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adenosine/hemorragia
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Arterial and venous plasma concentrations of adenosine during haemorrhage.
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A haemorrhage model was used to impose severe metabolic stress in anaesthetized cats by removing blood (15.3 ml min-1) to attain an arterial pressure of ca. 50 mmHg for a 2 h period. Adenosine levels in central venous blood rose by 5 min, reached a peak of about 3.5 times control levels by 15 min
Glutamine administration during total parenteral nutrition protects liver adenosine nucleotides during and after subsequent hemorrhagic shock.
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BACKGROUND
Glutamine supplementation of total parenteral nutrition (TPN) in stressed patients has been advocated. To determine whether glutamine supplementation affects the host response to conditions of stress, animals were given TPN with or without glutamine for 7 days. They were then subjected to
Intraperitoneal, but not enteric, adenosine administration improves survival after volume-controlled hemorrhagic shock in rats.
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OBJECTIVE
To circumvent the potential adverse systemic side effects of adenosine, this study explored the potential benefit of intraperitoneal or enteric adenosine on survival and inflammatory responses after volume-controlled hemorrhagic shock.
METHODS
Prospective, randomized, and blinded. A
Stimulation of the adenosine A3 receptor reverses vascular hyporeactivity after hemorrhagic shock in rats.
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OBJECTIVE
To investigate whether adenosine A(3) receptors (A(3)AR) stimulation restore vascular reactivity after hemorrhagic shock through a ryanodine receptor (RyR)-mediated and large conductance calcium-activated potassium (BK(Ca)) channel-dependent pathway.
METHODS
Rat hemorrhagic shock model (40
Adenosine triphosphate-sensitive potassium channels prevent extension of myocardial ischemia to subepicardium during hemorrhagic shock.
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Cardiac dysfunction during hemorrhagic shock (HS) is associated with myocardial ischemia, during which adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channels can be activated. We investigated the role of K(ATP) channels in HS-induced myocardial ischemia. Canine HS was induced using an
Parenteral administration of glipizide sodium salt, an inhibitor of adenosine triphosphate-sensitive potassium channels, prolongs short-term survival after severe controlled hemorrhage in rats.
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OBJECTIVE
Recent experimental evidence suggests that activation of adenosine triphosphate (ATP)-sensitive potassium channels contributes to vascular failure and early mortality after hemorrhagic shock. The present investigation evaluated the effects of the water-soluble sodium salt of glipizide, an
[Effects of exogenous adenosine on myocardial recovery after acute hemorrhage].
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This study was designed to investigate whether reperfusion with adenosine had an effect on myocardial high energy phosphate levels and cardiac function in hearts extracted from acutely hemorrhaged rats. Rats were bled to a mean arterial pressure of 0 mmHg for 5, 10 or 15 minutes and hearts were
Glaxo/MRS Young Investigator Medal. Molecular studies on adenosine deaminase deficiency and hereditary haemorrhagic telangiectasia.
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1. This manuscript describes two different strategies to progress from the clinical assessment of patients to the identification of disease-causing mutations. In the first disease, recognition of a metabolic abnormality allowed direct molecular analysis of the causal gene. In contrast, localization
Adenosine A2A receptor activation reduces lung injury in trauma/hemorrhagic shock.
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OBJECTIVE
Hemorrhagic shock and resuscitation trigger a global ischemia/reperfusion phenomenon, in which various inflammatory processes critically contribute to the ensuing tissue damage. Adenosine is an endogenous nucleoside that is released during shock. Activation of adenosine A(2A) receptors can
Erythropoietin production in healthy volunteers subjected to controlled haemorrhage: evidence against a major role for adenosine.
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1. This study was carried out to assess the role of adenosine in the regulation of human erythropoietin (EPO) production. To this end we investigated in healthy volunteers whether the nonspecific adenosine antagonist theophylline increases and the adenosine uptake inhibitor dipyridamole decreases
Determination of serum adenosine deaminase and xanthine oxidase levels in patients with crimean-congo hemorrhagic fever.
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OBJECTIVE
Crimean-Congo hemorrhagic fever is an acute viral hemorrhagic fever with a high mortality rate. Despite increasing knowledge about hemorrhagic fever viruses, little is known about the pathogenesis of Crimean-Congo hemorrhagic fever. In this study, we measured serum adenosine deaminase and
Na+ minus K+ transport and adenosine nucleotides in the lung in hemorrhagic shock.
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This study was undertaken to determine the effects of hemorrhagic shock on cellular energy production and utilization in the lung. Energy-dependent Na+ minus K+ transport was measured by quantitating tissue cation changes during a cold (0.5 degrees C.) and a subsequent warm (37 degrees C.)
Role of adenosine in noradrenergic neurotransmission during hemorrhagic hypotension.
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The purpose of this study was to test the hypothesis that endogenous adenosine suppresses noradrenergic neurotransmission during hemorrhagic hypotension. Rats were prepared for in situ blood-perfusion of their mesenteric vascular beds and received throughout the protocol an intramesenteric artery
Adenosine stimulates NA/K ATPase and prolongs survival in hemorrhagic shock.
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BACKGROUND
Hemorrhagic shock leads to the appearance of substances in plasma that can change Na/K ATPase activity. Our laboratory has reported the existence of a plasma inhibitor of Na/K ATPase that appears during shock. Recently, we have isolated a substance in plasma that stimulates Na/K
Maintenance of hepatic arterial blood flow during hemorrhage is mediated by adenosine.
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The effect of hemorrhage (1.91 mL/min, 10 mL/kg) on splanchnic blood flow was determined in cats anesthetized with pentobarbital. The hepatic artery (HA) is relatively protected during hemorrhage and does not constrict, whereas the superior mesenteric artery (SMA) undergoes significant
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