ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Continuous lumbar epidural anesthesia was instituted in 49 healthy parturients who were randomly assigned to three treatment groupos: 14 patients received chloroprocaine, 3 per cent; 19 received bupivacaine, 0.5 per cent, and 16 received a mixture containing chloroprocaine, 1.5 per cent, and bupivacaine, 0.375 per cent. Observations relating to the characteristics of the anesthetic block and to maternal and fetal well-being were made by a trained nurse observer. Times to onset of analgesia, times to maximum block, and adequacies of analgesia were similar in all groups. Bupivacaine lasted significantly longer than chloroprocaine or the mixtue (68 versus 50 and 52 min, respectively, for the first injection), and caused the least motor block. No clinical superiority could be demonstrated for the mixture as compared with bupivacaine or chloroprocaine used indivudually. There was no sign of maternal or fetal toxicity with any of the three treatment regimens.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

It is a clinical impression that less fentanyl is needed for anesthesia during hyperventilation and hypocarbia. If true, it might be due to both increased penetration of fentanyl, a highly lipid-soluble agent, into the brain and increased brain tissue binding. Serum and brain concentrations of fentanyl were determined in dogs anesthetized with halothane during normocarbia, hypocarbia by hyperventilation, and hypercarbia by addition of CO2to the inspired mixture. Fentanyl, 12.5 μg/kg, was injected iv, and serum and brain samples were taken for fentanyl analysis by radioimmunoassay. Brain fentanyl values peaked latest (15–20 min) and were highest during hypocarbia; brain fentanyl values peaked earliest (0–5 min) and were lowest during hypercarbia; values during normocarbia were intermediate in time to peak (10–15 min) and concentration. Thereafter, brain levels declined, but during hypocarbia were significantly higher and during hypercarbia were significantly lower than during normocarbia. Interestingly, serum fentanyl levels were also significantly higher during hypocarbia. The brain-blood fentanyl ratios for each of the three CO2levels increased for 30 min and thereafter stayed relatively constant. The brain-blood ratios were highest with hypocaria and lowest with hypercarbia. At 35 min, when clinical analgesia may be considered termineated, hypocarbic brain levels were double those of normocarbia. The authors feel this reflects, to a large extent, higher serum fentanyl concentrations and delayed cerebral wash-out because of decreased blood flow. To a small but unknown extent the higher brain fentanyl levels result from increased brain-blood penetration due to increased lipid solubility, and increased brain tissue binding of fentanyl during respiratory alkalosis.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Volatile anesthetics are known to decrease the requirements for neuromuscular blocking agents. To obtain a quantiative measure of the extent of this drug interaction, studies were performed on isolated guinea pig nerve-lumbrical muscle preparations exposed to methoxyflurane, halothane, isoflurane, diethyl ether, fluroxene, and enflurane in concentrations equal to MAC. From the relationship between indirect twitch height andd-tubocurarine concentration, the concentration depressing the twitch height by 50 per cent was determined. In the presence of MAC levels of anesthetic, the ED20was decreased by the following fractional amounts: methoxyflurane, 0.311; halothane, 0.334; isoflurane, 0.335, diethyl ether, 0.462; fluroxene, 0.580; enflurane, 0.697. Comparison of the fractional decrease ofd-tubocurarine dose requirement by an anesthetic at MAC and previously obtained values for the fractional depression of end-plate depolarization by an anesthetic at MAC showed that the more the anesthetic depresses depolarization, the smaller thed-tubocurarine dose requirement. Thus, clinically observed decreases in dose requirements may be explained by the effects of the anesthetics on chemosensitivity of the end-plate region.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Pulmonary-artery (PA) wedge pressure (Ppaw) is usually considered to be an accurate reflectiokn of left atrial pressure (Pla), Recent reports had demonstrated that during controlled positive-pressure ventilation (CV) in normal lungs, a progressive increase in positive end-expiratory pressure (PEEP) produced a progressive positive Ppaw-Pladiscrepancy when the PA catheter tip was positioned vertically above the left atrium (LA). In seven anesthetized dogs the Ppaw-Plarelationship (as transmural pressures) was studied at PEEP = 0, 5, 10, 15, and 20 torr, in two ways: 1) in compliant lungs with the PA catheter tip above the LA, CV was compared with spontaneous ventilation (SV); 2) during CV with PA catheter tip both above (Cup) and below (Cdown) the LA compliant lungs were compared with noncompliant lungs. A 35 per cent decrease in static pulmonary compliance was induced by administering oleic acid, 0.06 ml/kg, intravenously, and 0.01N HCI, 5 ml, intratracheally. In compliant lungs with the PA catheter tip above the LA during CV, Ppawwas significantly greater than Plaat PEEP ≥ 5 torr and equalled PEEP when PEEP ≥ 10 torr, whereas during SV, Plaat any PEEP. During CV in compliant lung, Ppawrecorded from Cupand Cdownwas significantly greater than Plaat PEEP ≥ 5 and PEEP ≥ 15 torr, respectively. During CV in noncomplicant lung, Ppawrecorded from Cupand Cdownwas significantly greater than Ppaw-Pladifference from Cupat PEEP ≥ 10 torr was significantly less in noncompliant lung than in compliant lung. It is concluded that SV affords complete protection of the Ppaw-to-Plarelationship even at high PEEP, whereas a decrease in pulmonary compliance affords moderate protection of the Ppaw-to-Plarelationship. These results are important because they further our ability to assess the accuracy of Ppawduring varying clinical situations.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The purpose of these experiments was to characterize the nature of tolerance to the analgesic action of nitrous oxide. Analgesia was assessed in rats using a tail-flick latency test and in mice using an abdominal constriction test. Rats and mice were exposed to nitrous oxide, 75 per cent, the balance oxygen, continuously for 16–18 hours. On re-exposure to nitrous oxide 30 min later, these animals were found tolerant to nitrous oxide in that the analgesic response was decreased by at least 50 per cent. Animals folerant to nitrous oxide were not tolerant to morphine. Morphine (0.25–1.5 mg/kg) produced equal degrees of analgesia in control and nitrous oxide-tolerant mice and rats. In contrast, rats made tolerant to morphine by repeated daily injections of as much as 400 mg/kg subcutaneously or by subcutaneous implantation of morphine pellets (75 mg, twice) showed a decreased analgesic response to nitrous oxide. Thus the cross-tolerance between nitrous oxide and morphine appears unique in that it is unidirectional.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Cerebral blood flow (CBF) is higher during drug-induced hypotension than during hypotension resulting from hemorrhage and, among the hypotensive drugs, CBF may be higher during nitroprusside (SNP) than during trimethaphan (TMP) administration. Increased perfusion of the brain does not guarantee better tissue oxygen supply, since perfusion of the capillary microcirculation may be inhomogeneous. In such a situation, minute areas of ischemia may exist while CBF values are normal. In this study, regional cerebral blood flow (rCBF) was measured in circles of parietal cortex approximately 1.5 cm in diameter in the cat. In addition, oxygen tension values (PB02) were measured in minute areas of cortical surface by use of 15-μm platinum oxygen electrodes. Control measurements were made during light anesthesia; blood pressure (BP) was then decreased to 30–35 torr by hemorrhage, TMP, or SNP. In the animals rendered hypotensive with TMP or SNP, a beta blocker, practolol, was also administered. It was found that rCBF was higher with SNP (68 ml/100 g/min) than with TMP (45 ml/100 g/min). PB02values showed a marked hypoxic shift during hemorrhagic hypotension, but no shift from control during SNP-induced hypotension. The PB02pattern with TMP was intermediate between the SNP and hemorrhage patterns. PB02were less than 10 torr in 25 per cent of cortical areas examined during hemorrhage, 12 and 7 per cent of areas examined during TMP-induced hypotension (two studies) and only 1 per cent of areas examined during SNP-induced hypotension. These results agree with those of others in showing higher rCBF during SNP-induced than during TMP-induced hypotension. The PB02values showed that the well-maintained cerebral perfusion during SNP administration was associated with homogeneous perfusion of the microcirculation. Therefore, brain tissue oxygen availability is greater during SNP-induced than during either TMP-induced or hemorrhagic hypotension.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Exposure of phenobarbital-pretreated male Sprague-Dawley rats to halothane, 1 per cent, for two hours under conditions of hypoxia (Fl020.14) resulted in extensive centrilobular necrosis within 24 hours. Accompanying the morphologic damage were an increase in serum glutamic pyruvic transminase (SGPT) and a decrease in hepatic microsomal cytochrome P-450. Glutathione levels in the liver were unchanged. Phenobarbital-pretreated rats anesthetized with halothane, 1 per cent, at FI020.21 had only minor morphologic changes at 24 hours. Hepatic injury was not appearent in any non-phenobarbital-induced rat or in any induced animal exposed to ether at Fl020.10 or to halothane at Fl020.99. There was a 2.6-fold increase in the 24-hour urinary excretion of fluoride in those rats in which extensive centrilobular necrosis developed. Thein-vivocovalent binding to lipids of14C from14C-halothane also was increased markedly when14C-halothane was administered intraperitoneally to phenobarbital-induced rats maintained hypoxic (FI020.14) for two hours. These results support the authors' hypothesis that halothane is metabolized to hepatotoxic intermediates by a reductive or non-oxygen-dependent cytochrome P-450-dependent pathway. This animal model of halothane-induced hepatotoxicity may be clinically relevant. A decrease in hepatic blood flow during halothane anesthesia may decrease the P02available to hepatocytes and thus direct the metabolism of halothane along its reductive, hepatotoxic pathway.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Other studies have indicated that hypoxia enhances the binding of halothane metabolites to components of the hepatic microsomal fraction. The authors pretreated Wistar rats with phenobarbital, 75 mg/kg, daily for four days to induce the hepatic drugmetabolizing enzyme system and subsequently made them hypoxic (FI02 = .08) while they were receiving halothane, 0.6 percent. Centrilobular hepatic necrosis was well developed by six hours following exposure, and early stages of resolution were evident by 48 hours. Hemorrhage occurred within the necrotic areas, and leukocytosis was not prominent. Normal rats or those depleted of hepatic glutathione did not experience hepatic necrosis when made hypoxic and given halothane. Rats receiving halothane in adequate oxygen (Fl02= 0.50) after phenobarbital pretreatment showed no hepatic necrosis. Plasma fluoride values were normal (<2 μM) immediately upon completion of halothane exposure when the animals received adequate oxygen, whether or not they had received phenobarbital pretreatment. When halothane was administered to hypoxic animals, plasma fluoride values averaged 19 ± 2 μM (Mean ± SEM), and pretreatment with phenobarbital caused a further increase in plasma fluoride to 24 ± 2 μM Plasma fluoride values thus increased indicate that the production of defluorinated halothane metabolites in caused primarily by hypoxia. In animals showing hepatic necrosis, cytochrome P-450 was decreased but cytochrome b5was not changed. The selective decrease in cytochrome P-450 suggests a specific, persistent involvement of this enzyme rather than a generalized destruction of microsomal enzymes. It is concluded that halothane anesthesia causes hepatic necrosis in rats when combined with phenobarbital stimulation of the hepatic drug-metabolizing enzme system and hypoxia.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

A capsule for regulated halothane delivery after abdominal implantation in experimental animals is described. The capsule is constructed of readily available medical-grade polyethylene and TeflonKtubing. At 37 C linear halothane release rates of 0.4 to 15 mg/hour may be obtained.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID