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:

Following the administration of a single 0.1 mg/kg dose of vecuronium bromide, satisfactory conditions for tracheal intubation developed in 156 ± 12 s (mean ± SEM), and the clinical duration of the initial dose was 36 ± 2 min. When the initial dose of vecuronium was administered in two increments, a 0.015 mg/kg “priming” dose, followed 6 min later by a 0.050 mg/kg “intubating” dose, intubation time decreased to 61 ± 3 s and clinical duration to 21 ± 1 min. The priming dose that had no unpleasant effect on premedicated, awake patients could be administered 3–4 min before, and the intubating dose 2 to 3 min after induction of anesthesia. With the described technique, comparable intubating conditions could be obtained just as rapidly with vecuronium as with succinylcholine chloride, without subjecting the patients to the side effects of and the complications occasionally encountered with succinylcholine. An added advantage of the use of a priming dose is that it will reveal undiagnosed, pathologic, or idiopathic increase of sensitivity to nondepolarizing muscle relaxants.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The authors sought to determine whether prior administration of a small, subparalyzing dose of nondepolarizing muscle relaxant would shorten the onset time of an intubating dose of muscle relaxant. Initially, in 60 anesthetized patients, twitch response of adductor pollicis to ulnar nerve stimulation was studied after a small dose of pancuronium 0.015 mg·kg−1, metocurine 0.03 mg·kg−1, ord-tubocurarine 0.04 mg·kg−1, followed 3 min later by pancuronium 0.08 mg·kg−1or atracurium 0.4 mg·kg−1administered iv. After 60 s, the minimum neuromuscular block, in all patients was 79.0 ± 5.0%. A 95% depression or twitch tension occurred between 59.1 ± 5.3 and 86.1 ± 5.9 s. In another 60 patients, intubating conditions under similar regimen were studied, except the small dose of muscle relaxant was given immediately prior to induction of anesthesia. At the end of 60 s, good to excellent intubating conditions were present in 100% of the patients following the second dose of pancuronium and in 83% of the patients following atracurium. In 17% of the patients, after atracurium intubating conditions were fair. When nondepolarizing neuromuscular blocking drugs are administered in divided doses, neuromuscular blockade adequate for endotracheal intubation is achieved in less than 90 s. This facilitates rapid endotracheal intubation in a time comparable to using succinylcholine, without undesirable effects of the depolarizing neuromuscular blocking drugs.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The effects of bupivacaine and lidocaine on cardiac conduction were compared in guinea pig ventricular muscle. Membrane potential was controlled using a single sucrose gap voltage clamp technique, and the maximum upstroke velocity of the action potential (Vmax) was used as an indicator of peak sodium current. Bupivacaine blocked cardiac sodium channels in a time- and voltage-dependent fashion. Although bupivacaine has a low affinity for rested and activated sodium channels, it avidly blocks inactivated channels (K4= 9 X 10−7M). Bupivacaine-associated channels do not conduct and have their voltage dependence of inactivation shifted by about 33 m V to more negative potentials. At bupivacaine concentrations above 0.2 μg/ml, a substantial fraction of the channels become blocked during the cardiac action potential, while recovery from block during diastole proceeds relatively slowly with a time constant (r) of 1,557 ± 304 ms (n = 8). Thus, bupivacaine blocks sodium channels in a fast-in-slow-out fashion, and substantial block accumulates at 60–150 beats/min. In comparison, 5–10 μg/ml lidocaine also blocks a substantial fraction of channels during the action potential, but diastolic recovery from block is more rapid (r= 153.8 ± 51.2 ms, n = 4). Thus, lidocaine blocks channels in a fast-in-fast-out fashion. Consequently, even at toxic doses of lidocaine (i.e., 10 μg/ml), little accumulation of block occurs at normal heart rates. Sodium channel block by bupivacaine can be minimized by reducing heart rate, hyperpolarization, and shortening of action potential duration. However, alteration of these variables over clinically applicable ranges does not produce marked changes in bupivacaine effect. Our results provide a possible explanation for the clinical observation that when bupivacaine accidently gains access to the general circulation, cardiac conduction can be depressed seriously and such depression may be difficult to reverse.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Twenty-seven pigtailed monkeys (Macaca nemestrina) were subjected to 17 min of complete cerebral ischemia followed by 96 h of intensive care treatment. Fourteen of the monkeys were assigned randomly to the treatment group and received nimodipine 10 μg·kg−15 min postischemia followed by 1 μg·kg−1·min−1for 10 h. Six monkeys (three treated) failed to meet preestablished protocol criteria and were excluded. The remaining treated and untreated monkeys were well matched for age, sex, and other physiologic variables. Neurologic outcome at 96 h postischemia was significantly better in the nimodipine-treated monkeys than in the controls. Eight of the 11 treated animals had an apparent normal level of consciousness; four of these had no detectable neurologic deficits and a fifth had only a slight motor apraxia. Only two of the 10 untreated animals had an apparent normal level of consciousness, and all had major neurologic deficits. Histopathologic examination showed variable ischemic neuronal change and infarction to involve gray matter in distal arterial perfusion zones. Significant white matter changes were not observed. A histopathologic scoring system yielded a significantly better mean score for the treated group than for the untreated group, and there was significant correlation between neurologic function and histopathologic findings. The authors conclude that nimodipine improves the neurologic outcome when given after an episode of complete cerebral ischemia in primates, and they recommend controlled clinical trials in patients resuscitated after cardiac arrest.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The authors previously demonstrated in dogs that a bolus dose of sodium thiosulfate maintained enhanced cyanide metabolism throughout a 1-h infusion of sodium nitroprusside (SNP). To further test this antidotal action, a bolus dose of thiosulfate (150 mg·kg−1) was given to eight dogs at theendof a 60-min near-lethal infusion of nitroprusside (3 mg·kg−1). Within 2 min of the antidote, mean plasma thiocyanate levels (70.3 μmol·1−1) were significantly higher than those of seven control dogs given nitroprusside only (45.9 μmol·1−1,P= 0.002) and plateaued at 153.8 μmol·1−1within 60 min, while the control values only reached 79.1 μmol·1−1(P< 0.001). Although differences between plasma cyanide levels in the two groups only attained significance 1 h after administering the antidote (0.8vs.2.74 μmol·1−1,P= 0.03), red blood cell cyanide concentrations were significantly lower in the antidote group within 5 min (166vs. 225μmol·1−1,P= 0.004) and remained so throughout the 2-h observation period. Compared with the controls, there was an impressive reduction in mean half-lives of plasma cyanide (25.1vs.74.1 min) and red blood cell cyanide (22.4vs.203.6 min). Similarly, peak cyanide levels occurred much sooner following the antidote (mean times: plasma cyanide 2.9vs.5.9 min; red blood cell cyanide 0.25vs.11 min). Whereas mean blood lactate levels remained elevated for at least 1 h after infusion in the controls, they showed a decrease within 5 min in the antidote dogs, becoming significantly lower 25 min later (P< 0.01). These results suggest that thiosulfate alone is a sufficient antidote for cyanide toxicity arising from excessive SNP administration. The data also suggest that red blood cells may be involved in the detoxication process.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Twenty patients (23–76 yr) were studied with regard to lung tissue changes prior to and following induction of general anesthesia with muscular relaxation, and another four subjects were studied for a longer period awake. The transverse thoracic area and the structure of the lung tissue were determined by computerized tomography. No abnormalities in the lung tissue were noted before anesthesia. Within 5 min after induction, including muscular relaxation, all subjects had developed crest-shaped changes of increased density in the dependent regions of both lungs. They were largest in the most caudal segment (4.8 ± 0.8% of the transverse lung area, mean ± SE) and smaller in the cephalad exposures (3.4 ± 0.7% of the transverse area). The size of the densities showed no correlation to age. The densities did not increase after a further 20 min of anesthesia and were not affected by the inspiratory oxygen fraction. When the subjects were moved from the supine to the lateral position, the crest-shaped densities disappeared in the nondependent lung and remained in the dorsal part of the dependent lung. The application of positive end-expiratory pressure of 10 cmH2O eliminated or reduced the densities. The four awake subjects showed no lung densities after 90 min in the supine position. It is suggested that these crest-shaped densities represent atelectases, which develop by compression of lung tissue rather than by resorption of gas.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The authors evaluated the systemic and cerebral hemodynamic and metabolic effects of 1 h of hypotension to a mean arterial pressure of either 50 mmHg or 40 mmHg induced by intravenous adenosine or ATP in dogs maintained on 70% nitrous oxide and 0.1% halothane. Following the hypotensive period, brain biopsy specimens were taken for the determination of cerebral metabolites and calculation of the energy charge. Hypotension induced by either adenosine or ATP produced a marked 40–62% decrease in systemic vascular resistance with little change in cardiac index or oxygen consumption but resulted in a mild metabolic acidosis. Because of a profound decrease in cerebral perfusion pressure with hypotension (to 31–33 mmHg at an MAP of 50 mmHg and 22–24 mmHg at an MAP of 40 mmHg) CBF decreased 54–65% and was inadequate to meet the unchanged cerebral oxygen demands, resulting in some anaerobic metabolism with an accumulation of lactate. While the ease with which one can induce and maintain hypotension with these agents may be advantageous in clinical practice, the effects of adenosine and ATP on cerebral hemodynamics and metabolism may offer no advantage over other hypotensive agents.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID