ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The effects of isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right (RV) and left (LV) ventricular performance (ultrasonic dimension technique), and on coronary, systemic, and pulmonary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Isofluraue caused dose-dependent decreases in LV and RV dP/dt, and in myocardial segment shortening in the presence of unchanged heart rate, unchanged or increased (RV) preload, and unchanged (RV) or decreased (LV) afterload. RV and LV functions were affected differently: at a mean aortic pressure of 70 mmHg (mean inspired isoflurane 1.2%), RV end diastolic dimensions and pressure remained unchanged, whereas those of the LV decreased. At a mean aortic pressure of 55 mmHg (mean inspired isoflurane 1.8%), RV end diastolic dimensions and pressure increased above control, whereas those of the LV remained unchanged. Within the RV, inflow and outflow tract were affected quantitatively similarly, but dyssynchrony developed in four animals. Isoflurane caused dosedependent decreases in coronary and systemic vascular resistances, but no change in pulmonary vascular resistance. At the lower concentration of isoflurane, coronary blood flow did not fall despite decreased LV and RV dP/dt, unchanged heart rate, unchanged or decreased preload, and unchanged or reduced afterload. The data indicate that isoflurane is a myocardial depressant and a potent coronary vasodilator. At both concentrations, LV function was better preserved than RV function, most likely due to the different effects of isoflurane on RV (unchanged) and LV (reduced) afterload.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To determine the site of isoflurane-associated coronary vasodilatation, the authors measured epicardial coronary artery diameter and examined the effects of isoflurane on coronary arteriolar tone. Angiograms of the left coronary system were obtained in seven fentanyl-pentobarbital anesthetized dogs and quantitated with a computerized analysis system. Cross-sectional areas of the proximal, mid, and distal left anterior descending and proximal circumflex coronary arteries were obtained at three arterial pressures, and then the measurement repeated following administration of 0.75%, 1.5%, and 2.25% end-tidal isoflurane. At the same time coronary blood flow was measured using a123Xe washout technique. Isoflurane was found to have no effect on epicardial coronary artery dimensions. No dilatation was observed throughout the range of isoflurane concentrations and coronary perfusion pressures investigated. However, despite the absence of epicardial coronary effects, coronary arterioles were dilated by both 1.5% and 2.25% isoflurane. Coronary blood flow corresponding to a myocardial oxygen consumption of 7.5 ml oxygen.100 gm−1.min−1was calculated as 99 ± 17 ml.100 gm−1.min−1(mean ± SD) during control conditions, and it increased to 150 ± 26 ml.100 gm−1.min−1at 1.5% isoflurane (P< .004) and to 197 ± 35 ml.100 gm−1.min−1at 2.25% isoflurane (P< .001). Although higher concentrations of isoflurane dilated intramyocardial arterioles, isoflurane had no effect on epicardial coronary arteries.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The hypothesis that isoflurane causes coronary steal was investigated in a canine model of chronic coronary occlusion. An ameroid constrictor was implanted in dogs to stimulate the development of intercoronary collateral vessels. During an acute experiment 3–4 weeks following implantation, heart rate, mean arterial pressure, and total coronary flow were held constant, and flow distribution was measured with microspheres in the presence and absence of isoflurane. Contractile function of the collateral-dependent zone and myocardial lactate extraction were also measured. Isoflurane produced a decrease in collateral flow and a decrement in collateral zone contraction, while, at the same time, enhancing flow in the normally perfused zone. In a second series of animals, isoflurane was found to have effects similar to those of adenosine, an arteriolar dilator known to produce coronary steal. In contrast, neither halothane nor nitrous oxide caused flow alterations or dysfunction of the collateral-dependent zone.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The effects of Isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right and left ventricular performance (ultrasonic dimension technique) and on coronary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs (anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium) with critical coronary artery stenoses (micrometer-controlled snares) of the right and left anterior descending coronary arteries. The stenoses reduced resting coronary blood flow by approximately 10% without affecting global or regional myocardial performance. During subsequent isoflurane administration, coronary blood flow fell markedly. In the areas supplied by the stenosed coronary arteries, segment length shortening decreased by 70% (P< 0.01), and regional akinesis, paradoxical motion, or postsystolic shortening developed in 9 of 12 animals. In contrast, in the areas supplied by normal coronary arteries, myocardial segment length shortening decreased significantly less and did not show signs of dysfunction. In these non-ischemic areas at both concentrations of isoflurane, end diastolic and systolic dimensions were greater in the right than in the left ventricle, probably related to differences in right (unchanged) and left (reduced) ventricular afterloads. The data indicate that in the presence of coronary artery stenoses, isoflurane-induced hypotension may cause regional myocardial dysfunction suggestive of ischemia.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Forty surgical patients were divided into two groups and anesthetized with either sevoflurane and oxygen or sevoflurane, oxygen, and nitrous oxide. The minimum alveolar concentration (MAC) for sevoflurane required to prevent movement in response to surgical incision in healthy patients was 1.71 ± 0.07% (SE). The AD95(anesthetic ED95) that prevented 95% of patients from moving was 2.07%. The addition of 63.5% end-tidal nitrous oxide allowed a reduction in the alveolar sevoflurane concentration to 0.66 ± 0.06% (SE). The reduction in sevoflurane MAC was 61.4%. The AD95for sevoflurane with 63.5% end-tidal nitrous oxide was 0.94%.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

This study tested the hypothesis that lidoflazine, a calcium entry blocking drug, will improve post-ischemic neurologic outcome when administered after a period of complete cerebral ischemia, and that the improvement in outcome is related to an increase in post-ischemic cerebral blood flow (CBF). Complete cerebral ischemia was produced in 31 dogs by temporary ligation of the aorta and venae cavae. In six dogs, 10 min of complete cerebral ischemia was followed by an infusion of lidoflazine 1.0 mg.kg−1iv over 10 min. CBF and cerebral metabolic rate for oxygen (CMRO1) were measured pre-ischemia, and for 90 min post-ischemia. The results from these six dogs were compared with results previously obtained from eight untreated dogs under similar, but not identical, conditions. The CBF measured post-ischemia in the dogs administered lidoflazine did not differ from the CBF measured post-ischemia in the untreated dogs. Both groups showed an initial hyperemia post-ischemia, followed by significant decreases in CBF from control values by 35 min post-ischemia. The post-ischemic CMRO2also did not differ between lidoflazine treated and untreated groups. In 25 dogs, 11 min of complete cerebral ischemia was followed by an iv infusion of either lidoflazine 1.0 mg.kg−1or saline placebo. The same iv infusions were repeated at 8 and 16 h post-ischemia. Seven dogs were excluded from data analysis for failure to meet pre-established protocol criteria. Neurologic injury was evaluated in the remaining dogs at 48 h post-ischemia by an observer blinded to the treatment groups. Only a suggestion of improved neurologic outcome was noted in the nine dogs having received lidoflazine, when compared to the nine dogs having received saline placebo (P= 0.077). If lidoflazine administered post-ischemia in the dog does improve neurologic outcome, then it must be by a mechanism which is independent of restitution of post-ischemic CBF.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The influence of isoflurane on hypoxic pulmonary vasoconstriction (HPV) was studied in eight subjects prior to elective surgery. The lungs were ventilated separately with a double-lumen endo-bronchial catheter. After oxygen ventilation of both lungs for 30 min during intravenous barbiturate anesthesia, the test lung was rendered hypoxic by ventilation with 8% O2in nitrogen. The control lung was ventilated continuously with 100% O2. Isoflurane was added to the inspired gas, so that end-tidal concentrations of 1% and 1.5% were obtained. Cardiac output (&OV0422;T) was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused, poorly soluble gas (SF6). The hypoxic challenge during intravenous anesthesia resulted in a reduction in the fractional perfusion of the test lung from 54% to 41% of &OV0422;T. Mean pulmonary arterial pressure increased by 46%, and pulmonary vascular resistance (PVR) of the test lung more than doubled. Arterial oxygen tension fell from 375 mmHg (50 kPa) to 101 mmHg (13.5 kPa). Adding isoflurane to the inhalation gas, first at a concentration of 1%, then 1.5%, caused no further significant change in the distribution of pulmonary blood flow, although six of the eight subjects showed a small increase in test lung blood flow at isoflurane 1.5%. There was no change in PVR or in any other circulatory variable. Arterial blood gases remained essentially unaltered. When the hypoxic challenge was discontinued, all variables returned to control values. It is possible that higher isoflurane concentrations would have caused a clear change in the blood flow distribution, but, at clinical concentrations, the effect of HPV in the human is all but immeasurable.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The authors studied the effects of dihydroergotamine (DHE) and etilefrine hydrochloride (E) on the regional distribution of99mTc-marked erythrocytes during epidural anesthesia in eight supine men to determine if vasoactive agents with venoconstrictor action would enhance cardiac filling during epidural anesthesia. Radioactivity was recorded with a gamma camera, and its distribution determined in the thorax, abdomen, and limbs. Arterial and central venous pressure, heart rate, and calf volume by plethysmography were measured. During epidural anesthesia with a sensory block up to T4/5, DHE (7.5 μg/kg) reduced the radioactivity,i.e., blood volume, in both the innervated (−5.9 ± 3.5%) and denervated muscle/skin (−16.9 ± 7%) regions, and increased it in both the intrathoracic (+7.0 ± 2.3%), and splanchnic vasculature (+4.2 ± 3.2). In contrast, E (6 μg.kg−1.min−1) decreased the blood volume most markedly in the splanchnic region (−5.4 ± 0.7%) and increased it in the thorax (+2 ± 0.6%). All these changes were statistically significant. The combined effects were estimated to be equivalent to a transfusion of nearly 1.01 of blood. Both drugs reversed the hypotensive action of epidural anesthesia. During epidural anesthesia, DHE preferentially constricted the capacitance vessels in skeletal muscle and skin irrespective of the state of innervation, whereas E preferentially constricted the splanchnic vasculature. In the doses used, the two agents replenished in an additive fashion the central circulation during epidural anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The pharmacokinetics of esmolol, a new, ultra-short-acting beta adrenergic blocking drug, were studied in 19 patients undergoing coronary artery surgery. Esmolol was administered as a continuous infusion, and blood concentrations were measured at intervals up to 40 min after discontinuation of the infusion. In all patients, a bi-exponential equation best described the esmolol concentration—time curve. Half-lives for the distribution and elimination phases were 1.34 ± 0.77 min and 9.9 ± 4.55 min (mean ± SD), respectively. The mean values for Vβand Vcwere 1.9 ± 1.24 1.kg−1and 0.41 ± 0.31 1.kg−1, respectively, and the total clearance was 128 ± 41 ml.kg−1.min−1.

ISSN:0003-3022    

出版商:OVID    

年代:1987

数据来源: OVID