摘要:

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 alterationsviaa cisterna magna infusion catheter. Hyperventilation (Paco2= 28–30 mmHg) and mannitol were used to shrink the brain to accommodate intracranial infusion of either air or lactated Ringer's (LR) solution, which was used to elevate ICP to between 10–15 mmHg from a baseline ICP of 2.1 ± 2.5 mmHg over a period of 8 to 10 min. Following stabilization at an elevated ICP, inhalation of nitrous oxide (75%) was either initiated or withdrawn (if already present during the induced ICP increase) and the subsequent changes in mean ICP and BP were recorded.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< 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 controlP< 0.001). Withdrawal of N2O after ICP had been elevated (15.2 ± 1.0 mmHg) by air infusion during N2O administration caused an abrupt and significant (P< 0.001) decrease in ICP ranging to 5.0 ± 4.6 mmHg, accompanied by a modest BP decline. These results confirm that N2O can diffuse back into the blood stream from a previously equilibrated intracranial gas cavity and lowers ICP when N2O is eliminated from the inspired gases. These findings suggest that discontinuance of N2O anesthesia after cranial-dural closure in patients who have a potential for developing significant pneumocephalus might reduce the potential for development of delayed tension pneumocephalus following craniectomy performed in the sitting position.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The effect of chronic alcohol intake on anesthetic responses to alcohol, thiopental, or diazepam was examined in adult male Sprague-Dawley rats. Alcohol-fed animals were maintained solely on a complete balanced liquid diet containing 6.54% ethanol (w/w) for 21 days; pair-fed control animals received equal amounts of the same diet with alcohol isocalorically replaced by sucrose or dextrin. Nine hours after diets were withdrawn on the twenty-second day, the following drug/dose combinations were administered intraperitoneally to separate groups of alcohol-fed and control rats (10–15 animals in each group): ethanol 2.4, 3.2, and 4.0 g/kg; thiopental 20, 40, and 80 mg/kg; and diazepam 10, 20, and 40 mg/kg. Three different responses were assessed in every animal: 1) loss of righting reflex (induction of anesthesia); 2) response to a painful stimulus (analgesia); and 3) sleeping time (duration of anesthesia). Alcoholfed rats compared with controls were significantly less tolerant of pain at an acute alcohol dose of 2.4 g/kg, and loss of righting reflex and sleeping time were reduced at 4.0 g/kg. All three anesthetic responses were also attenuated in alcohol-fed rats at a diazepam dose of 20 mg/kg. In contrast, none of the three responses was reduced in alcohol-fed rats at any of the three thiopental doses. Thus, chronic alcohol intake sufficient to produce tolerance to anesthetic doses of alcohol in rats also produced cross-tolerance to diazepam but not to thiopental in equianesthetic doses. These results suggest that blanket recommendations for adjusting intravenous anesthetic dosages in alcoholic humans may be inadequate as guides to anesthetic management.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To determine the percentage of anesthetic metabolized and to assess the role of metabolism in the total elimination of inhaled anesthetics, the authors administered isoflurane, enflurane, halothane, and methoxyflurane simultaneously, for 2 h, to nine healthy patients. Total anesthetic uptake during the 2 h of washin and total recovery of unchanged anesthetic in exhaled gases during 5 to 9 days of washout were measured, and from these the per cent of anesthetic uptake that was recovered was calculated. Of the isoflurane taken up, 93 ± 4% (mean ± SE) was recovered. To compensate for factors other than metabolism that limit complete recovery of unchanged anesthetic, the percentage recovery of each anesthetic was normalized to the percentage recovery of isoflurane (which it was assumed undergoes no metabolism). Deficits in normalized recovery were assumed to be due to metabolism of the anesthetics. The resulting estimates of metabolism of anesthetic taken up were: enflurane 8.5 ± 1.0%, halothane 46.1 ± 0.9%, and methoxyflurane 75.3 ± 1.6%. These results indicate that elimination is primarilyviathe lungs for isoflurane and enflurane, equallyviathe lungs andviametabolism for halothane, and primarilyviametabolism for methoxyflurane.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The authors tested the effects of injectate temperature and of changing cardiac output on the measurement of lung water by the thermoconductivity technique (ETVL). Cardiac output in dogs was increased and decreased with isoproterenol and halothane, respectively. Post mortem extravascular lung water (pulmonary extravascular tissue weight [PETW]) was determined using a weighing technique. Cardiac output varied between 0.7 and 8.8 1/min and did not influence the ETVLmeasurement. The authors conclude ETVLmeasured by the thermoconductivity technique is not influenced by large changes in cardiac output.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID