摘要:

This study on dogs determined whether the requirement for enflurane anesthesia was different pre-versuspostcardiopulmonary bypass (CPB). Male mongrel dogs (n = 16) were anesthetized with enflurane in oxygen. Tracheal intubation was performed, monitors placed, and end-tidal enflurane concentration measuredviaa Puritan-Bennett Anesthesia Agent Monitor.,® MAC was determined by the tail-clamp method. CPB was then initiated using aortoatrial (n = 6, group 1) or femoral artery-vein (n = 4, group 2) cannulation or none (n = 6, group 3, control). CPB was maintained for 1 h using a bubble oxygenator, a crystalloid prime, and flows of approximately 70–80 ml/kg with a mean systemic pressure maintained between 50–70 mmHg. Following separation from CPB, MAC was again determined. The reduction in enflurane MAC following CPB was 30.1 ± 21.5% (mean ± SD;P< 0.05vs.pre-CPB) in group 1 but there was a wide range of reduction produced (3.8–58.8%). The degree of MAC reduction (19.8 ± 8.6%;P< 0.05vs.pre-CPB) produced by CPB in group 2 was much less variable in degree (range 13.0–32.4%) but did not differ from group 1. Although pre-versuspost-CPB mean systemic pressure fell from 83 ± 13 to 69 ± 15 mmHg (P< 0.05), this is above the level likely to produce a reduction in MAC. No other significant hemodynamic changes were observed. Temperature pre-versuspost-CPB was not different. The degree of hemodilution and acid-base disturbances are unlikely to be the explanation. In group 3, MAC did not differ significantly when measured repeatedly over 8.7 ± 1.5 h (2.13 ± 0.26% at the beginning of the experiment vs. 2.14 ± 0.35% at the end), although the gradient between inspired and expired concentration was significantly reduced (0.15 ± 0.05 to 0.06 ± 0.05%;P< 0.05). This suggests that contamination of end-tidal gas by dead-space gas is also an unlikely explanation for our results. The authors conclude that normothermic CPB alters the requirements for enflurane anesthesia in dogs.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of HCl infusion on multipoint mean pulmonary arterial pressure (PAP)/cardiac index (CI) plots in pentobarbital-anesthetized dogs whose lungs were ventilated alternately in hyperoxia (fraction of inspired O2[FIO2], 0.4) and hypoxia (FIO2, 0.1) were investigated. Over the range of CI studied (1 to 51 · min−1· m−2), hypoxia increased PAP in 22 dogs (responders) and did not affect PAP in 16 other dogs (nonresponders). In eight nonresponders, two repetitions of alternated 0.4 and 0.1 FIO2exposures did not restore hypoxic pulmonary vasoconstriction (HPV), defined as a hypoxia-induced increase in PAP at a given flow. Intravenous infusion of 2 M HCI (2 mmol · kg−1· h−1) decreased arterialpH from normal to around 7.20 in eight responders and eight nonresponders. This metabolic acidosis increased PAP at all levels of CI in hyperoxia and in hypoxia in all the dogs, enhanced HPV in the responders, and restored HPV in the nonresponders. In eight responders, 2 M HCl infusion (2 mmol · kg−1· h−1) together with a 7% sodium bicarbonate infusion (adjusted to maintain arterialpH unchanged) did not affect hyperoxic or hypoxic PAP/CI plots. Pretreatment with 1 g acetyl-salicylic acid iv (6 dogs) did not affect the pulmonary vasoreactivity to HCl-induced (2 M HCl, 2 mmol · kg−1· h−1) metabolic acidosis. It was concluded that in intact dogs: 1) metabolic acidosis enhances HPV; 2) at the given dose, HCl does not produce pulmonary vascular effects unrelated to the circulating blood pH; and 3) it is unlikely that the pulmonary vasoreactivity to metabolic acidosis is mediated by products of the cyclooxygenase pathway.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The authors compared Paco2, with end-tidal CO2(ETco2,) sampled at multiple sites along the endotracheal tube (ETT) in seven anesthetized rabbits (weight, 2.7–3.6 kg) to determine the most convenient, yet accurate, sampling location. Comparisons were made during spontaneous and controlled ventilation with fresh gas flows (FGF) of two and ten times the minute ventilation using a Mapleson D circuit. An Engstrom Eliza analyzer with a continuous sampling rate of 100 ml/min was used to measure ETCO. A 0.75-mm ID polyethylene tube inserted in the side of the ETT sampled ETco2at the distal tip and at the 6-, 12-, and 15-cm marks on the ETT. ETco2, was also measured at the standard proximal connector. The differences (P< 0.05) between Paco2, and ETCO2at the distal, 6-, 12-, and 15-cm marks were 2.9 ± 0.4, 3.1 ± 0.4, 3.6 ± 0.4, and 4.6 ± 0.5 mmHg (x ± SEM), respectively, and did not change with FGF or mode of ventilation. The difference between Paco2, and ETco2, measured at the proximal connector was always large but significantly (P< 0.05) greater during spontaneous than controlled ventilation (24.2 ±1.5versus15.0 ± 1.4 mmHg) and at higher FGF (19.4 ± 1.3versus16.8 ±1.6 mmHg). The differences (P< 0.05) between ETCO2, at the distal tip and ETco2, at the 6-, 12-, and 15-cm marks were 0.24 ± 0.07, 0.73 ± 0.11, and, 1.77 ± 0.20 mmHg, respectively. This demonstrates that the change in ETco2, between the distal tip and the 12-cm mark on the ETT is less than 1 mmHg, and that this clinically insignificant difference is independent of FGF and mode of ventilation. The 12 cm-mark is outside of the mouth on a newborn, and sampling ETCO2, at that point, which may be accomplished simply by inserting a small needle in the side of the ETT, may be the most appropriate sampling location.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

There is controversy about whether N2O increases cerebral blood flow and cortical oxygen consumption (CMRO2) in rats. Cortical and subcortical blood flow and CMRO2were measured in awake, unrestrained rats while awake and during 70% N2O administration using radioactive microspheres. In the awake state, cortical and subcortical blood flow were 126 ± 10 and 98 ± 7 ml · 100 g−1· min−1, respectively, and CMRO2(cortical) was 10.0 ± 0.6 ml O2· 100 g−1· min−1(mean ± SE). After 15 min of 70% N2O, cortical and subcortical blood flow increased 100% and 40%, respectively, while CMRO2did not increase significantly. Cerebral blood flow remained increased after 60 min of N2O exposure, and CMRO2did not change. These results show that N2O produces cerebrovasodilation in rats that is not related to a change in metabolic demand. Plasma catecholamines do not change during N2O administration, indicating that the increase in blood flow is not due to a general stress response.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The electrical current thresholds for pain (ECTP) in the skin of the neck and tail were measured in rats with chronically implanted lumbar subarachnoid catheters. The effects of a benzodiazepine antagonist and a γ-aminobutyric acid (GABA) antagonist on the analgesic effects of equivalent doses of midazolam, fentanyl, and ketocyclazocine were studied. These were the minimum doses producing maximal segmental analgesia when given intrathecally (i.e., they all caused a significant and maximum increase in ECTP in the tail, which was similar for all three drugs, but no significant change in the ECTP in the neck). Flumazenil (Ro 15–1788) administration caused a parallel shift to the right of the dose-response curve for midazolam spinal analgesia. Segmental analgesia following midazolam was also significantly attenuated (P< 0.05) when the selective GABA antagonist bicuculline was given intrathecally at the same time as midazolam. The highest dose of bicuculline used (50 pmol) caused no significant attenuation of the segmental analgesic effects of either ketocyclazocine or fentanyl. The authors concluded that the segmental analgesia produced by intrathecal midazolam is mediated by the benzodiazepine-GABA receptor complex that is involved in other benzodiazepine actions.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Development of an index of myocardial contractility that is both load independent and easily quantifiedin vivohas been a difficult task. Recently, three measures of contractile state have been advocated that appear to fulfill these requirements: the end-systolic pressure-length relationship (ESPLR), the ESPLR area, and regional preload recruitable stroke work (PRSW). Because the effects of halo-thane and isoflurane on these indices of contractility have yet to be studied, the purpose of this investigation was to compare the effects of these volatile anesthetics on contractile function as evaluatedviathese techniques in chronically instrumented dogs. Because autonomic nervous system tone substantially influences systemic hemodynamicsin vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Four groups comprised the 36 experiments that were performed with nine dogs. Following inhalational induction, the dogs were maintained on 1.5 MAC and 2 MAC of halothane or isoflurane. Pressure-length loops were generated after 1 h of equilibration using preload reductionviapartial inferior vena caval occlusion or afterload augmentation by a phenylephrine infusion. The PRSW and ESPLR were then calculated, respectively. Slope and length intercept variables obtained from the ESPLR failed to significantly change from control with increasing levels of anesthetic depth despite substantial decreases in other indices of contractility. However, combination of slope and length intercept parameters into the ESPLR area model proved to be a sensitive and easily calculable measure of depressed myocardial function. Similarly, regional PRSW slope precisely reflected changes in contractile state when halothane (62 ± 10 for control to 30 ± 6 erg · cm−2· 10−3· mm−1at 2 MAC) or isoflurane (83 ± 14 for control to 55 ± 8 erg · cm−2· 10−1· mm−1at 2 MAC) were administered. The PRSW slope also demonstrated a significant difference in depressed contractility when equianesthetic concentrations of halothane and isoflurane were compared (63 ± 7% of control with halothane versus 86 ± 4% of control with isoflurane at 1.5 MAC; 50 ± 5% of control with halothaneversus70 ± 6% of control with isoflurane at 2 MAC). The ESPLR area also accurately demonstrated the differential depression in contractile function suggested by recentin vitrostudies when equianesthetic doses of halothane and isoflurane were comparedin vivo.Therefore, while ESPLR slope and length intercept variables fail as indices of myocardial contractility, ESPLR area and regional PRSW slope were shown to be useful indicators of contractile state in the conscious and anesthetized dog.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of transient hyperglycemia on brain glucose and the relationship between blood and brain glucose were studied in 76 Sprague-Dawley rats anesthetized with halothane 1% inspired. In a common control group, blood and brain glucose were determined prior to any intervention (n = 10). A second group of 30 rats was given an iv infusion of 3.9 ml of saline over a 30-min period, and blood and brain glucose were subsequently determined at several time points: 30 min (immediately after the saline infusion), 45, 60, 90, or 120 min (n = 6 for each time point). A third group of 36 rats was administered 3 g/kg of glucose in 3.9 ml of iv saline over a similar 30-min period, and blood and brain glucose were measured at the same time periods as in saline-treated rats and also when half of the glucose infusion was given (time = 15 min; n = 6 for each time point). In the common control group, blood glucose was 114 ± 14 mg/dl (6.4 ± 0.8 μmol/ml; mean ± SD) and brain glucose was 2.41 ± 0.59 μmol/g. Saline infusion had no effect on brain or blood glucose. In contrast, glucose infusion in the study group produced significant increases in both blood and brain glucose, achieving maximal values of 488 ± 60 mg/dl (27.4 ± 3.4 μmol/ml) and 7.62 ± 0.52 μmol/g, respectively, at the 30-min measurement period. The ratio of brain to blood glucose, normalized so that the common control group data achieved a value of 1, was less than unity during the period of glucose infusion. This ratio reached a nadir of 0.75 ± 0.07 at the 30-min measurement period (P< 0.05versussaline infusion). Thereafter, with the cessation of glucose infusion, the ratio returned to 1 and eventually exceeded unity: the peak ratios were 1.23 ± 0.13 and 1.16 ± 0.21 at the 60− and 90-min period, respectively (P< 0.05versussaline treatment). The authors concluded that during periods of rapidly fluctuating blood glucose, there is a hysteresis between blood and brain glucose values; hence, it may not be possible to accurately estimate brain glucose by measuring blood glucose.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The influence of age and volatile anesthetic agents on plasma concentrations and toxic effects of bupivacaine were studied in 2-day-old, 2-week-old, and 2-month-old pigs. Bupivacaine was infused at a constant rate while the pigs' ECGs and EEGs were recorded. Six pigs in each age group were lightly anesthetized with 70% N2O/ 30% O2during the bupivacaine infusion, and twelve 2-day-old pigs were anesthetized with 70% N2O/30% O2plus either 0.5 × MAC halothane or isoflurane. Two-day-old pigs were more resistant than older pigs to the toxic effects of bupivacaine despite higher plasma concentrations at all sample times. All pigs given N2O alone or N2O plus halothane had ventricular dysrhythmias, but only one pig in the N2O plus isoflurane group had a ventricular dysrhythmia. Threshold doses of bupivacaine for dysrhythmias in the N2O alone and N2O plus halothane groups did not differ. Seizures occurred in all pigs in the N2O alone group, in none of the N2O plus halothane group, and in two of the N2O plus isoflurane group. The doses required to depress cardiac index and cause asystole were less in the groups receiving halothane and isoflurane. It was concluded that N2O plus halothane and N2O plus isoflurane increase the lethality of bupivacaine while preventing early warning signs of toxicity.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Dexmedetomidine, a highly selective and potent agonist at alpha-2 adrenoceptors, produces a hypnotic-anesthetic action in rats. The mechanism for this response may involve an inhibitory G-protein and increased conductance through a potassium channel. To investigate this, the effects of pertussis toxin, a specific inactivator of inhibitory G-proteins, and 4-aminopyridine, a blocker of potassium channels, on the hypnotic-anesthetic response to dexmedetomidine were studied in rats. Pertussis toxin and 4-aminopyridine both decreased the hypnotic-anesthetic action of dexmedetomidine in a dose-dependent fashion. To preclude the possibility that pertussis toxin and 4-aminopyridine attenuated the hypnotic-anesthetic action of dexmedetomidineviaindirect central nervous system excitation, the effects of pertussis toxin and 4-aminopyridine on the hypnotic-anesthetic action of pentobarbital also were assessed. Pentobarbital-induced hypnosis was not attenuated by either treatment. These results suggest that the receptor-effector mechanism for the hypnotic-anesthetic action of dexmedetomidine involves an inhibitory G-protein and increased conductance through a potassium channel.

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