Journal of critical care
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Journal of critical care · Mar 1995
An increase in low aortic pressure increases coronary artery flow and coronary thrombolysis induced by intravenous administration of recombinant tissue plasminogen activator.
Our study investigated the effects of an increase in aortic pressure, induced by norepinephrine (NE) administration on coronary artery flow in a clotted artery, and rate of coronary thrombolysis induced by intravenous (i.v.) administration of recombinant tissue plasminogen activator (rtPA). ⋯ These results indicate that an increase in a low coronary artery perfusion pressure may enhance coronary artery flow and the rate of thrombolysis.
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Journal of critical care · Dec 1994
ReviewEndothelial and vascular smooth muscle function in sepsis.
The vascular abnormalities that arise during sepsis imply disturbances in the delicately tuned homeostatic mechanisms of vascular endothelium and smooth muscle. In the microvasculature, smooth muscle tone represents a complex equilibrium among metabolic stimuli, hemodynamic forces, and neurohumoral influences. ⋯ In sepsis, derangement of normal autoregulation of perfusion, together with toxic effects of mediators, may be severe enough to result in organ dysfunction. Recent advances in vascular biology have illuminated a variety of targets, such as adhesion molecules, platelet activating factor, and inducible nitric oxide synthase for potential therapeutic intervention in sepsis.
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Journal of critical care · Dec 1994
Mechanisms of myocardial depression after bolus injection of sodium bicarbonate.
The classic model for the effects of NaHCO3 on myocardial function predicts transient myocardial depression after an intravenous bolus of sodium bicarbonate in association with myocardial acidosis. ⋯ We could not confirm the predictions of the classic model and hypothesize that myocardial depression may be caused by decreased availability of free Ca++ of decreased Ca++ flux rather than intracellular acidosis.
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Journal of critical care · Dec 1994
Dextran 70 administration after trauma-hemorrhagic shock does not impair cellular immune functions.
Although the effects of the colloid dextran 70 on induction of anaphylactoid reactions or reticuloendothelial phagocytosis have been examined previously, its effects on specific cell-mediated immunity after trauma-hemorrhage shock remain unknown. ⋯ The combination of LRS and colloid dextran 70 does not adversely affect ex vivo cell-mediated immune functions during the first 24 hours after its administration after trauma-hemorrhage. Thus, from the immunological standpoint, dextran is a safe resuscitation adjunct.
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The release of oxygen-free radicals has been implicated in both peripheral vascular and myocardial alterations of septic shock. N-Acetylcysteine (N-AC), a substrate for the production of glutathione, has potent antioxidant effects. As a nitrosothiol, it may also improve capillary blood flow. We studied the effects of N-AC in a dog model of endotoxic shock. ⋯ These data indicate that N-AC administration in endotoxic shock is well tolerated, may increase oxygen availability to the tissues, and is associated with an attenuation of TNF release.