regulation of the cardiovascular and respiratory systems, as well as the properties of the blood and parenchymal cells, so that a fundamental understanding of the regulation of tissue oxygenation is achieved.

In recent years, there has been a wealth of new information on the physiological and biochemical consequences of hypoxia, or low blood levels of oxygen. This new volume discusses the implications of these new findings on the pathophysiology, development, and treatment of hypoxic metabolic acidosis. The volume is part of the Clinical Physiology series sponsored by the American Physiological Society, and is based on a FASEB symposium held in May 1988. Hypoxia was once thought to affect organs in a similar manner, but it is now known that each is affected differently. The author shows how hypoxia and metabolic acidosis affect the heart, lungs, blood vessels and other organs at the cellular level, the tissue level, and finally, at the level of the entire organ. The book then proceeds to a description of the situations in which hypoxic metabolic acidosis develops, such as during high altitude exposure, cardiac arrest, and lactic acidosis. The last few chapters give an overview of treatment. Traditional therapy has consisted largely of the intravenous administration of sodium bicarbonate. This method has come under increasing scrutiny however, and the range of problems associated with the use of sodium bicarbonate is examined fully. Newer alternative agents for managing hypoxic acidosis are reviewed as well. This up-to-date review of hypoxia and metabolic acidosis should be of interest to physiologists, internists, cardiologists, chest physicians, anesthesiologists, and intensive care specialists.

Just one of a series of volumes on differing aspects of hypoxia, this authoritative text focuses on cutting-edge research at the interface of hypoxia and biomedicine. Hypoxia – or lack of oxygen – is a constant threat to the human body and its vital organs, one that can take its toll in a number of situations. There are many situations in which the threat is heightened in health and disease, but mechanisms have evolved to lessen its detrimental effects. The International Hypoxia Symposia was founded to enable scientists, clinicians, physiologists, immunologists, mountaineers and other interested individuals to share their experiences of the situations associated with the lack of oxygen and the adaptations that allow us to survive.

Research centering on blood flow in the heart continues to hold an important position, especially since a better understanding of the subject may help reduce the incidence of coronary arterial disease and heart attacks. This book summarizes recent advances in the field; it is the product of fruitful cooperation among international scientists who met in Japan in May, 1990 to discuss the regulation of coronary blood flow.

All aspects of oxygen transport and tissue oxygenation that are relevant in clinical medicine are covered in this monograph. Experts from basic science as well as clinical research provide information that improves understanding of how to treat O2-transport disturbances in daily practice. Special interest is focussed on the question of supply dependency of O2-uptake and its role in multi-organ failure in the critically ill. Other topics are the clinical monitoring of O2-transport and O2-utilisation, oxygen toxicity, and the role of O2-radicals and the reperfusion syndrome in organ transplantation and cardiopulmonary resuscitation.

The aim of this treatise is to summarize the current understanding of the mechanisms for blood flow control to skeletal muscle under resting conditions, how perfusion is elevated (exercise hyperemia) to meet the increased demand for oxygen and other substrates during exercise, mechanisms underlying the beneficial effects of regular physical activity on cardiovascular health, the regulation of transcapillary fluid filtration and protein flux across the microvascular exchange vessels, and the role of changes in the skeletal muscle circulation in pathologic states. Skeletal muscle is unique among organs in that its blood flow can change over a remarkably large range. Compared to blood flow at rest, muscle blood flow can increase by more than 20-fold on average during intense exercise, while perfusion of certain individual white muscles or portions of those muscles can increase by as much as 80-fold. This is compared to maximal increases of 4- to 6-fold in the coronary circulation during exercise. These increases in muscle perfusion are required to meet the enormous demands for oxygen and nutrients by the active muscles. Because of its large mass and the fact that skeletal muscles receive 25% of the cardiac output at rest, sympathetically mediated vasoconstriction in vessels supplying this tissue allows central hemodynamic variables (e.g., blood pressure) to be spared during stresses such as hypovolemic shock. Sympathetic vasoconstriction in skeletal muscle in such pathologic conditions also effectively shunts blood flow away from muscles to tissues that are more sensitive to reductions in their blood supply that might otherwise occur. Again, because of its large mass and percentage of cardiac output directed to skeletal muscle, alterations in blood vessel structure and function with chronic disease (e.g., hypertension) contribute significantly to the pathology of such disorders. Alterations in skeletal muscle vascular resistance and/or in the exchange properties of this vascular bed also modify transcapillary fluid filtration and solute movement across the microvascular barrier to influence muscle function and contribute to disease pathology. Finally, it is clear that exercise training induces an adaptive transformation to a protected phenotype in the vasculature supplying skeletal muscle and other tissues to promote overall cardiovascular health. Table of Contents: Introduction / Anatomy of Skeletal Muscle and Its Vascular Supply / Regulation of Vascular Tone in Skeletal Muscle / Exercise Hyperemia and Regulation of Tissue Oxygenation During Muscular Activity / Microvascular Fluid and Solute Exchange in Skeletal Muscle / Skeletal Muscle Circulation in Aging and Disease States: Protective Effects of Exercise / References