摘要:

Nitrous oxide has a long clinical history, but its effects on the heart remain controversial. The direct effects of N2O on global myocardial function have not been reported. The authors' aim was to examine the inotropic, chronotropic, dromotropic, and vascular effects of N2O, compared with its N2control, on hearts isolated from the guinea pig. Hearts (N = 31) were isolated and perfused at 37° C with Krebs-Ringer solution at constant pressure. Isovolumetric left ventricular pressure (LVP) and its derivative (maximum rate of tension development [dP/dtmax) were measured by placing a saline-filled, latex balloon into the left ventricle. Bipolar electrodes were placed in the right atrium and right ventricle for measurement of heart rate (HR) and atrioventricular conduction time (AVCT). The venae cavae were ligated, and the right ventricle was cannulated through the pulmonic valve to collect coronary sinus effluent for measurement of coronary outflow O2tension, adenosine, and inosine. After stabilization and perfusion with 96% O2(plus 4% CO2), each heart was exposed for 10 min either to 48% N2O or to 48% N2with 48% O2. After repeated perfusion with 96% O2for 10 min, hearts were exposed in the reverse order to 48% N2O or 48% N2. In the postcontrol period, hearts were again exposed to 96% O2. Inflow Po2(in mmHg) was 506 ± 5 (standard error of the mean [SEM]) during 96% O2and 258 ± 5 during both 48% N2and 48% N2O. Effluent Po2was 155 ± 7 during 96% O2, 81 ± 5 during 48% N2and 83 ± 5 during 48% N2O. Adenosine increased coronary flow maximally 95 ± 5% in arrested and 50 ± 9% in paced hearts. Compared with in the O2controls, N2significantly increased coronary flow 26 ± 3%, reduced O2delivery 36 ± 2%, depressed LVP 20 ± 2% and +dP/dtmax15 ± 2%, and decreased myocardial O2consumption 36 ± 3%; effluent concentrations of adenosine and inosine increased 4.8 ± 0.8 and 2.7 ± 0.6 times. N2alone did not alter HR, AVCT, percentage O2extraction, or the O2supply-to-demand ratio. Substitution of 48% N2O for 48% N2, produced no additional change in these variables except for significant additional 5 ± 2% decreases in LVP and +dP/dtmax. N2O had no appreciable direct effects in addition to those of N2on coronary flow or O2consumption. Although the mild hypoxia caused by 48% N2or N2O decreased contractility and O2consumption and increased effluent release of adenosine and inosine, the increase in coronary flow was substantially less than maximal flow attained with adenosine. This suggests that reduced O2content, like reduced coronary flow, can itself potentially limit cardiac work. The findings also demonstrate that N2O adds little to the cardiac effects of reduced O2delivery except for a significant depression of contractility. The authors speculate that,in vivo, N2O may also be a mild direct cardiac depressant, especially in the presence of other cardiac depressant agents.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The antinociceptive interaction on the tail flick (TF) and hot plate (HP) tests between opioid analgesics and medetomidine after intravenous (iv) or intrathecal administration were examined by isobolographic analysis. Male Sprague-Dawley rats received fixed ratios of medetomidine to morphine, fentanyl, and meperidine of 1:10 and 1:30, 10:1, and 1:3, respectively, by iv administration or 10:1 3:1 and 10:1, and 1:3 by intrathecal administration, respectively. Data were expressed as the percentage maximal possible effect (%MPE). The A50(dose producing 50% MPE) for each drug or drug combination was determined from the dose-response curve. Isobolographic analysis revealed that the effect of medetomidine combined with fentanyl, morphine, or meperidine was additive after iv administration. The intrathecal administration of combinations of medetomidine with the opioids produced a synergistic antinociceptive effect in the TF but not HP test. These data confirmed that the interaction between medetomidine and opioids in producing antinociception may be additive or synergistic, depending on the route of administration, drug ratio administered, and level of processing of the nociceptive input (i.e., spinalvs.supraspinal). Moreover, these results were consistent with a spinal role for alpha-2 adrenoceptors in mediating antinociception. The authors suggest that the interaction between the opioid and alpha-2 adrenergic receptors occurs within the spinal cord.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The time course of changes in brain electrical activity during halothane anesthesia was examined in 12 malignant hyperthermiasusceptible (MHS) and 14 normal (nMHS) swine. Power densities in selected frequency bands were calculated from the electroencephalogram (EEG). EEG and systemic variables were determined over a period of 60 min after starting halothane (1% inspired). Malignant hyperthermia (MH) was triggered in all susceptible pigs. Initial changes in the EEG during development of MH consisted of a decrease in total power and a shift to lower frequencies (deltatheta activity) in all animals. These EEG alterations were noted when there was an increase in heart rate, but other systemic variables were still normal. EEG changes in all MHS animals started at an arterial oxygen tension (Pao2) greater than 90 mmHg and an arterial carbon dioxide tension (Paco2) less than 50 mmHg. In 5 MHS animals EEG became isoelectric at a Pao2of 61–82 mmHg and a Paco2of 53–68 mmHg. Mean arterial blood pressure at this time was 54–66 mmHg. To determine the effects of hypoxia on the EEG in 7 nMHS animals, oxygen was decreased over a period of 45–60 min to 7% inspired. In 7 other nMHS animals, hypercarbia was produced by admixture of carbon dioxide to the fresh gas supply to achieve incremental increases of Paco2to 110–120 mmHg. Significant EEG changes during hypoxia comparable to those seen at the onset of MH were noted at a Pao2below 40 mmHg and during hypercarbia at a Paco2greater than 68 mmHg. Our results do not support the hypothesis that early EEG changes during MH occur as a result of systemic hypotension, hypoxemia, or hypercarbia.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Short periods of coronary artery occlusion are known to produce prolonged periods of ventricular dysfunction. The effects of halothane or isoflurane on contractility and metabolism in postischemic “stunned” myocardium were studied in an open-chest canine model in which the left anterior descending artery (LAD) was occluded for 15 min and then reperfused. Regional function in the LAD and circumflex artery (CIRC) areas were measured with sonomicrometry, and metabolic data were determined from simultaneous arterial and venous measurements of oxygen and lactate. Halothane and isoflurane produced equivalent decreases in systolic shortening in both normal (CIRC) and stunned (LAD) areas of the heart. Furthermore, the amount of depression was similar with either halothane or isoflurane. Halothane 0.75 MAC significantly decreased systolic shortening in both the LAD region (from 38.8 ± 25.9% to 11.0 ± 21.8%) and in the CIRC region (from 116.7 ± 24.7% to 87.5 ± 23.3%). At equivalent MAC concentrations of isoflurane, the values were 42.5 ± 45.7 to −7.0 ± 49.9% in the LAD region and 91.5 ± 11.9% to 66.9 ± 23.9% in the CIRC area. At 1.5-MAC halothane, systolic shortening in the LAD region decreased from 47.9 ± 47.2% to –0.6 ± 20.3% and in the CIRC area from 114.6 ± 16.8% to 76.0 ± 18.7%. Isoflurane at 1.5 MAC produced significant decreases, from 23.4 ± 54.5% to –15.6 ± 27.1% in the LAD region and from 94.4 ± 33.2% to 61.3 ± 28.2% in the CIRC area. High concentrations of isoflurane (1.5 MAC) were associated with decreased lactate extraction (from 40 ± 16% to 32 ± 10%) and decreased oxygen extraction (from 46 ± 8% to 37 ± 11%), whereas halothane administration was not accompanied by any significant change in metabolic parameters. Although the decreases in systolic shortening produced by halothane and isoflurane are similar in normal and stunned myocardium, this depression of function after administration of volatile anesthetic agents may be of greater significance in postischemic stunned myocardium.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Since the increase in intracranial pressure produced by succinylcholine is temporally associated with intravenous administration, we investigatedin vitroa possible direct cerebrovascular effect of this nicotinic drug. Isometric responses were recorded from dog and guinea pig basilar artery rings suspended in modified Krebs' solution at 37° C. After precontracting with a voltage (KCl)- or a receptor (5-hydroxytryptamine)-mediated agonist, cumulative concentration-relaxation curves were established for: pure succinylcholine; Quelicin® from multidose vials containing 20 mg/ml succinylcholine 1.8 mg/ml methylparaben, and 0.2 mg/ml propylparaben; Anectine® from single-dose vials containing 20 mg/ml succinylcholine; multidose Anectine® containing 20 mg/ml succinylcholine and 1.0 mg/ml methylparaben; and methylparaben and propylparaben alone. When required, the endothelium of dog artery was removed by gentle mechanical rubbing and the response to the drugs reevaluated. Both Quelicin® and multidose Anectine® produced statistically significant (P< 0.05) relaxation; Quelicin® was the more potent of the two. Methylparaben and propylparaben produced relaxation in an additive manner and completely accounted for the relaxation produced by Quelicin® and multidose Anectine®. The vascular relaxation was found to be independent of the presence of a functional endothelium. Consistent with a nicotinic induced contraction, pure succinylcholine maintained vessel tone. It is concluded that the pharmaceutically ubiquitous preservatives methylparaben and propylparaben but not pure succinylcholine have vasoactive propertiesin vitro.

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

摘要:

The authors studied the particle size of aerosols of metaproterenol produced by three different actuators designed for use in patients with endotracheal tubes in place. These were compared with the metaproterenol aerosol produced by the actuator (provided by Boehringer-Ingelheim [BI]) that was supplied by the manufacturer for use in patients whose tracheas are not intubated. The volume of particles in the respiratory size range (1.0–5.1 μm) delivered to the end of the endotracheal tube were measured using adapters designed by Intec (IT), Instrumentation Industries (II), and Monaghan (MAIS). Particle numbers were measured using a CSAS 100 scatering-aerosol laser spectrometer, and volumes were calculated by assuming the particles were spheres. The authors found that the volume of particles in the respiratory range with the IT, II, and MAIS adapters plus endotracheal tube were 11, 31, and 66%, respectively, of the volume produced in the respiratory range by the BI. When particles likely to impact before reaching the lower airways (> 5 μm) were measured, almost none was produced by the adapters plus endotracheal tube, whereas the majority of drug volume in the BI aerosol was in the > 5 μm range. It was concluded that the aerosol produced by different actuators differ from each other, that all three produced less drug in the respiratory range than was produced by the manufacturer-supplied actuator, and that large particles are effectively removed by the adapter plus endotracheal tube.

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

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