Anesthesiology
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Nitrous oxide anesthesia has been implicated as contributing to the development of delayed tension pneumocephalus following surgery performed in the sitting position. The authors tested the hypothesis that withdrawal of nitrous oxide anesthesia administered during formation of an intracranial gas cavity would lead to a decrease in intracranial pressure (ICP) as N2O diffuses from the cavity back into the blood. Ten halothane-anesthetized rabbits were prepared for measurement of supracortical ICP and arterial blood pressure (BP) and for intracranial volume alterations via a cisterna magna infusion catheter. ⋯ Following stabilization at an elevated ICP, inhalation of nitrous oxide (75%) was either initiated or withdrawn (if already present during the induced ICP increase) and the subsequent changes in mean ICP and BP were recorded. Following ICP elevation with LR to 10 +/- 1 mmHg, initiation of 75% N2O administration resulted in no change in ICP and modest increases (P less than 0.05) in BP and cerebral perfusion pressure (CPP = BP - ICP) after 4 min. However, when ICP was raised (to 12 +/- 3.5 mmHg) with intracranial air infusion, subsequent initiation of 75% N2O inhalation caused an abrupt ICP increase to 22.3 +/- 9 mmHg (from control P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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To determine if clinical concentrations of halothane have direct relaxant effects on airway smooth muscle, the authors compared dose-response curves to histamine in the control state (thiopental) and during halothane anesthesia (1.0 and 1.5 MAC), in six basenji-greyhound (BG) dogs untreated and pretreated with atropine aerosols (10 mg X ml-1). Pulmonary resistance (RL) and dynamic compliance (Cdyn) were continuously monitored. Baseline airway tone was not significantly different during thiopental, halothane (1.0 MAC and 1.5 MAC), and after atropine aerosol administration. ⋯ There was no significant differences in the extent of antagonism of histamine-related bronchoconstriction between halothane (1.0 MAC and 1.5 MAC) and the atropine aerosol. Moreover, in four dogs halothane anesthesia in the presence of atropine offered no additional protection compared with atropine alone. Because the protection afforded by halothane was not greater than that of atropine pretreatment alone, and the addition of halothane to atropine failed to increase the protection, it is concluded that block of vagal reflexes was the major action of halothane responsible for the attenuation of histamine-induced bronchoconstriction.
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Randomized Controlled Trial Comparative Study Clinical Trial
A comparison of nitroglycerin and nitroprusside for inducing hypotension in children: a double-blind study.
Intravenous nitroglycerin (NTG) and sodium nitroprusside (SNP) were compared as hypotensive agents in anesthetized children and adolescents. The drugs were studied in a prospective, randomized, double-blind fashion in 14 patients anesthetized with nitrous oxide: oxygen, morphine, and thiopental. NTG in doses as high as 40 micrograms X kg-1 X min-1 was ineffective at decreasing mean arterial pressure (MAP) below 55 mmHg or causing a decrease in MAP greater than one-third of baseline values. ⋯ SNP use was associated with a slight metabolic acidosis (pH = 7.38 +/- 0.01; base excess [BE] = -6 +/- 1). Neither drug produced any other untoward reaction. SNP appears to be the agent of choice for the reliable and sustained induction of deliberate hypotension in children and adolescents.
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Whether succinylcholine causes an increase in intracranial pressure (ICP) in patients with brain lesions is uncertain and, if increased ICP does occur, its pathophysiology remains unknown. The authors investigated both the effect of succinylcholine on ICP and its modification with prior neuromuscular blockade by measuring ICP (subarachnoid bolt) in 13 consecutive patients with brain tumors who received succinylcholine both before and after complete neuromuscular blockade with vecuronium. Anesthesia was induced with thiopental, 6 mg X kg-1 iv, and nitrous oxide, 70% in oxygen, while ventilation was controlled (PaCO2 = 37.2 mmHg +/- 1.7 SE). ⋯ Following the first dose of succinylcholine, mean ICP increased from 15.2 mmHg +/- 1.3 SE to 20.1 mmHg +/- 2.0 SE (P less than 0.05), with five of the patients sustaining increases in ICP of 9 mmHg or greater. In contrast, when succinylcholine was given after vecuronium-induced paralysis, no patient developed an increase in ICP greater than 3 mmHg (P less than 0.05 compared with the incidence of ICP greater than or equal to 9 mmHg observed after the first dose of succinylcholine). A second group of six patients received two doses of succinylcholine according to the same protocol but without an intervening dose of vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)