摘要:

Critically ill patients requiring mechanical ventilation are particularly susceptible to malnutrition. A knowledge of the energy requirements of these patients is essential in designing nutritional regimens. This study examines 45 resting energy-expenditure measurements performed in a group (n = 40) of postoperative, critically ill patients who were hemodynamically stable, noncomatose, and receiving mechanical ventilation. It examines in particular to what degree the resting energy expenditure of such patients can be predicted using the Harris-Benedict and Aub-Dubois formulae. Resting energy expenditure was measured using indirect calorimetry. There was only a moderate correlation between measured resting energy expenditure and that predicted using the Harris-Benedict (r = 0.57) and Aub-Dubois (r = 0.59) formulae. There was little correlation between the ratio of the measured to the predicted (Harris-Benedict) resting energy expenditure and age, or the ratio of actual to ideal body weight and body weight. The measured resting energy expenditure differed widely (70–140%) from predicted, reflecting the many complex factors that influence these patients' metabolic rate. The role of standard predictive formulae in such patients is as an arbitrary reference point to be used to define hypermetabolism (measured greater than predicted) and hypometabolism (predicted greater than measured).

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Several inhalant anesthetics, including nitrous oxide and halothane, are known to be antimitotic in a variety of developing tissues, but none has been tested for antimitotic activity in developing brain. Concern about the safety of these agents has centered around behavioral effects reported in humans and animals after early exposure. Because interference with cell production during CNS development is a sufficient cause for later behavioral abnormalities, it is important to know whether cell production in the nervous system is altered by these agents. Mice were exposed to either nitrous oxide (75% N2O and 25% O2) or halothane (0.5% halothane in 75% N2and 25% O2) or a mixture of 75% N2and 25% O2. Prenatal treatment groups were exposed for 6 h on the 14th day of gestation, while postnatal treatment groups were exposed for 4 h on the second day after birth. Treated and control animals were then killed immediately after exposure, or 12, 24, or 48 h later, to be evaluated for CNS mitotic activity. Each of the four anesthetic-exposed groups showed some deviations from normal mitosis, but only the postnatal nitrous oxide group showed the pattern of reduced cell proliferation followed by a rebound that is characteristic of many antimitotic teratogens. Although prenatal nitrous oxides' effects on the fetal brain were not clearly interpretable, it did delay development of blood, as has been reported by other investigators. Both nitrous oxide and halothane significantly reduced body weight of fetusesin utero, but did not reduce body weight of neonates. The pattern of the body-weight effects suggests that they occur by some mechanism other than reduced cell production. The results indicate that nitrous oxide and halothane disrupt development in several ways, but are not antimitotic in all tissues at all times. Nitrous oxide does appear to be antimitotic to the late-forming cells of the cerebellar cortex.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

In order to correlate electroencephalogram (EEG) changes during anesthetic induction with level of consciousness, four-channel parasagittal EEG recordings were made during anesthetic induction with enflurane and enflurane–nitrous oxide in oxygen. The EEG was quantitated using power spectrum analysis. Significant EEG changes were identified during all anesthetic inductions; however, the frequency of occurrence of change was significant only during the development of amnesia (15 of 20 subjects,P= 0.04). The nature of the EEG changes at this time was agent-specific (P< 0.05 by chisquare), with high-frequency changes evident in the enflurane group and shifts in amplitude in the 8–12 Hz activity predominating in the nitrous oxide–enflurane group. Anterior dominance could not be documented as a correlate of amnesia or unresponsiveness. The identification of such EEG changes may be valuable in assessing anesthetic depth, but other effects, such as the response of the EEG to surgical stimulation, must be determined before the results are clinically applicable.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The molecular mechanisms by which general anesthetics act on postsynaptic membranes can only be worked out in a highly purified, homogeneous system. The nicotinic acetylcholine receptor-rich membranes from the electric tissue ofTorpedo californicaare currently the only postsynaptic membranes that fulfill this condition. Is this peripheral synapse acted on with a pharmacologic specificity similar to that for general anesthesia, and how much less sensitive is it to anesthetic action than the unknown central site? To answer these questions, the authors studied the effects of 13 anesthetic compounds, including volatile general anesthetics, alkanols, and urethane, on the equilibrium binding of3H-acetylcholine to these nicotinic receptors. As the anesthetic concentration was raised, all the agents first increased acetylcholine binding steeply and then, with few exceptions, decreased it again at higher concentrations. Anesthetics increased acetylcholine binding by decreasing acetylcholine's dissociation constant without changing the Hill coefficient or the number of sites. To a first approximation, the relative ability of these agents to increase3H-acetylcholine binding parallels that of anesthesiain vivoas predicted by the Meyer-Overton lipid solubility rule. On average, they produced half maximal increases in acetylcholine binding (EC50) at about four times the concentration that causes loss of righting reflex in one-half of a group of animals (ED50). However, a few agents deviated from this relationship. They were the agents with greatest general anesthetic potency in both the volatile anesthetic series (thiomethoxyflurane) and the normal alcohol series (octanol), and required up to 17 times their ED50s to achieve a half effect on acetylcholine binding. Although the concentrations required were high, these effects were reversible. These systematic deviations in the Torpedo model suggest either that: 1) lipid solubility is not a sufficient criterion for activity in Torpedo; 2) lipid solubility in Torpedo membranes deviates from that at the anesthetic site; or 3) more than one effect underlies the binding assay.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The effects of 1.2, 1.7, and 2.3 MAC enflurane (ENF), halothane (HAL), and isoflurane (ISO) on specialized atrioventricular (AV) conduction times were compared with awake (control) in 23 dogs that were chronically instrumented for His bundle studies. Compared with awake, 1.2 MAC ENF and HAL produced 17% and 18% increases in AV nodal conduction time, respectively. There was little added prolongation related to depth of ENF or HAL. ISO did not prolong AV nodal conduction time at 1.2 MAC compared with awake, but it did prolong conduction compared with awake at 1.7 (9%) and 2.3 MAC (12%). All agents produced an approximate 5% increase in His-Purkinje and ventricular conduction times compared with awake, with little additional effect related to depth of anesthesia. In separate experiments in ten of these dogs, anesthetic effects on conduction were determined following combined autonomic blockade with atropine and propranolol. During autonomic blockade, there was no effect of any anesthetic compared with awake, or to increased level of anesthesia, on specialized AV conduction times. The authors conclude that of the major inhalation anesthetics in current clinical use, ISO is least depressant of and ENF and HAL about equally depressant of AV nodal and His-Purkinje conduction times. Furthermore, depression of AV nodal conduction appears to be an indirect rather than direct effect of anesthesia. Finally, most depression of conduction occurs with light anesthesia, with little added depression related to depth of anesthesia over levels likely to be encountered clinically.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To compare the time course of neostigmine and edrophonium antagonism of varying intensity neuromuscular blockade induced by atracurium, pancuronium, or vecuronium, the authors studied 98 patients anesthetized with nitrous oxide (60%) and halothane or enflurane. Neuromuscular blockade, as monitored by single stimulusinduced twitch tension (TT), was antagonized at varying degrees of spontaneous recovery (2–80% of control TT). Time to antagonism (time from injection of neostigmine or edrophonium to 90% recovery of control TT) was not different between edrophonium, 0.5 mg/kg, and neostigmine, 0.04 mg/kg, when spontaneous recovery had been allowed to occur to at least 11 % of control TT prior to antagonist administration (P> 0.05). For profound neuromuscular blockade (TT ≤ 10% of control) induced by pancuronium or vecuronium, time (mean ± SD) to antagonism with neostigmine, 0.04 mg/kg, was 7.0 ± 2.2 min and 5.6 ± 1.7 min, respectively, while the same for edrophonium, 0.5 mg/kg, was 20.0 ± 8.0 min and 15.0 ± 12.5 min, respectively (P< 0.05). Time to antagonism of profound atracuriuminduced neuromuscular blockade was 8.5 ± 3.3 min for neostigmine, 0.04 mg/kg, and 9.8 ± 7.0 min for edrophonium, 0.5 mg/kg, (P> 0.05). For profound vecuronium- and pancuronium-induced neuromuscular blockade, time to antagonism by edrophonium, 1.0 mg/ kg, was 4.6 ± 3.0 min and 3.9 ± 1.6 min respectively. The authors conclude that neostigmine, 0.04 mg/kg, antagonizes neuromuscular blockade within 12 min when TT is greater than 2% of control at time of reversal. When TT is greater than 10% of control, edrophonium, 0.5 mg/kg, produces similar time to antagonism. However, when TT is 2–10% of control, the dose of edrophonium dose should be at least 1.0 mg/kg to be as rapid as neostigmine, 0.04 mg/kg.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Both ketamine and tracheal intubation are associated with increased heart rate (HR) and systolic blood pressure (SBP). Beta blockers prevent or attenuate this increase. Esmolol (E) is a new, intravenous, rapidly metabolized beta blocker. An open-label study was performed in 41 ASA Class II and III patients divided into groups 1–4: control, 100, 200, and 300 µg·kg−1· min−1(n = 10, 10, 11, and 10, respectively). E was infused over 10 min, the first onefourth of which was a loading dose of 500 µg · kg−1· min−1; at 4 min, ketamine was followed by succinylcholine, intubation, and enflurane–N2O–O2. HR, SBP, blood E, and plasma catecholamine levels were obtained during the 40 min of study. The control group had a baseline HR of 83 ± 5 beats/min while esmolol groups 2–4 had an HR of 73 ± 3, 72 ± 3, and 68 ± 4 beats/min, respectively (P< 0.05). After ketamine, the control group HR increased to 93 ± 6 beats/ min and groups 2–4 remained at the baseline level, 73 ± 3, 73 ± 3 and 67 ± 4 beats/min, respectively (P< 0.05). Postintubation, the control increased further to 113 ± 5 beats/min while groups 2–4 were significantly less, 91 ± 5, 84 ± 3, and 78 ± 4 beats/min, respectively. The mean SBP in most E groups was less than the control within groups, but only in group 4 between groups was the SBP less at postintubation (P< 0.05). Catecholamine levels were the same in all groups and were increased at postintubation. Blood E levels were dose-related and at minutes 4 and 9 the higher levels corresponded to lower HR; there was no active drug or clinical effect at 10 and 30 min postinfusion. No adverse effects of the drug were seen. E, therefore, prevents the tachycardia and attenuates the hypertension associated with ketamine and subsequent tracheal intubation.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Positive end-expiratory pressure (PEEP) may decrease venous air embolism (VAE) by increasing venous pressure at the incision level. Because PEEP and VAE can both increase pulmonary vascular resistance, it is possible that the application of PEEP during VAE may increase right atrial pressure (RAP) relative to left atrial pressure (LAP) and thereby reverse the normal interatrial pressure gradient, allowing paradoxical air embolism in patients with a probe-patent foramen ovale. We studied atrial pressures during 0, 4, and 8 mmHg PEEP before and during continuous VAE in both supine and upright tilted dogs. Both PEEP and VAE increased pulmonary artery pressure and resistance. Prior to VAE, PEEP increased both RAP and LAP but did not affect the interatrial pressure gradient. VAE alone did not affect RAP, LAP, or the interatrial pressure gradient. Application of PEEP during VAE had similar effects as at baseline, namely an increase in RAP and LAP with no change in the interatrial pressure gradient. Although RAP exceeded LAP more frequently in the upright than in the supine dogs, the effects of PEEP and VAE on atrial pressures were similar in both groups. Our finding that PEEP and VAE did not disproportionately increase RAP compared with LAP is consistent with other studies demonstrating preservation of right ventricular function in situations of increased right ventricular afterload.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Lipid peroxidation by free radicals has been suggested as a mechanism of a lung injury caused by breathing higher than normal concentrations of oxygen. The appearance of hydrocarbons such as n-pentane in the expired gas of mammals has been proposed asin vivoevidence of lipid peroxidation. The excretion of n-pentane was studied in 15 healthy volunteers in whom excretion of exogenous n-pentane was determined over a 60- to 90-min period while breathing hydrocarbon-free gases. N-pentane elimination rates (mean ± SEM) in the expired gas at 0, 30, 60, 90, and 120 min were 10.2 ± 1.5, 1.6 ± 0.2, 1.2 ± 0.9, 1.3 ± 0.4, and 1.3 ± 0.3 (pmol · kg−1· min−1), respectively. Using a specially assembled circuit, a 2-h oxygen exposure study was performed on six healthy volunteers, in whom basal n-pentane excretion varied ten-fold among individuals, from 0.25 to 2.25 pmol · kg−1· min−1. After breathing 100% oxygen, npentane excretion was augmented 62–420% within 30 to 120 min. The authors conclude that lipid peroxidation may occur in humans within 30 min of breathing 100% oxygen.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Adrenergic receptor interaction with isoflurane was studied in anin vitrorat parotid gland model in which beta-adrenoceptor agonists evoke amylase release and alpha-adrenoceptor agonists induce potassium secretion from parotid cells. The amylase secretory studies were performed using a batch-incubation technique, and potassium efflux was evaluated using86Rb+as a probe for K+. Isoflurane was dissolved in a fat emulsion, which of its own had no secretory effect. Isoflurane induced a dose-dependent amylase release that was unaffected by beta-adrenergic blockade with propranolol and metoprolol. Isoflurane also induced a significant efflux of86Rb+that could not be inhibited by the alpha-adrenoceptor antagonist, phentolamine. Dinitrophenol, an uncoupler of oxidative phosphorylation, had no effect on the isoflurane-induced enzyme release, indicating that amylase secretion occurred by passive leakage. It is suggested that isoflurane has no direct action on alpha- or beta-adrenoceptors. Isoflurane, however, induces potent cellular events that might be due to an unspecific effect on the cell membrane, thereby causing changes in membrane permeability.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID