Immune complexes in aids with chronic viral hepatitis B and/or C . UMDNJ-New Jersey Medical School Liver Center, Newark, New Jersey
Journal: Hepatology (1995)

1.Introduction2.Cardiovascular Function and Energetics2.1.Oxygen Transport by the Cardiovascular System2.2.Responses to Hypoxia2.3.Elasmobranch Cardiac Anatomy2.4.Cardiac Metabolic Biochemistry3.Factors Controlling and Effecting Cardiovascular Function3.1.Heart Rate and Stroke Volume3.2.Body Fluid Volume and Blood Pressure Regulation4.Signaling Mechanisms Effecting Blood Vessel Diameter4.1.Gasotransmitters4.2.Endothelins and Prostaglandins (Prostacyclin)4.3.Autonomic Nervous System Signaling Mechanisms (Adrenaline and Noradrenaline)4.4.Other Vascular Signaling Mechanisms (Acetylcholine, Adenosine, CNP, Serotonin, Vasoactive Intestinal Polypeptide, Bombesin, and Neuropeptide Y)4.5.Substances Affecting Gill Blood Flow Patterns5.The Action Potential and Excitation–Contraction (EC) Coupling in Elasmobranch Hearts: The Influences of Environmental, Biochemical, and Molecular Factors5.1.The Action Potential5.2.EC Coupling5.3.Effects of Catecholamines and Acetylcholine5.4.Effects of Temperature and Acidosis6.Practical Applications: Physiology in the Service of Elasmobranch Conservation6.1.Global Climate Change and Ocean Acidification6.2.Surviving Interactions with Fishing Gear7.SummaryThe functional characteristics of elasmobranch and teleost cardiovascular systems are similar at routine metabolic rates. Differences do become apparent, however, in cardiovascular function of high-energy-demand species (e.g., mako shark and yellowfin or skipjack tunas) at maximum metabolic rates. Elasmobranchs have an autonomic nervous system separable into parasympathetic and sympathetic components. The vagus nerve has a major role in controlling heart rate, although sympathetic innervation of the heart and blood vessels is absent. Elasmobranchs increase cardiac output primarily by increasing stroke volume which, in turn, is primarily determined by ventricular end diastolic volume. End diastolic volume is determined by filling time and venous filling pressure; with the latter being effected by venous tone and venous capacitance. Blood volume and pressure in elasmobranchs are controlled by endocrine (e.g., renin-angiotensin, kallikrein-kinin, and natriuretic peptides) and paracrine (e.g., endothelins, prostaglandins, the gasotransmitters NO and H2S,) mechanisms. Excitation-contraction (EC) coupling in elasmobranch hearts largely fits the accepted model for vertebrates, although the rise in cytoplasmic calcium is primarily from trans-sarcolemmal sources, which includes Na+-Ca2+ exchanger (NCX).Some elasmobranchs populations are severely depleted due to the intersection of life history characteristics, unsustainable rates of fisheries-associated mortality, and environmental degradation. To address these issues effectively will require a better understanding of the elasmobranch cardiovascular physiology – including the ability of various species to withstand the physiological consequences of the increasing temperature and expanding hypoxic zones accompanying global climate change, and the severe acidosis and the plasma ionic imbalances resulting from interactions with fishing gear.