摘要:

Ventricular tachycardia likely secondary to a reentrant mechanism may be reliably induced by programmed electrical stimulation in dogs 4–6 days after creating a 2-h experimental, occlusion-reperfusion myocardial infarction. The effects of 1.1 and 1.8 MAC halo-thane, isoflurane, and enflurane on pacing-induced arrhythmias were studied in this model. The ease of initiation of ventricular tachycardia was measured in both awake and anesthetized dogs (n = 18). Excitation thresholds, conduction times, and refractory periods in both normal and infarcted myocardium were also determined to understand changes in the ease of induction of the arrhythmias secondary to anesthetic exposure. Halothane and enflurane administration suppressed the induction of ventricular tachycardia compared with the unanesthetized control (P < 0.01 for both). During isoflurane anesthesia, there was a trend that was not statistically significant for pacing-induced ventricular tachycardia to be less frequent than during the conscious state (P = 0.11). Halothane and enflurane prolonged refractory periods in both normal and infarcted myocardium, whereas isoflurane had that effect only in normal myocardium. In addition, halothane and enflurane tended to increase refractory periods more than isoflurane in both regions. Conduction times and excitation thresholds were not altered by anesthetic administration. It is concluded that halothane and enflurane suppress inducible ventricular arrhythmias secondary to a prior myocardial infarction. In addition, the increased efficacy of halothane and enflurane as antiarrhythmic agents compared with isoflurane in this model may be related to their greater prolongation of refractory periods.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The present study investigated the actions of halothane, isoflurane, and enflurane on spontaneous discharge and evoked action potential activity in mammalian A-δ and C fiber nociceptors from the in vitro rabbit cornea. At 1 MAC halothane, isoflurane, and enflurane significantly (P < 0.001) increased spontaneous discharge frequency of C fibers to 410%, 388%, and 569% of control, respectively. The anesthetics produced burst discharge activity over the concentration range of 0.25–1.5 MAC and depressed discharge activity at higher concentrations (<3.0 MAC). Similar excitatory effects were produced by the potassium channel blocker 4-aminopyridine (250–500 μM). Variable effects on evoked discharge activity of A-δ fibers were observed. Halothane reduced action potential amplitude (77.3 ± 4.5% of control ± SD; n = 6 at 1 MAC) and increased spike latency (0.42 ± 0.075 ms). In contrast, the ethers decreased both spike latency (isoflurane by 0.31 ± 0.064 ms and enflurane by 0.35 ± 0.058 ms) and action potential amplitude. Halothane and the ether anesthetics produced a common excitatory action on C fibers; however, the differential depressant effects on A-δ fibers suggest that diferent membrane mechanisms of action are involved.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Using positron emission tomography, cerebral blood flow (CBF) and cerebral blood volume (CBV) were measured after the addition of isoflurane (1.3 vols %, end-tidal concentration) to neuroleptanesthesia (fentanyl/droperidol) in hypocapnic baboons. The study was designed to determine whether isoflurane, when administered during hypocapnia, acted as a cerebral vasodilator to increase either CBF or CBV. Mean arterial pressure was maintained within 10% of preisoflurane levels with an angiotensin infusion. In the first protocol (A), CBF and CBV were measured as close together in time as possible in order to detect divergent effects of isoflurane on these variables. When Paco2, was reduced from 40 mmHg to 25 mmHg, CBF decreased from 44 ± 4 to 31 ± 4 ml · 100 g-1· min-1(P < 0.05) and CBV decreased from 3.1 ± 0.3 to 2.6 ± 0.3 ml/100 g (P < .05). Neither CBF nor CBV was significantly changed by the addition of isoflurane. In the second protocol (B), serial CBV scans were performed frequently during the addition of isoflurane in a fashion designed to detect transient changes in CBV at the time isoflurane was first added to the breathing circuit. Induction of hypocapnia again reduced CBV from 3.1 ± .3 to 2.7 ± .2 ml/100 g, (P < .05) and addition of isoflurane did not change CBV. From these results the authors conclude that in the normal hypocapnic baboon the addition of 1.3% isoflurane does not significantly change cerebral blood flow or volume.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

A rat model of tourniquet-induced ischemia was created to observe the changes in sciatic afferent neuronal activity associated with prolonged tourniquet inflation on the hind leg. The sciatic nerve was divided in the proximal thigh and a two-electrode microfilament recording technique and signal averaging computer were used to survey afferent neuronal activity prior to and after tourniquet inflation. This method was able to determine both firing rate and conduction velocity of spontaneously active or mechanically sensitive nerve fibers. In 14 rats observed prior to tourniquet inflation there was much spontaneous activity. These fibers all had rapid conduction velocities (30 ± 6.9 m/s) (mean ± SD) and firing rates (16.3 ± 1.9 H). All fibers could be stimulated by movement of distal joints or by probing the skin of the leg. After tourniquet inflation, a pressure-induced conduction block occurred stopping all spontaneous and mechanically induced activity. After a short interval, (55 ± 16 min) a different group of spontaneously active fibers were observed that had both slow conduction (2.04 ± 0.77 m/s) and firing rates (0.54 ± 0.9 H). These fibers did not respond to mechanical stimulation of the limb distal to the tourniquet, or local anesthetic or cold block of the nerve distal to the tourniquet. Blockade of the sciatic nerve just proximal to the tourniquet and deflation of the tourniquet did abolish activity in these fibers. In ten separate rats in which tourniquets were placed but no surgical incision made, mean arterial blood pressure rose significantly after tourniquet inflation. With tourniquet deflation, blood pressure fell significantly from levels observed during tourniquet inflation. This study showed the presence of a group of spontaneously active fibers with velocities in the C-fiber range that were not observed prior to tourniquet inflation. The receptive fields of these fibers were most likely in the ischemic tissue or axons directly under or just proximal to the tourniquet. The neurophysiologic changes noted in this experimental model could represent the physiologic basis of tourniquet pain.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The neurologic outcomes following incomplete cerebral ischemia in rats treated by fasting, nonfasting, or glucose administration (6 ml/kg of 50% glucose solution intraperitoneal) were compared. Rats were anesthetized with 1.4% inspired isoflurane in air and incomplete ischemia was produced by temporary unilateral carotid occlusion and hypotension of 30 mmHg for 30 min. The rats were recovered and neurologic outcome was scored every 8 h for 3 days using a 6-point scale ranging from 0 (normal) to 5 (death associated with stroke). Brain histopathology was scored using a four-point scale on 19 of 30 rats surviving the 3-day postischemic neurologic examination and was correlated with neurologic deficit scores. Fasted rats had plasma glucose concentrations of 79 ± 7 mg/100 ml (mean ± SE) during ischemia and a significantly better neurologic outcome (P < 0.001) than glucose-loaded rats (plasma glucose = 496 ± 43 mg/100 ml). Nonfasted rats had blood glucose values (292 ± 28 mg/ 100 ml) and deficit scores not significantly different from fasted but better than glucose-loaded rats (P = 0.054). Brain histology showed the greatest neuronal damage in caudate followed by hippocampus and cortical tissue. Histopathologic evaluation showed a correlation of r = 0.87 (P < 0.01) with neurologic outcome. In separate experiments brain samples were collected at the end of the ischemic period in each of the experimental groups and regional tissue lactate and brain phosphocreatine and adenosinetriphosphate (ATP) concentrations were measured. Ischemic tissue lactate was similar in fasted, nonfasted, and glucose-loaded rats in caudate and hippocampus but was significantly higher in glucose loaded rats in cortical and thalamic tissue. Phosphocreatine and ATP were decreased by ischemia and were lower in fasted than in nonfasted and glucose-loaded rats. These results confirm previous reports that fasting and lower plasma glucose concentrations protect the brain from ischemic damage but question the influence of tissue lactate or maintenance of brain energy metabolites.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Intraventricular conduction disorders and reentrant arrhythmias in dogs can be produced by high plasma bupivacaine concentrations. The authors' aim was to determine if these conduction disturbances also occurred at moderate plasma bupivacaine concentrations (2.2–3.7 μg/ml) when in association with other factors which affect in-tracardiac conduction, such as hyponatremia and hyperkalemia. Thus, duration of the QRS complex, ventricular conduction time, and effective refractory period (ERP) was measured during ventricular pacing at 180 beats per min in 46 anesthetized, closed-chest dogs separated into five treatment groups as follows: group I, an iv bolus of 4 mg/kg of bupivacaine plus an infusion of 0.1 mg-kg-1· min-1of bupivacaine followed in 50–60 min by 10 ml · kg-1· min-1of 1.5% glycine iv to produce dilutional hyponatremia; group II, 1.5% glycine alone, as above; group III, bupivacaine, as above, followed in 50–60 min by 0.05 mmol · kg-1· min-1of KC1 iv to produce hyperkalemia; group IV, KCl alone, as above; and group V, bupivacaine, as above, except that the duration of infusion was 90 min. QRS duration and ventricular conduction time, which were prolonged approximately 33% and 61%, respectively, by bupivacaine alone were additionally prolonged 29% and 44%, respectively, when serum sodium concentration was lowered to 114 mmol/ 1 and potassium concentration was raised to 7.7 mmol/1. The combinations of bupivacaine and hyponatremia, and bupivacaine and hyperkalemia tended to increase ERP more than did bupivacaine alone, although these changes were not statistically significant. Wave burst arrhythmias and episodes of ventricular tachycardia occurred spontaneously or were triggered by pacing in those dogs in which conduction time was most prolonged. The authors conclude that the effects of hyponatremia and hyperkalemia on cardiac conduction, when superimposed on the effects of moderate plasma concentrations of bupivacaine, may result in severe or even fatal cardiac arrhythmias in dogs.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

It has been suggested that halothane inhibits contraction of airway smooth muscle in vivo mainly by reducing reflex activity in nerves innervating the muscle with only minimal direct effects on the muscle itself. To examine possible mechanisms of action of halothane at clinically relevant concentrations the authors studied the effect of halothane on increases in pulmonary resistance (RL) produced by either vagus nerve stimulation (VNS, which caused neurally mediated constriction) or the inhalation of nebulized acetylcholine (ACh, which directly stimulated the smooth muscle cell) in nine mongrel dogs. The frequency of bilateral VNS and the dose of nebulized ACh were adjusted to produce approximately equal increases in RL. Halothane reduced the response to both types of stimulation in a dose-dependent fashion. At halothane concentrations greater than or equal to 0.4 MAC, the VNS response was significantly less than the ACh response. When tetrodotoxin was given to block neural activity, the ACh response was unchanged, confirming that neural activation did not contribute significantly to smooth muscle contraction in response to ACh. The authors conclude that in addition to neurally mediated effects, halothane at clinically used concentrations has significant direct effects on airway smooth muscle stimulated by ACh. The relative importance of each factor invivoshould depend on the stimulus that causes contraction of airway smooth muscle.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

An in situ electrophysiologic technique was developed to study the effects of intrathecal chloroprocaine and sodium bisulfite on spinal reflex activity in the anesthetized rat. By not surgically invading the subarachnoid space, this procedure allows drugs to be administered remotely through an indwelling catheter while monitoring drug effects on the spinal monosynaptic reflex with noninvasive electrophysiologic methods. In this way the normal pharmacokinetic factors are left intact so that time-action relations can be monitored under conditions that may resemble spinal anesthesia in conscious animals. Using this technique it was established that chloroprocaine with and without 0.2% sodium bisulfite blocks the monosynaptic reflex in a fully reversible manner. The reflex block of a higher concentration of bisulfite (0.6%) was poorly reversible in some preparations. These results correlate well with a previous invivobehavioral study on the motor and sensory blocking actions of intrathecal chloroprocaine and bisulfite in the same animal species. The authors feel this technique can be used to study the temporal changes in reflex activity caused by other drugs administered via the intrathecal route.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID