Journal of critical care
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Journal of critical care · Dec 1996
The effects of high dose NG-nitro-L-arginine-methyl ester on myocardial blood flow and left ventricular function in dogs.
Nitric oxide (NO) synthase inhibition has been reported to cause elevation in mean arterial pressure (MAP) and a decrease in cardiac index (CI), the cause of which is not completely understood. It has been shown that increased concentrations of NO synthase inhibitors cause a further drop in cardiac output without a corresponding increase in arterial pressure, prompting the conclusion that NO inhibition results in direct myocardial depression. However, myocardial ischemia was not completely ruled out as a cause for myocardial dysfunction in these studies. The purpose of this study was to examine the effects of 30 mg/kg of the NO synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) to those of 300 mg/kg and assess the effects on coronary ischemia and myocardial function. ⋯ L-NAME at 30 mg/kg caused a rise in MAP and systemic vascular resistance; however, it had no effect on ventricular function. High dose NO synthase inhibition causes myocardial depression not related to increased afterload, coronary vasoconstriction, or myocardial ischemia.
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The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (Cv), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized. ⋯ Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.
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Journal of critical care · Dec 1996
Central venous pressure, pulmonary artery occlusion pressure, intrathoracic blood volume, and right ventricular end-diastolic volume as indicators of cardiac preload.
Central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and right ventricular end-diastolic volume (RVEDV) are often regarded as indicators of both circulating blood volume and cardiac preload. to evaluate these relationships, the response of each variable to induced volume shifts was tested. The relationships between these variables and cardiac index (CI) and stroke volume index (SVI) was also recorded to assess the utility of each variable as an indicator of cardiac preload. The responses of the new variable intrathoracic blood volume (ITBV) to the same maneuvers was also tested. To examine the effects of changes in cardiac output alone on ITBV, the effects of infusing dobutamine were studied. ⋯ Under the experimental conditions chosen neither CVP, PAOP, nor RVEDV reliably indicated changes in circulating blood volume, nor were they linearly and tightly correlated to the resulting changes in SVI. ITBV reflected both changes in volume status and the resulting alteration in cardiac output. The possibility that ITBV might be cardiac output-dependent was not supported. ITBV, therefore, shows potential as a clinically useful indicator of overall cardiac preload.
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Journal of critical care · Dec 1996
Anti-CD18 antibodies improve cardiac function following cardiopulmonary bypass in dogs.
Cardiopulmonary bypass is associated with activation of neutrophils, which may adhere to vascular endothelium causing lung, heart, and brain injury. We tested whether blocking neutrophil adherence would improve organ function following cardiopulmonary bypass in dogs. ⋯ Monoclonal antibodies to CD18 can prevent the deterioration in cardiac function routinely observed following cardiopulmonary bypass.
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Journal of critical care · Dec 1996
Editorial Comment ReviewCardiovascular derangement in septic shock and nitric oxide.