摘要:

This study was designed to determine if spinally administered epinephrine is capable of suppressing noxiously evoked activity of wide dynamic range (WDR) neurons in the dorsal horn of the spinal cord. Extracellular activity was recorded from single WDR neurons in the dorsal horn of decerebrate, spinal cord-transected (T-12) cats. Activity was evoked by the presentation of a noxious radiant heat stimulus (51°C) to the cells' receptive fields on the hind paws. Evoked activity was monitored both before and after the spinal administration of either 50 μg (n = 6) or 100 μg (n = 6) epinephrine. Both doses of epinephrine produced a significant suppression of noxiously evoked activity, which was dose-dependent. In addition, the 100-μg dose produced a suppression that was of longer duration than that seen following the 50-μg dose. Recovery from suppression was recorded following both the 50-and 100-μg dose. These results indicate that spinally administered epinephrine is capable of suppressing noxiously evoked activity of WDR neurons in the dorsal horn of the spinal cord. Since WDR neurons have been identified as cells of origin for the spinothalamic tract, such an action may block the central transmission of afferent pain information. This may be a mechanism by which spinally administered epinephrine enhances the duration or intensity of spinal anesthesia produced by local anesthetics and may also explain spinal analgesia resulting from the spinal administration of adrenergic agonists.Interactions between spinally administered epinephrine and spinally administered opioids also were studied. Following spinal fentanyl administration, 10μg of spinally administered epinephrine produced significant suppression of noxiously evoked activity within 6 to 9 min (n = 3). In contrast, 10 μg of spinally administered epinephrine by itself produced no significant suppression of noxiously evoked activity (n = 4). Interpretation of these results suggests that adrenergic agonists may act in a multiplicative fashion with spinally administered opiates to produce a profound suppression of noxiously evoked activity.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Halothane is a well known cerebral vasodilator that can produce dangerous increases in intracranial pressure (ICP) in certain neurosurgical patients. It has been suggested that isoflurane may be a less potent cerebral vasodilator. The authors therefore undertook a direct comparison of the effects of halothane and isoflurane on cerebral blood flow (CBF), cerebral vascular resistance (CVR), intracranial pressure, and cerebral metabolic rate for oxygen (CMRO2). Studies were carried out in normocarbic mechanically ventilated cats, using the intracarotid133Xe injection technique to measure CBF. The effects of three doses were examined: 0.5, 1.0, and 1.5 MAC, studied in the continued presence of 75% N2O. Autoregulation also was tested at 1.0 MAC (plus 75% N2O) by recording CBF and CVR before and after elevation of blood pressure with angiotensin.Both agentes had similar effects on blood pressure and ICP. However, while halothane produced significant increases in CBF at all doses, with values of 61 ± 5 ml · 100 g-1· min-1(123 ± 8% of control, mean ± SE) at 1.0 MAC, isoflurane anesthesia caused no significant changes in CBF at any level, (e.g.,48 ± 8 ml · 100 g-1· min-1or 94 ± 12% of control at 1.0 MAC). Both drugs produced dose-related decreases in CVR, but the changes were greater with halothane,e.g.,CVR at 1.0 MAC halothane = 1.46 ± 0.20 mmHg · ml-1· 100 g · min (47 ± 7% of control) compared with 2.23 ± 0.40 mmHg · ml-1· 100 g · min (72 ± 9% of control). In addition, isoflurane produced greater decreases in CMRO2than did halothane, and also impaired autoregulation less.The results indicate that isoflurane possesses cerebrovascular properties that are different from halothane. These differences suggest that isoflurane may come to play an important role in future neuroanesthetic practice.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Neurophysiologic studies have demonstrated epileptoid activity during high-dose narcotic anesthesia. The authors utilized the14C-2-deoxyglucose method to evaluate the local cerebral glucose metabolism (1-CMRg) during high-dose fentanyl-induced epileptoid discharges as evaluated by electroencephalography (EEG) in ventilated rats. Fentayl was administered intravenously at two dose levels (200 μg · kg-1, n = 5; and 400 μg · kg-1, n = 8). Seven unanesthetized animals served as controls. During fentanyl administration, the EEG was characterized by the appearance of isolated high voltage (>100 μV) spike and polyspike and wave complexes at a frequency of one every 1–4 s, superimposed on a baseline of reduced frequency and voltage. Isolated ictal discharges (spike or sharp waves at a frequency of 12–20/s) rarely were superimposed upon the spike and polyspike activity.As a general trend, fentanyl administration induced a significant (P<0.05) decrease of the 1-CMRg in the majority of the 37 brain structures surveyed. A clear relationship between 1-CMRg and epileptoid activity appeared when the anatomic areas were grouped into functional systems. Cerebral metabolism was globally decreased in the visual and snesorimotor systems (53–78%), in the white matter structures (76–78%), and reticular formation (59–69%) with both fentanyl treatments. The largest deviation from this trend appeared in the limbic system. Here with both treatments, the 1-CMRg in the claustrum, septal nucleus, amygdala, and ventral areas of CA1 and CA3 of the hippocampus remained at control values. At the higher fentanyl dosage, there was a more widespread depression of 1-CMRg in the rest of the brain, while in the limbic system this effect was reversed, with the 1-CMRg returning to control values in the hippocampus (CA1), dentate gyrus, and interpeduncular nucleus.The relative hypermetabolism in limbic system structures during fentanyl-induced epileptoid activity, coupled with a significant reduction of glucose utilization in the rest of the brain, suggests a role for the limbic system in the genesis of seizure activity during fentanyl administration.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Power spectrum analysis of 4-channel EEGs was performed during cooling and rewarming using cardiopulmonary bypass. During rewarming, linear correlations of temperature with the total power and with peak power frequency of the high-frequency band were observed in a significant number of cases (85%,P< 0.0001 and 76%,P< 0.002, respectively). The magnitude of these changes were 1,215 μV2/°C (±150 [SEM]) and 0.39 Hz/°C (± 0.04 [SEM]). Two other descriptors of the EEG power spectrum (the spectral edge and average frequencies) did not correlate with the temperature changes in a significant number of cases. Changes during cooling followed a similar trend but were more variable, presumbaly because of other physiologic changes associated with the start of bypass. Knowledge of the relationship of the EEG to temperature should permit distinguishing EEG changes secondary to hypothermia from those caused by acute hypoxia.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The effects of intravenous (iv) verapamil (0.01 to 1.0 mg/kg) on the constant neuromuscular block produced by an iv infusion of either pancuronium or succinylcholine were studied on the indirectly stimulated gastrocnemius and tibialis-anterior muscles of the rabbit anesthetized with halothane in oxygen. Verapamil alone (n = 6) had no significant effect. However, the drug did significantly potentiate the 50% twitch depression of the gastrocnemius muscle produced by a constant iv infusion of either pancuronium (n = 5) or succinylcholine (n = 5) to 36 ± 6% and 45 ± 1% of control, respectively. This effect of verapamil occurred with doses of 0.1 mg/kg for pancuronium and 0.01 mg/kg for succinylcholine; these doses of verapamil were the lowest which produced a significant effect. In contrast, verapamil had no significant effect on the progression of the neuromuscular blockade of either the gastrocnemius or tibialis-anterior muscles produced by alpha-bungarotoxin (n = 5). Verapamil also significantly prolonged the P-R interval of the ECG from a control value of 71 ± 2 ms to 78 ± 3 ms at a dose of 0.1 mg/kg and to 93 ± 6 ms at a dose of 0.3 mg/kg. The possible mechanisms of the neuromuscular actions of verapamil are discussed and it is concluded that verapamil can produce potentiation of either pancuronium- or succinylcholine-induced neuromuscular block at doses within the therapeutic range.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Rat lungs were ventilated and perfused at a constant ratein vitro.The maximal hypoxic pulmonary vasoconstrictor (HPV) response was recorded by measuring the pulmonary artery pressure change when the inspired oxygen concentration was changed from 21% to 3% (with 5.5% carbon dioxide) in the absence of anesthetic vapor.In different experimental groups, the effects of halothane, enflurane, and isoflurane on HPV were examined. In random order the anesthetics were added to the inspired gas in concentrations of 0.25, 0.5, 1, 1.5, and 2 or 2.5 MAC units. The HPV pressor response to 3% oxygen in the presence of anesthetic agent was expressed as a per cent of the pressure response observed in the absence of anesthetic (R%MAX).All three agents depressed HPV in a dose-related manner. The concentrations in MAC units at which 50% depression of HPV (ED50) occurred was 0.47, 0.60, and 0.56 for halothane, isoflurane, and enflurane, respectively, and neither the ED50values nor the slopes of these dose response curves were significantly different.It was concluded that these halogenated general anesthetics inhibit HPV with essentially the same potency.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Effects of halothane on the excitation-contraction coupling or neuro-effector transmission in the dog tracheal muscle were observedin vitroin an attempt to clarify the cellular mechanisms involved in anesthetic-induced bronchodilation.Double sucrose gap, microelectrode, and tension recording methods were used. Application of halothane evoked an initial induction of phasic contraction with no alteration in the electrical membrane properties, and secondarily a reduction in muscle tone with membrane hyperpolarization.Halothane suppressed the amplitude of the twitch contractions evoked by indirect (nerve mediated) or direct muscle stimulation, the degree of suppression being greater with the former stimulation. The threshold membrane depolarization required for the generation of tension development was increased. In the presence or absence of TEA, halothane completely suppressed the generation of an action potential or a local response in the muscle membrane, following stimulation by outward current pulses.Therefore, halothane has complex actions on Ca++economy in the tracheal smooth muscle cell,i.e.,initial release of Ca++from the store sites followed by inactivation or a reduction in free calcium ions in the cytoplasm, and/or suppression of the influx of Ca++across the cell membrane.Low concentrations of halothane (≤1%) suppressed the amplitude of excitatory junction potential (EJP) without altering the membrane potential, membrane resistance, or muscle sensitivity to acetylcholine. Therefore, this anesthetic probably suppresses the release of transmitter from the nerve terminals. Halothane also suppressed the facilitation phenomena of EJP during repetitive nerve stimulation.These direct inhibitory effects of halothane on smooth muscle cells and excitatory neuro-effector transmission could account for the potent bronchodilator action of this anesthetic.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The results of erroneous filling of agent-specific anesthetic vaporizers were studied. The fraction of gas flow through the vaporizer was calculated for three vaporizers set to deliver essentially equipotent final concentrations: halothane, 1% (1.25 MAC); enflurane, 2% (1.19 MAC); and isoflurane, 1.5% (1.30 MAC). These fractional flows, at 22°C, were 0.0188 for 1% halothane, 0.0615 for 2% enflurane, and 0.0295 for 1.5% isoflurane. Concentrations were calculated for cases of total filling of a vaporizer with one of the other two agents. In terms of potency of delivered agent, fourfold underdoses or overdoses could result from such errors. Refilling a 25% full vaporizer with the wrong agent then was considered. In order to calculate the concentrations of each agent that would be delivered in such a case, vapor pressures of each were determined in mixtures of two agents. Enflurane and isoflurane could not be separated satisfactorily by gas chromatography. Halothane, when mixed with enflurane or isoflurane, enchanced vaporization of each agent, as well as being somewhat more easily vaporized itself. Halothane, enflurane, and isoflurane do not form ideal solutions when mixed and the resultant vapor concentrations of each of two agents when mixed may be far from those predicted by an assumption of ideality.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID