Plasma ATP Research Articles

On reactive heat conduction for multiple ionized two-temperature argon plasma

Two models to computer equilibrium composition of a two temperature plasma with degree of ionization larger than one have been evaluated, and the range of validity of each model is discussed. These are then applied further for the calculation of the ambi-polar diffusion coefficient and the reactive heat conduction coefficient for the electrons and the heavy particles. Numerical results for multiple-ionized two-temperature argon plasma atp=1 bar are presented.

A proposal for the role of ecto-enzymes and adenylates in traumatic shock

It is proposed that the biochemical mechanisms which lead to the pathology of irreversible traumatic shock are based on the vasodilatory action of adenylates and failure of ecto-enzymes to clear these substances from the vascular bed. Following massive injury, or another assault which produces significant cytolysis, cytoplasmic ATP is released into the circulation. Ecto-phosphoesterhydrolases on erythrocytes normally control plasma adenylate concentrations to be maintained below 10 −7 M. If a critical ATP (or ADP) concentration between 10 −5 and 10 −4 M is reached, erythrocytes become semi-permeable and themselves release additional ATP into the plasma compartment. When ecto-ATPase activity becomes insufficient in metabolizing plasma ATP at rates which are needed to compensate for the release of cytoplasmic ATP, the vasodilatory effects of adenylates will manifest themselves in a sustained manner. It is suggested that ecto-phosphoesterhydrolases on blood formed elements and endothelial cells serve a protective function. Circulatory shock ensues under conditions when these ecto-enzymes are rendered incompetent or when plasma adenylate concentrations exceed their catabolic capacity.

CARDIOPULMONARY DYSFUNCTIONS CAUSED BY INTRAVENOUS COLLAGEN-INDUCED RELEASE OF ADP AND ATP FROM PLATELETS

Bovine tendon collagen suspension (4.5 mg/kg) was injected rapidly into the femoral vein of 14 normal (untreated) and 8 busulfan treated rats. Trasient effects included decreased platelet counts and arterial PO2, increased central venous pressure, apnea, bradycardia and variable A-V block. These findings were most prominent within 1 minute after injection and subsided or disappeared by 10 minutes. During this period, ADP and ATP in platelet-free plasma from carotid arterial blood were measured in a liquid scientillation counter using the firefly luciferase assay. In normal (untreated) rats, collagen injection was followed by increases in plasma ADP and ATP, a rise in plasma hemoglobin and minimal changes of fibrinogen and hematcrit. Pathological observations indicated the platelet emboli in pulmonary vessels. In contrast, rats made thrombocytopenic by intraperitoneally infected busulfan prior to collagen injection had minimal or no change in platelet count, plasma ADP, ATP, hemoglobin, fibrinogen, or cardiopulmonary functions following collagen injection. These findings suggest that collagen injection causes release of ADP and ATP from platelets; released ADP induces platelets to form aggregates which lodge in the coronary and pulmonary microcirculations and elsewhere, resulting in thrombocytopenia and the cardiopulmonary dysfunction, in the presence of shear, of red cells with vessel surfaces altered by platelet aggregates.

Rest and exercise plasma nucleottoes

Previous studies have reported an increase in ventilatory rate with injections of adenosine triphosphate and adenosine diphosphate. The present study considers the possibility that ATP or ADP could be released from exercising skeletal muscle into the circulation and produce part of the ventilatory response to exercise. Plasma levels of ATP and ADP from both venous and arterial blood were determined in resting and exercising subjects. There was no detectable plasma ATP or ADP with the method used. Either these nucleotides are not released into the circulation, or they are rapidly altered, or they are present in amounts too small to be detected by this method.

Local effect of adenosine mono-, di-, and triphosphate vessel resistance.

The local effects of adenosine mono-, di-, and triphosphate (AMP, ADP, and ATP) on resistance to blood flow through large and small vessels of the forelimb were studied in 14 anesthetized dogs. This was accomplished by holding blood flow constant to the forelimb while pressures in the brachial artery, cephalic vein, and a small artery and vein in the forepaw were recorded. Acute local elevation of plasma AMP, ADP, and ATP concentration greatly decreased resistance to blood flow in the small vessels over a wide dose range. It is concluded that AMP, ADP, and ATP act primarily on small vessels, and particularly arterioles, to produce active vasodilatation.

保存血球の溶血,電解質移動,並びに炭酸脱水酵素活性に及ぼす糖質, ATP, Thiol化合物,血漿の影響

保存血球の溶血,電解質移動,並びに炭酸脱水酵素活性に及ぼす糖質, ATP, Thiol化合物,血漿の影響