摘要:

BackgroundDeep hypothermic circulatory arrest is a widely used technique in pediatric cardiac surgery that carries a risk of neurologic injury. Previous work in neonates identified distinct changes in cerebral oxygenation during surgery. This study sought to determine whether the intraoperative changes in cerebral oxygenation vary between neonates, infants, and children and whether the oxygenation changes are associated with postoperative cerebral dysfunction.MethodsThe study included eight neonates, ten infants, and eight children without preexisting neurologic disease. Cerebrovascular hemoglobin oxygen saturation (ScO2), an index of brain oxygenation, was monitored intraoperatively by near‐infrared spectroscopy. Body temperature was reduced to 15 degrees Celsius during cardiopulmonary bypass (CPB) before commencing circulatory arrest. Postoperative neurologic status was judged as normal or abnormal (seizures, stroke, coma).ResultsRelative to preoperative levels, the age groups experienced similar changes in ScO2during surgery: Scosub 2 increased 30 plus/minus 4% during deep hypothermic CPB, it decreased 62 plus/minus 5% by the end of arrest, and it increased 20 plus/minus 5% during CPB recirculation (all P < 0.001); after rewarming and removal of CPB, ScO2returned to preoperative levels. During arrest, the half‐life of ScO2was 9 plus/minus 1 min in neonates, 6 plus/minus 1 min in infants, and 4 plus/minus 1 min in children (P < 0.001). Postoperative neurologic status was abnormal in three (12%) patients. The ScO2increase during deep hypothermic CPB was less in these patients than in the remaining study population (3 plus/minus 2% versus 33 plus/minus 4%, P < 0.00l). There were no other significant ScO2differences between outcome groups.ConclusionsBrain oxygenation changed at distinct points during surgery in all ages, reflecting fundamental cerebral responses to hypothermic CPB, ischemia, and reperfusion. However, the changes in Sc sub O2half‐life with age reflect developmental differences in the rate of cerebral oxygen utilization during arrest, consistent with experimental work in animals. Certain intraoperative cerebral oxygenation patterns may be associated with postoperative cerebral dysfunction and require further study.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundUnintended hypothermia occurs frequently during surgery and may have adverse effects on the cardiovascular system. Although the mechanisms responsible for the cardiovascular manifestations of hypothermia are unclear, it is possible that they are sympathetically mediated. In this prospective study, relationships between body temperature, the neuroendocrine response, and hemodynamic changes in the perioperative period were examined.MethodsSeventy‐four elderly patients, undergoing abdominal, thoracic, or lower extremity vascular surgical procedures, were randomly assigned to either “routine care” (n = 37) or “forced‐air warming” (n = 37) groups. Throughout the intraoperative and early postoperative periods, the routine care group received standard thermal care, and the forced‐air warming group received forced‐air skin‐surface warming. Core temperature, forearm minus fingertip skin‐surface temperature gradient, and plasma concentrations of epinephrine, norepinephrine, and cortisol were measured throughout the perioperative period, and the two groups were compared. In addition, heart rate and arterial blood pressure were compared between groups.ResultsThe routine care and forced‐air warming groups did not differ with regard to age, sex, type of surgical procedures, anesthetic techniques, or postoperative analgesia. Mean core temperature was lower in the routine care group on admission to the postanesthetic care unit (routine care, 35.3 plus/minus 0.1 degree Celsius; forced‐air warming, 36.7 plus/minus 0.1 degree Celsius; P = 0.0001) and remained lower during the early postoperative period. Forearm minus fingertip skin‐surface temperature gradient (an index of peripheral vasoconstriction) was greater in the routine care group in the early postoperative period. The mean norepinephrine concentration (pcg/ml) was greater in the routine care group immediately after surgery (480 plus/minus 70 vs. 330 plus/minus 30, P = 0.02) and at 60 min (530 plus/minus 50 vs. 340 plus/minus 30, P = 0.002) and 180 min (500 plus/minus 80 vs. 320 plus/minus 30, P = 0.004) postoperatively. Mean epinephrine concentrations were not significantly different between groups. Mean cortisol concentrations were increased in both groups during the early postoperative period (P < 0.01), but the differences between groups were not significant. Systolic, mean, and diastolic arterial blood pressures were significantly higher in the routine care group.ConclusionsCompared with patients in the forced‐air warming group, patients receiving routine thermal care had lower core temperatures, a greater degree of peripheral vasoconstriction, higher norepinephrine concentrations, and higher arterial blood pressures in the early postoperative period. These findings suggest a possible mechanism for hypothermia‐related cardiovascular morbidity in the perioperative period.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundThe goal of this study was to identify interventions that anesthesiologists can make to decrease total costs of a postanesthesia care unit (PACU).MethodsData were collected retrospectively from patients who underwent ambulatory surgery at our tertiary care center.ResultsSupplies and medications accounted for only 2% of PACU charges. Personnel costs, which depend on the peak number of patients in the PACU, accounted for almost all PACU costs. If nausea and vomiting could have been eliminated in each patient who suffered this complication, without causing sedation, the total time to discharge for all patients would have been decreased by less than 4.8% (95% confidence interval < 7.3%). Arrival rates to and times to discharge from the PACU followed triangular and log‐normal distributions, respectively. Computer simulations, using published times to discharge for drugs with “faster recovery,” such as propofol, showed that the use of these drugs would only decrease PACU costs if operating rooms were consistently scheduled to run later each day. Such earlier discharge also might be beneficial if used at night, but only if the PACU could close after a single patient leaves. However, reasonably achievable decreases in the times to discharge for all patients undergoing general anesthesia are unlikely to substantively decrease PACU costs. In contrast, arranging an operating room schedule to optimize admission rates would greatly affect the number of PACU nurses needed.ConclusionsAnesthesiologists have little control over PACU economics via choice of anesthetic drugs. The major determinant of PACU costs is the distribution of admissions.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundThe intracellular mechanisms involved in the alpha‐adrenoceptor‐ or hyperventilation‐induced bronchoconstriction remain unknown. Because there is a direct relationship between phosphatidylinositol (PI) metabolism and airway smooth muscle contraction induced by muscarinic agonists, the authors examined the effects of carbachol (CCh), norepinephrine (NE), and hypocapnia on PI turnover in the airway smooth muscle.MethodsRat tracheal slices were incubated in Krebs‐Henseleit solution containing LiCl and [sup 3 Hydrogen]myo‐inositol in the presence of NE, CCh, or neither. The PCO2in the solution was 36 plus/minus 3 mmHg (normocapnia), 19 plus/minus 2 mmHg (moderate hypocapnia), or 5 plus/minus 2 mmHg (severe hypocapnia), respectively. [sup 3 Hydrogen]inositol monophosphate (IP1) formed was counted with a liquid scintillation counter.ResultsBasal IP1formed was greater at severe hypocapnia than at normocapnia. Norepinephrine‐ and CCh‐induced IP1formation were also greater at hypocapnia than at normocapnia.ConclusionsThese results indicate that CCh, NE, and hypocapnia stimulate PI turnover in the airway smooth muscle, which would cause bronchoconstriction, and hypocapnia also augments NE‐ and CCh‐induced PI turnover, which could cause worsening of exercise‐induced asthma and vagotonic asthma, respectively.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundPerturbation of neuronal calcium homeostasis may alter neurotransmission in the brain, a phenomenon postulated to characterize the anesthetic state. Because of the central role of plasma membrane Calcium2+ ‐ATPase (PMCA) in maintaining Calcium2+ homeostasis, the authors examined the effect of several inhalational anesthetics on PMCA function in synaptic plasma membranes (SPM) prepared from rat brain.MethodsCalcium2+ ‐ATPase pumping activity was assessed by measurement of ATP‐dependent uptake of Calcium2+ by SPM vesicles. ATPase hydrolytic activity was assessed by spectrophotometric measurement of inorganic phosphate (Pi) released from ATP. For studies of anesthetic effects on PMCA activity, Calcium2+ uptake or Pi release was measured in SPM exposed to halothane, isoflurane, xenon, and nitrous oxide at partial pressures ranging from 0 to 1.6 MAC equivalents. Halothane and isoflurane exposures were carried out under a gassing hood. For xenon and nitrous oxide exposures, samples were incubated in a pressure chamber at total pressures sufficient to provide anesthetizing partial pressures for each agent.ResultsDose‐related inhibition of Calcium2+ ‐ATPase pumping activity was observed in SPM exposed to increasing concentrations of halothane and isoflurane, confirmed by ANOVA and multiple comparison testing (P < 0.05). Concentrations of halothane and isoflurane equivalent to one minimum effective dose (MED) depressed PMCA pumping approximately 30%. Xenon and nitrous oxide also inhibited Calcium2+ uptake by SPM vesicles. At partial pressures of these two gases equivalent to 1.3 MAC, PMCA was inhibited approximately 20%. Hydrolysis of ATP by SPM fractions was also inhibited in a dose‐related fashion. An additive effect occurred when 1 vol% of halothane was added to xenon or nitrous oxide at partial pressures equivalent to 0–1.6 MAC for the latter two agents.ConclusionsPlasma membranes Calcium2+ ‐ATPase is significantly inhibited, in a dose‐related manner, by clinically relevant partial pressures of halothane, isoflurane, xenon, and nitrous oxide. Furthermore, these anesthetics inhibit PMCA activity in accordance with their known potencies, and an additive effect was observed. How inhalational anesthetics inhibit the PMCA pump is not known at this time. It is noteworthy that the only shared characteristic of this group of agents of widely different structure is anesthetic action. The relevance of this dual commonality, anesthetic action and PMCA inhibition, to actual production of the anesthetic state remains to be determined.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundThe authors recently showed that plasma membrane Calcium2+ ‐ATPase (PMCA) activity in cerebral synaptic plasma membrane (SPM) is diminished in a dose‐related fashion during exposure in vitro to halothane, isoflurane, xenon, and nitrous oxide at clinically relevant partial pressures. They have now extended their work to in vivo studies, examining PMCA pumping in SPM obtained from control rats decapitated without anesthetic exposure, from rats decapitated during halothane anesthesia, and from rats decapitated after recovery from halothane anesthesia.MethodsThree treatment groups were studied: 1) C, control rats that were decapitated without anesthetic exposure, 2) A, anesthetized rats exposed to 1 minimum effective dose (MED) for 20 min and then decapitated, and 3) R, rats exposed to 1 MED for 20 min and then decapitated after recovery from anesthesia, defined as beginning to groom. Plasma membrane Calcium2+ ‐ATPase pumping and Calcium2+ ‐dependent ATPase hydrolytic activity, as well as sodium‐calcium exchanger activity and Sodium sup + ‐Potassium sup + ‐ATPase hydrolytic activity, were assessed in cerebral SPM. In addition, halothane effect on smooth endoplasmic reticulum Calcium2+ ‐ATPase (SERCA) was examined.ResultsPlasma membrane Calcium2+ ‐ATPase transport of Calcium2+ into SPM vesicles from anesthetized rats was reduced to 71% of control (P < 0.01) compared with 113% of control for the recovered group (NS). No depression by halothane of SERCA activity, sodium‐calcium exchanger, or Sodium sup + ‐Potassium sup + ‐ATPase activity was noted among the CAR treatment groups.ConclusionsPlasma membrane Calcium2+ ‐ATPase is selectively and stably inhibited in cerebral SPM from rats killed while anesthetized with halothane, compared with rats killed without anesthesia or after recovery from anesthesia. The studies described in this report, in conjunction with previously reported inhibition of PMCA activity in vitro by a wide range of anesthetic agents, indicate a relationship between inhibition of PMCA and action of inhalational anesthetics.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundThe autonomic nervous system plays a critical role in the central modulation of cardiac dysrhythmias. Because sympathetic blockade by thoracic epidural anesthesia has been documented to protect patients from various stress responses, the authors speculate that epidural anesthesia can attenuate the dysrhythmogenic interaction between halothane and epinephrine.MethodsIn adult mongrel dogs anesthetized with halothane, the dysrhythmogenic dose (DD) of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15‐s period, was determined in the presence of thoracic epidural mepivacaine or saline. To address the effect of circulating mepivacaine after epidural administration, the authors examined the DD of epinephrine in the presence of intravenous mepivacaine. They also investigated the effect of thoracic epidural anesthesia in bilaterally vagotomized dogs.ResultsEpidural mepivacaine significantly increased the DD of epinephrine compared with epidural saline. However, intravenous mepivacaine did not affect the DD of epinephrine, even when the plasma concentration of mepivacaine during the dysrhythmias was twice that in the epidural mepivacaine group. The beneficial effect of epidural mepivacaine was not seen in bilaterally vagotomized dogs.ConclusionsThoracic epidural anesthesia attenuated the myocardial sensitization by halothane, and vagal activity had an essential role in this action.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundThe endogenous vasodilator endothelium‐derived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow.MethodsRadioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by NW‐nitro‐L‐arginine methyl ester (L‐NAME) compared with either conscious or barbiturate‐anesthetized rats.ResultsNW‐nitro‐L‐arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate‐anesthetized rats, L‐NAME increased blood pressure (BP) by 24 plus/minus 2 (P < 0.001) and 20 plus/minus 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 plus/minus 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). NW‐nitro‐L‐arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate‐anesthetized rats, L‐NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane‐anesthetized rats, L‐NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L‐NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate‐anesthetized rats, L‐NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane‐anesthetized rats, L‐NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate‐anesthetized rats.ConclusionsHalothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L‐NAME. These data indicate that halothane anesthesia inhibits EDNO‐mediated regulation of systemic and organ hemodynamics.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundPrevious studies have shown that the region of the nucleus of the solitary tract (NST) is involved in the control of electrocortical activity and in sleep mechanisms. It also is well known that this region contains the highest concentration of opioid receptors within the medullary brainstem. The involvement of the NST opioid system in sleep‐wakefulness states was evaluated.MethodsTen cats were implanted with electrodes for chronic polygraphic recordings of their sleep‐wakefulness states and provided with an implanted guide cannula stereotaxically aimed at the NST region. Microinjections of saline, morphine sulfate, morphiceptin (specific micro agonist), D‐pen‐2‐D‐pen‐5‐enkephalin (delta agonist), and U‐50488H (kappa agonist) were given to the freely moving animals (doses 0.8–2.4 x 10 sup ‐9 M, in a volume of 0.05 micro liter of saline). After microinjections, sleep‐wakefulness recordings were obtained for 8 h.ResultsMorphine microinjections in NST provoked a dose‐dependent enhancement of all the polygraphic and behavioral manifestations of slow wave sleep. This effect was blocked by the prior intraperitoneal administration of naloxone. The micro and delta agonists also produced a hypnotic effect by enhancing slow wave sleep. By contrast, the kappa agonist caused no changes in sleep‐wakefulness states.ConclusionsThese results indicate that endogenous opioids could be involved in controlling electrocortical activity generated by NST and that activation of micro and delta NST opioid receptors enhanced the electroencephalographic synchronization associated with behavioral slow wave sleep in cats.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

BackgroundThis study examined the effects of halothane on arterial pressure after central nervous system (CNS) pressor site stimulation in anesthetized cats, cats rendered unconscious by midcollicular transection, and conscious cats.MethodsTwo anesthetized groups and two nonanesthetized groups were used. Cats were anesthetized with either alpha‐chloralose and urethane or pentobarbital. Nonanesthetized groups were cats with midcollicular transections or conscious cats with chronically implanted electrodes. Stimulating electrodes were placed into vasomotor areas of the hypothalamus (HYP), reticular formation (RF), and medulla, and arterial pressure responses to increasing stimulus currents were examined during different halothane concentrations. Two groups of cats were also anesthetized with either pentobarbital or urethane and underwent bilateral carotid artery occlusion.ResultsStimulation at each CNS site produced increases in arterial pressure and heart rate. Halothane attenuated pressor responses evoked by stimulation of all loci in all groups of cats. The inhibition by halothane on these cardiovascular responses was greatest at HYP and RF sites, while the medulla was more resistant to the effects of halothane in the anesthetized animals. Midcollicular transection decreased this medullary resistance. The inhibition of pressor responses by halothane was also greater in pentobarbital‐ than chloralose urethane‐anesthetized animals. In contrast, pressor responses elicited by bilateral carotid occlusion were attenuated by halothane similarly in both anesthetic groups. Reticular formation stimulation in conscious animals resulted in “alerting responses” in addition to pressor effects, both of which were attenuated by halothane.ConclusionsModulation of CNS cardiovascular control centers contribute to halothane‐induced hemodynamic alterations. Baseline anesthesia, CNS stimulation site, and the suprabulbar system influence the effects of halothane.

ISSN:0003-3022    

出版商:OVID    

年代:1995

数据来源: OVID