摘要:

In order to compare the responses to increasing depths of anesthesia with inhalational anesthetic agents of the phrenic nerve and cranial nerves supplying upper airway muscles, the effects of acute administration of halothane (2.5%) or enflurane (5.0%) on the activities of the hypoglossal nerve (HN), the recurrent laryngeal nerve (RLN), and the phrenic nerve (PN) were investigated in artificially ventilated, vagotomized cats. Following administration of halothane or enflurane, rhythmic inspiratory activities of all three nerves decreased progressively, but the decrease in HN activity was more pronounced than the decreases in HN and RLN activities. During the course of respiratory depression due to increasing depth of anesthesia with halothane or enflurane, rhythmic inspiratory activities of PN and RLN decreased linearly and approximately at the same rate, indicating that the response of RLN more closely resembles that of PN. However, at a relatively deep level of anesthesia, rhythmic inspiratory RLN activity was replaced by strong tonic RLN activity, while PN activity was completely abolished, causing quantitatively and qualitatively different responses of RLN and PN. These peculiar responses of RLN activity to increasing depth of anesthesia were examined in more detail with the use of single- or few-fiber preparations. Increasing depth of anesthesia depressed the inspiratory RLN units while recruiting other units, originally silent, indicating that there are two different groups of fibers in RLN whose response to increasing depth of anesthesia is exactly opposite to one another. The effects of halothane on HN, RLN, and PN were not identical to those of enflurane, since enflurane administration caused characteristic spike-like activities in HN and RLN, which were never observed following halothane, although the overall responses of the activities of all three nerves to increasing depth of anesthesia with halothane were similar to those with enflurane. The dissimilarities observed in all three nerves potentially could affect the balance of activity among upper airway and chest wall muscles and lead to obstruction in the upper airway.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Redistribution of lidocaine and bupivacaine was studied after intrathecal injection in mice qualitatively by whole-body autoradiography or quantitatively by determining spinal cord concentration of the drugs. The composition of the drug solutions then were changed to see if drug distribution could be altered. Changing thepH of the lidocaine solution from 7.5 to 5.0 by adding hydrochloric acid had no effect on spinal cord distribution. Simultaneous injection of bupivacaine and epinephrine increased the bupivacaine concentration in the spinal cord. By adding sucrose to a lidocaine solution, rostral spread of lidocaine was considerably less when the animals were restrained in a vertical position as compared with those injected with a plain solution. When lidocaine and bupivacaine were injected simultaneously, the spinal cord concentration was only changed to a small extent as compared with when the drugs were given separately. Whole body autoradiography revealed that both lidocaine and bupivacaine were rapidly redistributed rostrally from the lumbar area, but quantitatively the rostral redistribution is small. Whole body autoradiography also illustrated the elimination pathways from the spinal subarachnoid space. The authors conclude that alterations in the composition of the injected drug solution can affect rostral redistribution in the spinal cord tissue.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Embolized nitrogen appears in alveolar gas during clinical and experimental venous air embolism (VAE). Since early detection of VAE is believed to reduce morbidity and mortality, this study was done to compare the sensitivity of end-tidal nitrogen (ETn2) monitoring with other detection methods in current clinical use—precordial Doppler (PD), end-tidal CO2(ETCO2), and pulmonary artery pressure (PAP). Ten mongrel dogs (10–17 kg) were anesthetized, placed in the supine position, immobilized, and ventilated (FIO21.0; PaCO235–40 mmHg). Anesthesia and muscle relaxation were maintained with constant infusions of thiamylal and pancuronium. Maintenance fluids were administered at 5 ml · kg−1· h−1, Mean arterial pressure (MAP), PAP, and ETN2and ETCO2(Medspec II® mass spectrometer) were displayed on a strip chart recorder. The dogs were divided into two equal groups and given either a step-wise sequence of 1-min air infusions (0.1–1.5 ml · kg−1· min−1) or 5-s bolus air injections (0.25–1.0 ml · kg−1). Changes in PD sounds occurred in all animals at all air doses. Changes in cardiovascular variables and PaO2were minimal. The threshold dose for ETCO2and ETN2to reach significance was 0.1 and 0.25 ml · kg−1, respectively, while PAP increases were significant at >0.5 ml · kg−1air doses. The time to maximum change (Δmax) ETN2was 30–90 s earlier than Δmax ETCO2(P< 0.05) and 6–105 s earlier than Δmax PAP. The Δmax for all variables was dose related and statistically significant except for the smallest infusion VAE, where only ETCO2was significantly changed. At 0.5 ml · kg−1and greater air doses, increases in ETN2after bolus VAE were double those following infusion of the same amount of air. The magnitude of the changes in ETCO2and PAP were comparable following bolus and infusion VAE. It is concluded that changes in ETN2following low-dose infusion VAE are less sensitive than changes in ETCO2, while during the bolus doses studied, they are equally sensitive. Changes in ETN2and ETCO2are more sensitive than changes in PAP during bolus and infusion VAE. Continuous mass spectrometry monitoring of ETN2may not provide early warning of air entry after small emboli, however, when a significant increase in ETN2occurs following VAE, it precedes changes in ETCO2and PAP.

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

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