Charles E. Reier

Acute respiratory effects of ethanol in man

Six healthy subjects received ethanol 0.35, 0.70, and 1.05 ml per kilogram intravenously in 1 hour, causing average blood ethanol concentrations of 40, 99, and 121 mg per milliliter, respectively. Resting ventilatory minute volume (VE) and end tidal carbon dioxide tension (PACO2) were inconsistently affected. The ventilatory response to CO1 was depressed in a dose‐dependent manner. The PACO2 at a VE of 20 I per minute was 3.9 torr greater than control after the 1.05 ml per kilogram dosage. Respiratory exchange ratio decreased from 0.779 to 0.709 1 hour after the 1.05 ml per kilogram infusion. Vital capacity decreased from 5.42 to 5.09 1, and expiratory reserve volume decreased from 1.14 to 0.9311 hour following this dosage. Irregular ventilatory patterns with transient inspiratory and expiratory apnea were observed frequently following the 0.70 and 1.05 ml per kilogram dosages.

Cortisol and growth hormone response to surgical stress during morphine anesthesia.

HE recent popularity of morphine anesT thesia emanates in part from numerous observations suggesting an absence of cardiovascular depression following large doses of the drug. These immediate observations relate primarily to the direct effect of the drug on the heart, vessels, and autonomic nervous system. Equally important, although subtle, are the delayed drug effects, usually mediated through humoral mechanisms. In this respect, the ability of morphine to inhibit ACTH releasel and to block the pituitary-adrenal (PA) response to certain stimuli2,3 must be considered. Therefore, we elected to observe the effects of large doses of intravenous morphine on some aspects of the hypothalamic-pituitary-adrenal (HPA) function during major surgical procedures. METHODS A total of 38 patients scheduled for elective major operations were divided into six groups, a11 of whom received nitrous oxide plus: (1) halothane (control-general surgery); (2) morphine, 1 mg./kg.; (3) halothane (controlopen-heart surgery) ; (4) morphine, 2 mg./kg.; (5) morphine, 4 mg./ kg.; (6) morphine, 4 mg./kg. plus ACTH, 25 units.

Cardiac Output and Postganglionic Sympathetic Activity during Acute Respiratory Alkalosis

The effects of acute respiratory alkalosis on the cardiovascular system (particularly cardiac output) and spontaneous activity of postganglionic sympathetic nerves in anesthetized dogs has been examined. Fifteen experiments were performd on ten dogs. Reducing mean Paco2 from 39.7 to 18.3 mm Hg without changing ventilation decreased both stroke volume and cardiac output (P > 0.05). Simultaneously with reduction in cardiac output, spontaneous postganglionic activity diminished. Alterations in cardiac output and postganglionic activity were reversed when the animal was returned to normocapnia. The authors conclude that a reduction in sympathetic nervous system activity contributes to the reduction of cardiac output observed during respiratory alkalosis.

The Effects of d-Tubocurarine on Spontaneous Postganglionic Sympathetic Activity and Histamine Release

The effects of d-tubocurarine on mean arterial pressure (MAP) spontancous postganglionic sympathetic activity (SPGSA) and histamine release were studied in cats. The muscle-paralyzing dose of d-tubocurarine (0.4 mg/kg) produced an average decrease in MAP of 44 mm Hg together with a marked decrease in SPGSA to 7.8 per cent of the control value and a twofold increase in blood histamine concentration. A larger dose of d-tubocurarine (1 mg/kg) produced a profound fall in MAP (average decrease 78 mm Hg), followed by signs of histamine-induced catecholamine release (transient rebound increases in MAP, PP, and HR) and more than a four-fold increase in circulating histamine. The authors conclude that the decreased SPGSA and the histamine release contributed to the fall in MAP with the muscleparalyzing dose of d-tubocurarine and that histamine release became physiologically more significant in the cardiovascular changes following the larger dose of d-tubocurarine.

The effect of dimethyl tubocurarine iodide on cardiovascular parameters, postganglionic sympathetic activity, and histamine release.

HE value of succinylcholine in facilitatT ing endotracheal intubation has been well established. However, recent reportsl-4 indicate that severe cardiovascular disturbances may follow the intravenous use of succinylcholine in patients with massive trauma, burns, war injuries, and central nervous system disease or injury associated with paralysis. In this group of patients, although endotracheal intubation under topical anesthesia is possible, most anesthesiologists prefer endotracheal intubation under general anesthesia, with adequate masseter muscle relaxation.

Methoxyflurane analgesia: a clinical appraisal and detailed description of stage I in man.

N 1779, Sir Humphrey Davy discovered I the analgesic property of nitrous oxide during inhalation of the gas while suffering from a t0othache.l Since that time analgesia associated with subanesthetic concentrations has been reported for most anesthetic agents.z.8 Unfortunately, each of these agents has certain undesirable characteristics (explosiveness, neurotoxicity, unpleasant odor) which have limited its clinical use in this manner.

Effects of neuromuscular blocking agents on uterine contractions in vitro

Abstract The direct effect of competitive and noncompetitive neuromuscular blocking agents on uterine contractions was observed in vitro. Exposure of human gravid myometrial strips to succinylcholine chloride, decamethonium iodide, gallamine triethiodide, and d -tubocurarine chloride in concentrations equivalent to one hundred times the paralyzing dose failed to significantly affect spontaneous or oxytocin stimulated contractions. By contrast, halothane produced complete inhibition of spontaneous contractions, which was completely reversed by discontinuance of the agent. These results support the contention that the role of neuromuscular blocking agents in the management of obstetric emergencies requiring uterine relaxation is limited to relaxation of the abdominal and perineal musculature, and to facilitation of anesthetic management.

Respiratory Interaction of Alcohol

ABSTRACT To the Editor.— Alcohol is widely thought to depress respiration, yet our previous studies have demonstrated minimal ventilatory depression during acute alcohol intoxication (JAMA 222:486,1972; Clin Pharmacol Ther 14:501, 1973). Since concomitant ingestion of drugs and alcohol occurs frequently and respiratory depression is a major physiologic effect of sedative drugs in large doses, interaction between alcohol and tranquilizers in small doses might dangerously depress respiration.To study this problem, we recently measured resting ventilation and response to CO2 in six healthy volunteers who received clinical doses of pentobarbital (100 mg) or glutethimide (500 mg) plus ethanol (0.7 ml/kg). No resting ventilatory measurements changed after drug ingestion. Pentobarbital and glutethimide moderately depressed, but ethanol did not significantly increase, the ventilatory response to CO2.We think that the respiratory depression due to combinations of alcohol and tranquilizers is unlikely to be clinically hazardous if the patient is awake and without