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Biomedical subjects

G Blaise

Publications and source records attributed to G Blaise.

At least 19 recordsLinked to original sources
PubMed1992

Mechanism of halothane attenuation of isometric tension induced by serotonin in isolated canine coronary artery rings.

We explored the mechanism of halothane's interaction with the serotoninergic contractile response of isolated canine coronary artery rings. The serotoninergic contractile response of both intact and denuded rings was measured with and without halothane. In some experiments, rings were pretreated with methiothepin, a 5-HT1 and 5-HT2 antagonist, or ketanserin, a 5-HT2 antagonist. The contractile responses to 5-carboxamidotryptamine (5-CT) and alpha-methylserotonin, a 5-HT1 and a 5-HT2 receptor agonist, respectively, were measured with and without halothane. Finally, the response to prostaglandin F2-alpha, another spasm mediator, was also measured with and without halothane. Halothane attenuated the coronary artery response to serotonin (5-hydroxytryptamine, 5-HT), and specific 5-HT1 and 5-HT2 agonists, and prostaglandin F2 alpha (PGF2 alpha). Its inhibitory effect on the serotoninergic response was abolished in vessels pretreated with either 5-HT1 or 5-HT2 blockers. These data suggest that halothane is not a direct smooth muscle depressant, that it is not a specific 5-HT1- or 5-HT2-subtype antagonist in canine coronary arteries, and that it might interfere with intracellular pathways activated by agonist-receptor interactions.

Animals↗
PubMed1991

Beneficial effects of volatile anesthetics on decrease in coronary flow and myocardial contractility induced by oxygen-derived free radicals in isolated rabbit hearts.

Oxygen-derived free radicals have been implicated in reperfusion injury whereas volatile anesthetics have been shown to enhance myocardial recovery during reperfusion. To explore the mechanism by which these agents improve myocardial recovery, we measured the effect of volatile anesthetics on the free radical-induced reduction in left ventricular pressure (LVP), coronary flow, and endothelium-dependent dilation induced by acetylcholine (Ach). Isolated rabbit hearts were perfused in a Langendorff apparatus. Isovolumetric LVP and coronary flow were measured throughout the study. Oxygen-derived free radicals were produced by the electrolysis (direct current of 0.6 mA) of the perfusate. The following volatile anesthetics were used: halothane 0.5 or 1.0%, isoflurane 0.7 or 1.4%, and enflurane 1.0 or 2.0%. Oxygen free radicals induced a significant decrease in systolic LVP and coronary flow. Pretreatment of the heart with enflurane 1.0 or 2.0%, halothane 1.0%, or isoflurane 0.7% attenuated the effect of the free radicals on both systolic LVP and coronary flow. Free radicals reduced the dilating response induced by 0.1 microM Ach with or without addition of volatile anesthetics. These data suggest that the volatile agents have beneficial effects on the free radical cell damage pathway and that this protection is not related to the preservation of endothelium-dependent dilation.

Anesthetics↗
PubMed1991

Halothane 1.5 MAC, isoflurane 1.5 MAC, and the contractile responses of coronary arteries obtained from human hearts.

Active vasoconstriction of epicardial coronary arteries can cause myocardial ischemia in patients with coronary artery disease. Relief of vasoconstriction can improve blood flow to the heart. The purpose of this study was to determine if 1.5 MAC halothane and 1.5 MAC isoflurane would each attenuate contractions evoked by three putative mediators of coronary constriction in coronary arteries removed from the hearts of human beings. Hearts were obtained in the operating room from five patients undergoing cardiac transplantation and from six brain-dead patients undergoing organ donation procedures. Coronary arteries were dissected free, cut into rings, and studied in organ chambers. Endothelium-dependent relaxations to 10(-6) M bradykinin were examined; they indicated a variable degree of endothelial dysfunction in vessels used in the experiments. Contractile responses to 40 mM KCl were tested and were used as control contractions. Contractions evoked by serotonin, histamine, and prostaglandin F2 alpha were measured and were expressed as a percent of contractile responses evoked by 40 mM KCl. Halothane depressed the agonist-induced contractions. Maximal contractile responses to serotonin were 130% +/- 28% in untreated rings and 63% +/- 10% in rings exposed to halothane (P less than 0.03). Responses to histamine were 183% +/- 46% untreated and 121% +/- 26% during halothane administration (P less than 0.05), and responses to prostaglandin F2 alpha were 227% +/- 42% untreated and 148% +/- 18% with halothane (P less than 0.05). Isoflurane had no effect on contractions. The results demonstrate that 1.5 MAC halothane, but not 1.5 MAC isoflurane, attenuates contractile responses evoked by putative mediators of coronary vasoconstriction in coronary arteries removed from the hearts of human beings.

Adult↗
PubMed1991

Electrophysiologic effects of bupivacaine in the isolated rabbit heart.

To assess the direct electrophysiologic effects of bupivacaine, we examined the spontaneous sinus rhythm and induced rapid and premature atrial and ventricular pacing in 11 isolated rabbit hearts perfused in the Langendorff apparatus with varying concentrations (designated by []) of bupivacaine (control, n = 2; 0.3 microgram/mL, n = 3; 1.5 micrograms/mL, n = 3; 3.0 micrograms/mL, n = 3). There was no change in sinus node automaticity or sinus node recovery time at any concentration and no evidence of abnormal automaticity. Depression of conduction was reflected by prolongation of the PR interval at the following concentrations: 1.5 micrograms/mL (65.0 ms before, 96.6 ms after) and 3.0 micrograms/mL (61.6 ms before, 103.3 ms after) and increase in atrial and ventricular pacing thresholds at 3.0 micrograms/mL (atrial: 0.86-8.6 mA, ventricular: 2.0-10.0 mA). No spontaneous tachyarrhythmias occurred; 2:1 spontaneous atrioventricular block (n = 1) and a decrease in maximal paced rate with 1:1 anterograde or retrograde atrioventricular conduction were noted at all concentrations of bupivacaine. Thus bupivacaine did not change automaticity but had a depressant effect on conduction at the atrial, ventricular, and atrioventricular levels, providing a basis for clinically occurring atrioventricular block and reentrant arrhythmias.

Action Potentials↗
PubMed1991

Isoproterenol corrects the effects of bupivacaine on the electrophysiologic properties of the isolated rabbit heart.

The purpose of this study was to test the hypothesis that isoproterenol could reverse bupivacaine toxicity. In eight isolated rabbit hearts an electrophysiologic evaluation was performed then repeated during infusion of bupivacaine (1 microgram/mL) alone and bupivacaine plus isoproterenol (1-2 micrograms/mL). Bupivacaine alone increased electrocardiographic intervals (P wave, QRS complex, PR, AV, and QTc interval) and refractory periods of the myocardium and atrioventricular junction as well as the Wenckebach cycle and pacing thresholds. The addition of isoproterenol corrected partially or completely all bupivacaine-induced abnormalities, and decreased sinus cycle length, suggesting a potential therapeutic value in the treatment of bupivacaine intoxication.

Action Potentials↗
PubMed1989

Metabolic effects of acetate on the heart.

The effects of various substrates (15 mM glucose, 5 mM glucose, 20 mM acetate, or a combination of these substrates) on the coronary blood flow and on the energetic status of myocytes were studied in isolated perfused rat hearts. We demonstrate that low level glucose (5 mM) or high concentration of acetate (20 mM) leads to a simultaneous fall in tissue ATP, rise in tissue adenosine, and significant increment in coronary blood flow. The latter effect is especially marked with 20 mM acetate. Dipyridamole (10(-6) M) does not enhance the vasodilatation induced by acetate. The provision of 15 mM glucose together with 20 mM acetate fully prevents these changes, indicating that the vasodilatation induced by acetate is probably mediated by metabolic changes. The evidence supports the concept that a redistribution of blood flow together with a fall in tissue ATP may explain some of the adverse effects of acetate dialysis in man, and suggests that the provision of glucose may alleviate these changes.

Acetates↗
PubMed1988

Inhibitors of cyclooxygenase augment serotonergic responsiveness in canine coronary arteries.

Experiments were designed to determine the role of products of cyclooxygenase in contractions of coronary smooth muscle evoked by serotonin. Rings of canine coronary artery without endothelium were suspended in organ chambers filled with modified Krebs-Ringer bicarbonate solution. Serotonin caused concentration-dependent contractions followed by secondary relaxations at higher doses. Indomethacin and meclofenamate augmented both the contraction and the relaxation. Indomethacin did not affect contractions evoked by increasing concentrations of either phenylephrine, prostaglandin F2 alpha, or potassium chloride. Propranolol did not affect the concentration-response curve to serotonin under control conditions; it prevented the facilitated contraction to the monoamine but not the augmented secondary relaxation caused by the inhibitors of cyclooxygenase. These results suggest that endogenous prostanoids simultaneously inhibit the contractile process and brake relaxations induced by higher concentrations of serotonin. As a consequence, inhibitors of prostanoid formation facilitate the vasospastic component of the response to the monoamine in large coronary arteries. For unknown reasons, propranolol prevents this facilitation.

Animals↗
PubMed1987

Isoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteries.

The authors sought to determine if isoflurane would attenuate effects of three different types of vasoconstrictors on isolated segments of canine epicardial coronary arteries removed from healthy dogs. As the endothelium has a major role in regulating epicardial coronary artery tone, and as it modulates the effect of many vasoactive substances, experiments were conducted both on normal rings and on rings whose endothelium had been mechanically removed. In addition, the endothelium is thought to be damaged in human atherosclerosis. Rings were suspected in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% oxygen and 5% carbon dioxide, and connected to strain gauges for the measurement of isometric tension. Isoflurane 2.3% (1.5 MAC in the dog) was added to the aerating gas mixture in half the preparations, while the other rings served as control. The vasoconstrictors serotonin, phenylephrine, or prostaglandin F2 alpha were added in increasing concentrations to the bath solution. In the presence of endothelium, vasoconstrictor evoked contractions were attenuated by isoflurane. Maximal tension generated by prostaglandin F2 alpha in untreated rings was 114 +/- 18% (mean +/- SEM) of a reference contraction, while, following isoflurane, it was 46 +/- 8% (P less than 0.005). In the absence of endothelium, isoflurane attenuated neither prostaglandin F2 alpha nor serotonin evoked contraction, and had decreased effectiveness against phenylephrine mediated contraction (P less than 0.001). It is concluded that isoflurane attenuates vasoconstrictor-evoked contraction of isolated canine epicardial coronary arteries, and that this effect is mediated by the endothelium.

Animals↗
PubMed1986

The sleep apnoea syndrome and epidural morphine.

A patient not known in advance to have the sleep apnoea syndrome (SAS) was administered a combined epidural-general anaesthetic for a proposed radical prostatectomy. After surgery which had to be discontinued due to extensive tumoural spread, morphine 5 mg was administered through the epidural catheter for analgesia. Severe respiratory depression occurred eight hours later and was successfully reversed by repeated injections of naloxone. The potential danger of epidural morphine administration to SAS patients is discussed.

Aged↗
PubMed1979

Preoperative autotransfusion for total hip protheses.

The authors describe a method of preoperative autotransfusion for scheduled total hip prothesis. Blood is collected in the patients 10 days before the operation. This blood is retransfused at the end of surgery, done under continuous epidural anesthesia. Of the 15 patients, 85% had a total hip prothesis without receiving bank blood.

Aged↗
PubMed1977

Technique of general anesthesia for tonsillectomy and adenoidectomy.

This article reports a technique of general anesthesia for tonsillectomy, according to the method of Sluder-Ballanger. For induction of the anesthesia the children receive: ketamine (1 to 1.5 mg/kg), succinylcholine (1 mg/kg). They are intubated through the nose and then ventilated by a mixture of N2O and O2 (50% - 50%). For the intervention they are brought in sitting position. The authors discuss the advantages of this technique as much from the anesthetic as from the surgical point of view.

Adenoidectomy↗
PubMed1977

Treatment of gas gangrene. Interest of hyperbaric oxygen therapy.

We report 27 cases of gas gangrene treated at the University Hospital of Liège since the Anesthesiology Department has been using a caisson for hyperbaric oxygen therapy. Frequency of gas gangrene does not appear to have decreased during recent years. The etiologies now encountered are mainly of post-traumatic and post-operative origin (especially surgery on the digestive tract); arterial insufficiency is a predisposing factor. The prognosis depends on the speed with which an effectual treatment is started; the latter consists in intensive hyperbaric oxygen therapy, antibiotic therapy and resuscitation. Surgery should be as conservative as possible and is undertaken only when progress of the disease has been checked by hyperbaric oxygen therapy. The association of these various modes of treatment proves effectual despite a still significant mortality.

Adolescent↗