ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Alterations in the skin temperature of the trunk during spinal anesthesia, using either tetracaine, 6 mg, or lidocaine, 50 mg, were monitored at intervals by means of a General Electric Spectrotherm 2000® Thermographic Imager and recorded on Polaroid® 107C photographic film. The upper level of sensory blockade was determined with each thermograph by recording the most cephalad dermatome at which analgesia to pinprick occurred. The upper limit of diminished sympathetic activity was assumed to be the most cephalad dermatome at which skin temperature elevation occurred. In all cases, the uppermost level of temperature elevation was cephalad to the upper limit of sensory blockade. Assuming that temperature elevation reflects diminished sympathetic activity, the mean sympathetic-sensory differential for lidocaine, 50 mg, was 6.00 (±SE 0.70) segments, and for tetracaine, 6 mg, was 6.70 (±SE 0.50) segments. Arrival of the temperature elevation “front” at the fourth thoracic dermatome and above was associated with decreases in mean arterial pressure.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Volatile anesthetic agents have profound and heterogeneous effects on global and local cerebral blood flow (I-CBF) and metabolism. The relationship between I-CBF and local cerebral glucose uptake (I-CMRg) during isoflurane anesthesia is unknown. Because these relationships might influence neuronal homeostasis during periods of cerebral ischemia of different causes, it becomes important to understand them. Accordingly, the authors evaluated the I-CBF and I-CMRgeffects of isoflurane with quantitative autoradiography in normal rats. As the dose of isoflurane increased in a stepwise fashion to 0.5, 1.0 (1.38%), 1.5, and 2.0 MAC levels, the number of structures with a significant (P < 0.05) I-CBF increase or I-CMRgdecrease became greater. At each respective MAC level I-CBF was increased in 0%, 11%, 34%, and 30%, while I-CMRgdecreased in 11%, 70%, 74%, and 81% of the structures in which autoradiographic measurements were performed. Between 1.5 MAC and 2.0 MAC the I-CMRgdecrease stabilized at about −50% to −70% of cerebral metabolic values obtained in awake control rats in association with attainment of a burst-suppression of isoelectric electroencephalogram. In contrast to these general changes, I-CMRgin two subcortical limbic system structures (dentate gyrus and interpeduncular nucleus) did not decrease, even at the highest doses of isoflurane. L-CBF was significantly (P < 0.05) increased only at the highest dose ranges (1.5–2.0 MAC) and increased from 34% to 238% in about one-third of the structures evaluated. Isoflurane anesthesia causes heterogeneous changes in I-CBF and metabolism, which are most apparent at doses at or above 1.0 MAC. Differences in I-CBF/I-CMRgratio patterns during isoflurane anesthesia suggest, at least in part, that cerebral flow and metabolic changes may proceed through unrelated regulatory mechanisms.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The effect of isoflurane anesthesia on local rate of glucose utilization was investigated in the rat brain by means of the autoradiographic14C-2-deoxyglucose method. Local cerebral glucose utilization (LCGU) was measured in 26 neuroanatomic structures of awake and isoflurane-anesthetized rats. Isoflurane anesthesia (1.5% inspired) caused both increases and decreases in LCGU. Significant reductions were found in all cortical areas examined and in primary sensory relay nuclei of central visual and auditory pathways. Among regions of the extrapyramidal motor system, LCGU was increased in substantia nigra pars compacta, and decreased in cerebellum, red nucleus, and ventral thalamus. Large increases in LCGU were observed in some structures of the limbic system such as the medial habenulo-interpeduncular system and the CAsfield of hippocampus. LCGU was significantly reduced by isoflurane in the CA1-CA2field and dentate gyrus of hippocampus. These results are similar to previous findings on the LCGU response to other inhaled and intravenous anesthetics and further confirm the regional specificity of the effects of anesthetics on brain metabolism.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The safety and efficacy of esmolol during high-dose fentanyl anesthesia were studied in 37 patients undergoing coronary artery bypass grafting (CABG). The anesthetic management consisted of fentanyl 75 μg/kg, pancuronium 0.15 mg/kg, and O2. To assess the safety of esmolol, it was administered in a double-blind manner to 17 anesthetized patients prior to surgical incision. Infusion of the drug was increased in stepwise fashion to obtain administration rates between 100 and 300 μg · kg−1' min−1. Esmolol produced smail but significant increases in pulmonary capillary wedge pressure (PCWP) (8.3 ± 1.7 to 13.2 ± 2.0 mmHg) when compared with placebo (10.9 ± 1.0 to 12.1 ± 0.6 mmHg) (P < 0.05). For the other studied parameters (heart rate, mean arterial pressure, central venous pressure, cardiac index, stroke index, left ventricular stroke work index, systemic vascular resistance, and peripheral vascular resistance), no significant differences were observed between esmolol and placebo. To evaluate the efficacy of esmolol, 20 patients were randomly assigned to an esmolol group (n = 11) or a placebo group (n = 9). The study medication was infused from 5 min before induction through initiation of cardiopulmonary bypass. Infusion of esmolol at 200 μg · kg−1· min−1prevented tachycardia in response to intubation. In the esmolol group the heart rate increased from 63.4 ± 2.7 to 67.6 ± 2.9 beats/min after intubation, while in the placebo group it increased from 61.4 ± 4.3 to 72.4 ± 3.4 beats/min (P < 0.05). Furthermore, the increases in mean pulmonary artery pressure and PCWP observed in unstimulated, anesthetized patients were absent during surgical stimulation. Thus, in CABG patients anesthetized with fentanyl, esmolol appears safe and effective in preventing increases in heart rate during stimulation.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Whether succinylcholine causes an increase in intracranial pressure (ICP) in patients with brain lesions is uncertain and, if increased ICP does occur, its pathophysiology remains unknown. The authors investigated both the effect of succinylcholine on ICP and its modification with prior neuromuscular blockade by measuring ICP (subarachnoid bolt) in 13 consecutive patients with brain tumors who received succinylcholine both before and after complete neuromuscular blockade with vecuronium. Anesthesia was induced with thiopental, 6 mg · kg−1iv, and nitrous oxide, 70% in oxygen, while ventilation was controlled (Paco2= 37.2 mmHg ± 1.7 SE). Succinylcholine, 1 mg · kg−1iv, was administered and ICP, heart rate (HR), and blood pressure (BP) were recorded until normal twitch tension was restored. Complete neuromuscular blockade was then established with vecuronium, 0.14 mg · kg−1iv; 3 min later, succinylcholine, 1 mg · kg−1iv, was repeated. The resulting changes in ICP, HR, and BP were recorded for 3 min. Following the first dose of succinylcholine, mean ICP increased from 15.2 mmHg ± 1.3 SE to 20.1 mmHg ± 2.0 SE (P < 0.05), with five of the patients sustaining increases in ICP of 9 mmHg or greater. In contrast, when succinylcholine was given after vecuronium-induced paralysis, no patient developed an increase in ICP greater than 3 mmHg (P < 0.05 compared with the incidence of ICP ≥ 9 mmHg observed after the first dose of succinylcholine). A second group of six patients received two doses of succinylcholine according to the same protocol but without an intervening dose of vecuronium. These patients sustained increased ICP after both doses of succinylcholine. The authors conclude that increases in ICP may be induced by succinylcholine in patients with compromised intracranial compliance and the possibility of such an increase should be considered in their anesthetic management. While the exact mechanism of this phenomenon remains unknown, the results indicate that complete neuromuscular blockade with vecuronium prevents succinylcholine-induced increases in ICP.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To determine if clinical concentrations of halothane have direct relaxant effects on airway smooth muscle, the authors compared dose-response curves to histamine in the control state (thiopental) and during halothane anesthesia (1.0 and 1.5 MAC), in six basenji-greyhound (BG) dogs untreated and pretreated with atropine aerosols (10 mg · ml−1). Pulmonary resistance (RL) and dynamic compliance (Cdyn) were continuously monitored. Baseline airway tone was not significantly different during thiopental, halothane (1.0 MAC and 1.5 MAC), and after atropine aerosol administration. During thiopental anesthesia, histamine produced dose-related increases in RLand decreases in Cdyn. Both halothane and atropine significantly attenuated the bronchoconstriction induced by histamine 1 mg · ml−1. There were no significant differences in the extent of antagonism of histamine-related bronchoconstriction between halothane (1.0 MAC and 1.5 MAC) and the atropine aerosol. Moreover, in four dogs halothane anesthesia in the presence of atropine offered no additional protection compared with atropine alone. Because the protection afforded by halothane was not greater than that of atropine pretreatment alone, and the addition of halothane to atropine failed to increase the protection, it is concluded that block of vagal reflexes was the major action of halothane responsible for the attenuation of histamine-induced bronchoconstriction.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Intravenous nitroglycerin (NTG) and sodium nitroprusside (SNP) were compared as hypotensive agents in anesthetized children and adolescents. The drugs were studied in a prospective, randomized, double-blind fashion in 14 patients anesthetized with nitrous oxide: oxygen, morphine, and thiopental, NTG in doses as high as 40 μg · kg−1· min−1was ineffective at decreasing mean arterial pressure (MAP) below 55 mmHg or causing a decrease in MAP greater than one-third of baseline values. SNP was uniformly successful at inducing hypotension in all patients, including those patients in whom NTG failed. The dose of SNP required to induce hypotension was 6–8 μg · kg−1· min−1. Both NTG and SNP decreased systemic vascular resistance, although SNP did so to a much greater degree than NTG (64% vs. 29%; P < 0.01). Only SNP increased cardiac index significantly (2.27 ± 0.35 to 4.44 ± 1.36; P < 0.003). Both drugs reflexly increased heart rate, necessitating the use of intravenous propranolol (range from 1 to 3 mg) in all patients. Both drugs produced small decreases in arterial oxygen tension and increases in the average alveolar-arterial oxygen tension gradient (SNP, 44 ± 13vs.NTG, 41 ± 6). SNP use was associated with a slight metabolic acidosis (pH = 7.38 ± 0.01; base excess [BE] = −6 ± 1). Neither drug produced any other untoward reaction. SNP appears to be the agent of choice for the reliable and sustained induction of deliberate hypotension in children and adolescents.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The dose-response effects of intravenous ranitidine given 45min to 5 hearlier on gastricpH and volume were evaluated in six groups of 25 outpatients, each undergoing elective surgery under general anesthesia. Patients in Group 1 received no ranitidine and served as controls. Patients in Groups 2–6 received ranitidine intravenously in incremental doses of 0.5 mg · kg−1body weight from 0.5 mg to 2.5 mg (Group 2, 0.5 mg; Group 3, 1.0 mg; Group 4, 1.5 mg; Group 5, 2.0 mg; and Group 6, 2.5 mg). Ninety-six per cent of patients in the control group (Group 1) had gastricpH ≤ 2.5 while 36% of the patients had gastric content volumes ≥ 25 ml withpH ≤ 2.5. Ranitidine, in incremental doses of 05.-2.5 mg · kg−1body weight, caused a significant reduction of gastric acidity and volume. The ED30of ranitidine producing a gastricpH ≥ 2.5 was 0.36 mg · kg−1, and the ED95was 0.98 mg · kg−1body weight. The ED95of ranitidine producing a gastric volume ≤ 25 ml was 1.96 mg · kg−1. At the dose of 1.5 mg · kg−1of ranitidine, 100% of the patients had gastric contents withpH ≥ 2.5. The proportion of patients with volume ≤ 25 ml was 68% with ranitidine, 0.5 mg · kg−1, and gradually increased to 100% with 2.5 mg · kg−1body weight. It is concluded that a significant number of outpatients are at risk for aspiration of acid gastric contents and that this risk is lowered by preoperative administration of ranitidine.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The dose-dependent actions of bupivacaine on the microvasculature were evaluated by television microscopy in an invivorat cremaster muscle preparation. Animals were anesthetized with chloralose and urethane. Mean arterial pressure was measuredviaa carotid artery cannula; heart rate was calculated from the phasic pressure trace. The cremaster muscle was suffused with a balanced electrolyte solution that was controlled for temperature,pH, PO2, PCO2, and osmolarity to provide a physiologic environment. Internal diameters of fourth-order arterioles were measured with an electronic vernier displayed on the video monitor. Arteriolar diameters were measured every 30 s during a 10-min control period, a 10-min period of topical application of bupivacaine hydrochloride, and a 30-min recovery period. Bupivacaine 10−1, 100, 101, and 102μg · ml−1produced progressive vasoconstriction to 82.7 ± 2.9%, 75.0 ± 5.6%, 71.0 ± 7.0%, and 65.7 ± 9.4% of control (P ≤ 0.05 for each), respectively. Bupivacaine, 103and 2.5 X 103μg · ml−1, did not alter arteriolar diameters significantly, although there was a tendency for vasodilation. In a second group of animals, arteriolar diameters were measured during intravenous bupivacaine infusion that produced stable plasma concentrations of 2.3 ± 0.2 μg · ml−1. Vasoconstriction of 91.4 ± 2.2%, of control (P ≤ 0.01) was observed. These results demonstrate that dose-dependent arteriolar constriction occurs even with blood bupivacaine levels that are at the upper limits of those expected to occur during regional anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID