ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The authors hypothesized that laudanosine, a metabolite of atracurium and a central nervous system stimulant, might increase the minimum alveolar concentration (MAC) of halothane. An initial study in five rabbits anesthetized with halothane used a two-compartment model to produce estimates of pharmacokinetic variables for laudanosine. These estimates were used to determine the rates of infusion that would produce steady state plasma concentrations of laudanosine of approximately 200, 400, and 800 ng.ml-1. Subsequent infusion of laudanosine in eight rabbits produced mean (±SD) steady state plasma concentrations of laudanosine of 234 ± 56, 457 ± 66, and 873 ± 105 ng.ml-1. The control value for MAC of halothane was 1.08 ± 0.28%. At the lowest steady state plasma laudanosine concentration, MAC did not significantly differ from control (MAC = 1.15 ± 0.23%,P< 0.1). However, at 457 and 873 ng.ml-1, laudanosine significantly increased the MAC of halothane by 23% and 30%, respectively. Infusion with saline in two additional rabbits did not affect MAC. Therefore, at the plasma concentrations of laudanosine found in humans after administration of atracurium, laudanosine increased the MAC of halothane in rabbits.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Pancuronium decreases the minimal alveolar anesthetic concentration (MAC) of halothane in humans, while atracurium has a metabolite, laudanosine, which is a known cerebral stimulant. To determine if these muscle relaxants significantly alter cerebral function, their effects on cerebral metabolic rate (CMRO2), cerebral blood flow (CBF), intracranial pressure (ICP), EEG, and the cerebral energy state were studied in halothane-anesthetized dogs. Group A dogs (n = 6) were maintained at 0.86% end-expired (1.0 MAC) halothane. Thereafter, a sequence of 1) pancuronium 0.1 mg.kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; and 3) pancuronium 0.2 mg.kg-1produced no changes in CMRO2CBF, ICP, or EEG. Group B dogs (n = 6) also were maintained at 0.86% end-expired halothane and received the following in sequence: 1) atracurium 0.5 mg.kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; 3) atracurium 1.0 mg.kg-1; and 4) atracurium 2.5 mg.kg-1. There were no changes in CMRO2, CBF, or ICP; EEG evidence of cerebral arousal occurred in only one dog with the final dose of atracurium. Group C dogs (n = 6) received tetracaine spinal anesthesia and the minimal halothane concentration (mean ± SE = 0.69 ± 0.03% end-expired) that would maintain an “anesthetic” EEG pattern. Each Group C dog received the following in sequence: 1) atracurium 1.0 mg.kg-1, and 2) atracurium 2.5 mg.kg-1. EEG evidence of cerebral arousal occurred in all six Group C dogs. Arousal was not accompanied by significant increases in CBF, CMRO2, or ICP. In Groups B and C, neuromuscular blockade always preceded arousal. Once arousal occurred, the EEG never returned to the asleep pattern. Cerebral stimulation by atracurium in the dog is modest in magnitude, is probably independent of the neuromuscular effects of the drug, and is presumed to be secondary to the metabolite laudanosine.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

To compare the effects of continuous positive airway pressure (CPAP) with those of ambient end-expiratory pressure (T-tube) on lung mechanics and blood gas exchange, transpulmonary pressure (Ptp), tidal volume (VT), respiratory frequency, and arterial oxygen and carbon dioxide tensions were measured in 16 spontaneously breathing patients recovering from acute respiratory failure. These variables were measured during breathing through a T-tube; with 18, 12, and 6 cm H2O CPAP; and again during breathing through a T-tube. During all levels of CPAP, mean effective lung compliance (Ceff) was higher and mean total pulmonary power during inspiration lower than during breathing through a T-tube before CPAP (P< 0.05). The data obtained at the level of CPAP producing maximum Ceff(optimum CPAP) were grouped and compared with values obtained during breathing through a T-tube. Mean total pulmonary power of inspiratory muscles during breathing through a T-tube before CPAP (0.7 ± 0.14 kg.m.min-1) decreased during optimum CPAP (0.44 ± 0.07 kg.m.min-1) and increased during breathing through a T-tube after CPAP (0.63 ± 0.12 kg.m.min-1). Mean VTwas higher (557 ± 63 mlvs.474 ± 47 ml) and frequency lower (17.5 ± 1.6 breaths/minvs.22.5 ± 2.5 breaths/min) during optimum CPAP than during breathing through a T-tube before CPAP, and inspiratory time was significantly longer. Mean minute ventilation was also lower during optimum CPAP (8.7 ± 0.6 1/min) than during breathing through a T-tube (9.6 ± 0.8 1/min); Paco2did not change significantly. Mean alveolar-to-arterial oxygen pressure difference decreased significantly during optimum CPAP. The authors conclude that CPAP, when adjusted to the appropriate levels, improves lung mechanics in patients recovering from acute respiratory failure. Continuous positive airway pressure reduces total pulmonary power during inspiration and at the same time improves oxygen and carbon dioxide exchange. In these respects, it is preferable to breathing through a T-tube without CPAP.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Hypoxic pulmonary vasoconstrictor (HPV) responses were measured with repeated intermittent hypoxic challenges in eight non-traumatized closed chest dogs anesthetized with pentobarbital. The right lung was ventilated continuously with 100% O2while the left lung was either ventilated with 100% O2(control) or ventilated with a gas mixture containing 3–4% O2(hypoxia). Mean per cent left lung blood flow for all four normoxic periods was 43.1 ± 1.5% (mean ± SE) of the total blood flow by the SF6excretion method and 40.8 ± 1.1% by the differential CO2excretion method, corrected for the Haldane effect. With hypoxic ventilation, flow diversion from the hypoxic lung was maximal with the first exposure and did not change subsequently with a total of four alternating exposures to normoxia and hypoxia. Flow diversion during hypoxia was approximately 50.5 ± 2.4% by the SF6method and 50.3 ± 3.5% by the Vco2method. This result contrasts with the increasing flow diversion response with intermittant hypoxic exposure that has been reported in animals exposed first to thoracotomy and surgical dissection. It is concluded that in the absence of surgical trauma the initial response to hypoxia is maximal and is not potentiated by repeated hypoxic stimulation.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The authors determined whether increasing alpha1-adrenergic blockade resulted in progressively less arrhythmic activity in the canine halothane-epinephrine arrhythmia model. Dogs (n = 7) were anesthetized with halothane (1.5%) in oxygen. Stepwise increases in steady-state plasma levels of either of two alpha1-adrenoceptor antagonists (droperidol, doxazosin) were produced by applying Wagnerian principles to the known pharmacokinetic parameters of these drugs. At each steady state plasma level of these antagonists, the extent of the alpha1-adrenergic blockade produced was assessed by defining a phenylephrine (PE) dose pressor response curve. The degree of alpha1-blockade produced was quantitated as the dose of PE that caused a 25-mmHg increase in mean arterial pressure (ED25) as derived by polynomial regression analysis. By analysis of variance (ANOVA) the ED25increased significantly for each targeted steady state plasma level of either droperidol (P< 0.001) or doxazosin (P< 0.001). For an assessment of the antiarrhythmic activity of these alpha1-antagonists, the arrhythmogenic dose of epinephrine (ADE) was determined at each of the states of alpha1-adrenergic blockade previously defined. By ANOVA there was a significant increase in the ADE over the range of alpha blockade produced for either droperidol (P< 0.001) or doxazosin (P< 0.001). A close correlation (r2) existed between the ED25and the ADE for the target steady state levels that were achieved for either droperidol (0.99) or doxazosin (0.74). These data support the contention that the antiarrhythmic activity of these antagonists is on the basis of their alpha, adrenergic blockade, and the authors suggest that this antiarrhythmic action is mediated by blockade of the myocardial alpha, adrenoceptors.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID