Critical care medicine
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Critical care medicine · Jan 1996
Adrenergic vasopressor agents and mechanical ventilation for the treatment of experimental septic shock.
Vasopressor agents and mechanical ventilation are routine interventions for the treatment of sepsis complicated by hypotension. It was our hypothesis that such treatment singly or in combination increases the duration of survival. ⋯ No benefit or detriment was demonstrated when vasopressor agents were administered to sustain arterial pressure in the course of experimental peritonitis in this murine model of septic shock. This finding contrasted with highly significant prolongation of survival when animals were mechanically ventilated. There was no evidence that routine vasopressor therapy, under these controlled experimental conditions in rats, improved duration of survival.
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Critical care medicine · Jan 1996
Hypertonic saline does not improve cerebral oxygen delivery after head injury and mild hemorrhage in cats.
To investigate the effects of hypertonic saline for resuscitation after mild hemorrhagic hypotension combined with fluid-percussion traumatic brain injury. Specifically, the effects of hypertonic saline on intracranial pressure, cerebral blood flow (radioactive microsphere method), cerebral oxygen delivery (cerebral oxygen delivery = cerebral blood flow x arterial oxygen content), and electroencephalographic activity were studied. ⋯ After a combination of hemorrhage and traumatic brain injury, neither 10% hydroxyethyl starch nor 3.0% hypertonic saline restored cerebral oxygen delivery. Although neither trauma alone nor hemorrhage alone altered electroencephalographic activity, the combination produced significant decreases in electroencephalographic activity at 60 and 120 mins after resuscitation in groups 3 and 4, suggesting that cerebral oxygen delivery is inadequately restored by either resuscitation fluid. Therefore, traumatic brain injury abolished compensatory cerebral blood flow increases to hemodilution, and neither hydroxyethyl starch nor 3.0% hypertonic saline restored cerebral blood flow, cerebral oxygen delivery, or electroencephalographic activity after hemorrhagic hypotension after traumatic brain injury.
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Critical care medicine · Jan 1996
Burn injury alters beta-adrenergic receptor and second messenger function in rat ventricular muscle.
The molecular pharmacologic bases for the attenuated cardiovascular and metabolic responses to catecholamines, after burn injury, have not been elucidated. In the present study, myocardial tissues were used as a model of beta-adrenergic receptors to study burn injury-induced alterations in receptors and in signal transduction. ⋯ The etiology of the decreased responses in the myocardium to exogenous and endogenous beta-adrenergic receptor agonists after burn injury may be attributed to decreased affinity for ligands, and also to impaired receptor-mediated signal transduction and to decreased adenylate cyclase enzyme activity, resulting in decreased basal and stimulated second messenger (cAMP) production.
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Critical care medicine · Jan 1996
Comment Letter Comparative StudyPropofol vs. midazolam for sedation.