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Biomedical subjects

N T Smith

Publications and source records attributed to N T Smith.

125 records · Page 7Linked to original sources
PubMed1967

Pressor agents.

Explore the source record for details and available documents.

Humans↗
PubMedDate not supplied

Pretreatment with sedative-hypnotics, but not with nondepolarizing muscle relaxants, attenuates alfentanil-induced muscle rigidity.

STUDY OBJECTIVE: To evaluate and compare the efficacy of various pretreatment agents to attenuate or prevent opioid-induced muscle rigidity using a well-established, previously described clinical protocol. DESIGN: Prospective, controlled, single-blind, partially randomized study. SETTING: Large medical center. PATIENTS: ASA physical status I-III patients undergoing elective surgical procedures of at least 3 hours' duration. INTERVENTIONS: The effect of pretreatment with nondepolarizing muscle relaxants (atracurium 40 micrograms/kg or metocurine 50 micrograms/kg), benzodiazepine agonists (diazepam 5 mg or midazolam 2.5 mg), or thiopental sodium 1 mg/kg on the increased muscle tone produced by alfentanil 175 micrograms/kg was compared with a control group (given no pretreatment). MEASUREMENTS AND MAIN RESULTS: Rigidity was assessed quantitatively by measuring the electromyographic activity of five muscle groups (biceps, intercostals, abdominals, quadriceps, and gastrocnemius). Rigidity also was rated qualitatively by attempts to initiate and maintain mask ventilation, attempts to flex an extremity, and the occurrence of myoclonic movements. Pretreatment with the two nondepolarizing muscle relaxants had no effect on the severe muscle rigidity produced by high-dose alfentanil. Whereas thiopental was only mildly effective, the benzodiazepines midazolam and diazepam significantly attenuated alfentanil rigidity (p < 0.05). CONCLUSION: This study suggests that benzodiazepine pretreatment is frequently, but not always, effective in preventing opioid-induced muscle rigidity.

Abdominal Muscles↗
PubMedDate not supplied

Acetate fails to reverse myocardial depression in dogs anesthetized with halothane.

Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.

Acetates↗
PubMedDate not supplied

Electroencephalographic abnormalities following halothane anesthesia.

In 7 subjects, serial EEGs, serum bromide determinations, and psychological tests were done prior to and following 13.83 +/- 0.74 (SEM) MAC-hours of halothane anesthesia. Significant psychological impairment demonstrated 2 days following anesthesia in these subjects was absent 2 weeks following exposure to halothane. Nonspecific postanesthetic slowing of the EEG was found, qualitatively similar to but more marked than that following exposure to enflurane. Generalized EEG slowing, with a tendency toward posterior delta activity and significant reduction of frequency and amplitude of the alpha rhythm, persisted for 6 to 8 days following anesthesia. Rare sharp-wave activity developed in 3 subjects in the 1st week after halothane. A potentially psychoactive postanesthetic serum bromide level of 2.97 +/- 0.17 mEq/L (SEM) was found 5 days following anesthesia. Electroencephalographic changes characteristic of mild bromide intoxication were absent, suggesting that the psychological impairment noted after halothane anesthesia is probably not due to this metabolite; these psychological changes are probably due instead to persistence in the circulation of unchanged halothane.

Adult↗
PubMedDate not supplied

Changes in blood chemistries following prolonged enflurane anesthesia.

Blood chemistries revealed minimal or no injury to the kidney or liver in 12 young healthy male volunteers subject to 9.6 MAC hours of enflurane anesthesia without surgical stress. The results were similar to those previously obtained with halothane, isoflurane, fluroxene, and diethy ether.

Adult↗