PubMed Health⌕ Search

Biomedical subjects

G A Blaise

Publications and source records attributed to G A Blaise.

At least 19 recordsLinked to original sources
PubMed1997

Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus.

BACKGROUND: Although epidural corticosteroid injections are commonly used for sciatica, their efficacy has not been established. METHODS: In a randomized, double-blind trial, we administered up to three epidural injections of methylprednisolone acetate (80 mg in 8 ml of isotonic saline) or isotonic saline (1 ml) to 158 patients with sciatica due to a herniated nucleus pulposus. All patients had Oswestry disability scores higher than 20 (on a scale of 1 to 100, with scores of 20 or less indicating minimal disability, and higher scores greater disability). RESULTS: At three weeks, the Oswestry score had improved by a mean of -8.0 in the methylprednisolone group and -5.5 in the placebo group (95 percent confidence interval for the difference, -7.1 to 2.2). Differences in improvements between the groups were not significant, except for improvements in the finger-to-floor distance (P=0.006) and sensory deficits (P=0.03), which were greater in the methylprednisolone group. After six weeks, the only significant difference was the improvement in leg pain, which was greater in the methylprednisolone group (P=0.03). After three months, there were no significant differences between the groups. The Oswestry score had improved by a mean of -17.3 in the methylprednisolone group and -15.4 in the placebo group (95 percent confidence interval for the difference, -9.3 to 5.4). At 12 months, the cumulative probability of back surgery was 25.8 percent in the methylprednisolone group and 24.8 percent in the placebo group (P=0.90). CONCLUSIONS: Although epidural injections of methylprednisolone may afford short-term improvement in leg pain and sensory deficits in patients with sciatica due to a herniated nucleus pulposus, this treatment offers no significant functional benefit, nor does it reduce the need for surgery.

Adult↗
PubMed1994

Platelet-induced vasomotion of isolated canine coronary artery in the presence of halothane or isoflurane.

To determine the effect of 1.5 MAC of two volatile anesthetics (halothane and isoflurane) on platelet-induced contraction of canine coronary artery, isolated, denuded coronary rings were suspended between two stirrups, placed into organ chambers filled with an oxygenated Krebs-Ringer solution, and connected to an isometric force transducer. Human platelets were obtained from healthy donors and introduced into the organ chambers in increasing amounts to reach 20,50 and, 70 x 10(9) platelets/L. The tension generated in both the control and anesthetic-treated rings was recorded; only halothane reduced the tension induced by platelet activation in the organ chambers. In some experiments, aliquots of Krebs-Ringer solution were taken to determine the amount of 5-HT and TB2 released by 70 x 10(9) human platelets in the presence and absence of the anesthetics. Only halothane reduced TA2 production by the activated platelets. Finally, the contractile response of isolated denuded canine coronary artery rings to U46619, a thromboxane analog, was measured in the presence and absence of the anesthetics. Neither halothane nor isoflurane attenuated the response. In another series of experiments, in vitro platelet aggregation was induced by epinephrine, collagen, ADP, or arachidonic acid in the presence or absence of 1.5 MAC isoflurane or halothane. Both anesthetics significantly reduced the aggregation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Effect of rapamycin on rat aortic ring vasomotion.

Rapamycin (RAPA) is an antifungal antibiotic with interesting new immunosuppressive properties. We evaluated RAPA's effects in vitro on basal and stimulated tension of isolated intact or denuded rat aortic rings. Rings were prepared in an organ chamber and contracted with 40 mM KCl (reference 100%). Some rings were treated with either RAPA's polysorbate/polyethylene glycol-based (PEG) vehicle (0.8% vol/vol) or with different concentrations of RAPA (10, 100, and 1,000 ng/ml) diluted in PEG; untreated rings were used as controls. Variation in tension with time (2 h) and the dose-response to thromboxane A2 analogue (U46619) and phenylephrine (PE) were measured in controls and treated rings. PEG potentiated the increase in basal tension in rings with endothelium after 2-h treatment (44.66 +/- 3.59 vs. 14.82 +/- 2.43% for controls, p < 0.05, n = 10). RAPA antagonized the contraction induced by its own vehicle dose dependently. At 1,000 ng/ml, RAPA caused relaxation of intact rings below the control level (4.29 +/- 2.20 vs. 14.82 +/- 2.43%, p < 0.05, n = 10), but not in rings without endothelium. RAPA did not modify the response to PE or U46619 in rings with endothelium. RAPA relaxed the vessels by an endothelium-dependent mechanism, and this effect can be modulated by its vasoconstrictive PEG vehicle.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Acetylcholine stimulates release of endothelium-derived relaxing factor in coronary arteries of human organ donors.

OBJECTIVE: To determine whether cholinergic stimulation of human coronary endothelial cells induces the release of endothelium-derived relaxing factor (EDRF), denuded human coronary artery rings or denuded rabbit aorta rings were either directly perfused or superfused by the effluent of intact or denuded human coronary artery segments in a perfusion bioassay system. DESIGN: Coronary vessels were dissected from hearts of organ donors and prepared for use as donor segments and detector rings in the perfusion bioassay system. Segments were continuously perfused by an oxygenated Krebs-Ringer solution. Rings were suspended between two stirrups, one of which was connected to an isometric force transducer. They were either directly perfused (no tissue had been previously perfused by the same Krebs-Ringer) or superfused by the effluent of an endothelium-intact or -denuded coronary segment. Human rings were contracted with prostaglandin F2 alpha (2 x 10(-6) M) and rabbit rings were contracted with phenylephrine (10(-6) M). RESULTS: Tension in detector tissue did not change during superfusion with effluent from endothelium-denuded or -intact human coronary artery segments, showing that there was no basal release of EDRF/nitric oxide (NO) in this preparation. Acetylcholine (ACh) (10(-6) or 10(-5) M) added to the perfusate increased the tension of the precontracted endothelium-denuded human rings directly perfused (50 +/- 32%) but not of the precontracted rabbit rings, showing that ACh is a potent agonist of human coronary vascular smooth muscle. ACh added to the coronary segment in the endothelium-intact superfusion mode had no effect in 33% or induced a small relaxation (8.8 +/- 1.6%) in 66% of the preparations. Hemoglobin (10(-5) M), a scavenger of EDRF/NO, caused a further increase in tension (32 +/- 15%). Adding calcium ionophore (A 23187;10(-5) M), which stimulates EDRF/NO release through a nonreceptor-mediated mechanism, to the coronary artery segment induced a relaxation in the endothelium-perfused detector rings which did not relax to ACh (30 +/- 2%); this relaxation was reversed by methylene blue (10(-5) M), a blocker of soluble guanylate cyclase. NO endothelin, a potent vasoconstrictor released by the endothelial cells, was detected in the effluent of intact coronary vessels. CONCLUSION: The results suggest that in two-thirds of the six preparations studied, cholinergic stimulation can release EDRF from human donor coronary artery endothelial cells.

Acetylcholine↗
PubMed1992

Maternal inspired oxygen concentration and fetal oxygenation during caesarean section.

This study was designed to determine whether fetal arterial and venous PO2 could be increased by increasing maternal FIO2 in the period between hysterotomy and birth. Two groups of ten patients were studied. All were anaesthetised with the same technique except for the FIO2 after hysterotomy. One group inspired 50% oxygen and the second group inspired 100% oxygen. Although the maternal arterial PO2 was higher at birth in the 100% O2 group (177.4 +/- 42.3 mmHg vs 281.0 +/- 94.2 mmHg), there were no differences between the arterial umbilical cord PO2 (19.3 +/- 5.7 mmHg vs 18.5 +/- 7.3 mmHg) and the venous umbilical cord PO2 (31.1 +/- 7.6 mmHg vs 33.0 +/- 10.8 mmHg). Awareness was present in one patient in the 50% O2 group and in four patients in the 100% O2 group but this difference was not statistically significant. It is concluded that a higher inspired maternal oxygen concentration between hysterotomy and birth does not result in any increase in fetal PO2.

Anesthesia, Inhalation↗
PubMed1991

Attenuation of contraction of isolated canine coronary arteries by enflurane and halothane.

Contraction of vascular smooth muscle such as that existing in coronary arteries is regulated in part by Ca++ entry into cells via Ca++ channels. Volatile anaesthetics are known to attenuate agonist-induced coronary artery constriction. The purpose of this experiment was to determine if 1.5 MAC concentrations of halothane or enflurane attenuated contractions evoked by activation of one type of Ca++ channel--the potential operator channel. In the current experiment, potential operator channels were activated by depolarizing isolated canine coronary artery rings with high concentration of K+, causing Ca++ entry and vessel contraction. Rings without endothelium were suspended for isometric force measurement in organ chambers containing aerated Krebs-Ringer solution. Maximum response to Ca++ in rings depolarized with K+ was 120 +/- 5 per cent in untreated versus 101 +/- 3 per cent in rings treated with enflurane (P less than 0.01). The maximum response was 123 +/- 6 per cent in untreated versus 111 +/- 5 per cent during halothane administration (P less than 0.05). In contrast, nifedipine 10(-9) M depressed maximum contractions from 114 +/- 5 per cent to 37 +/- 4 per cent (P less than 0.01) and nifedipine 10(-8) M depressed contractions to 30 +/- 4 per cent (P less than 0.01). In a further series of experiments, sustained contractions were depressed by continued administration of the anaesthetics, indicating no loss of anaesthetic effect with time. The results indicate that 1.5 MAC halothane and enflurane attenuate contractions of canine coronary arteries evoked by depolarization and Ca++ entry through potential operated channels. However, neither halothane nor enflurane exhibited the marked depressant effect exerted by nifedipine.

Animals↗
PubMed1991

Effects of isoflurane, halothane, and enflurane on myocardial flow and energy stores in the perfused rat heart.

The effect of three volatile anesthetics (halothane, enflurane, and isoflurane) on coronary flow and metabolic state of isolated rat hearts was studied. These anesthetics are coronary dilators and their effects are dose dependent. At 2 MAC (minimum alveolar concentration), isoflurane, enflurane, and halothane increase coronary flow by 114 +/- 5.9, 93 +/- 6.1, and 77 +/- 6.4%, respectively (p less than 0.001). At these concentrations, they also have a modest but significant metabolic effect causing a 30% reduction in myocardial ATP and phosphocreatine levels, with no significant modification in ADP and AMP concentrations. Energy charge and lactate/pyruvate ratio were also unaffected by these anesthetics. The vascular and metabolic effects were reversible within 2 and 30 min, respectively. Perfusion of the hearts with a Krebs-Henseleit solution without Pi did not interfere with the vascular and the metabolic effect of the anesthetics; however, in this case, ATP and phosphocreatine concentration did not return to control levels after their discontinuation despite full recovery of the vascular effect. These data suggest that the volatile anesthetics have direct coronary vascular and myocardial metabolic effects and that these effects occur independently.

Adenosine Diphosphate↗
PubMed1990

Side effects of nalbuphine while reversing opioid-induced respiratory depression: report of four cases.

Nalbuphine hydrochloride, an agonist-antagonist opioid, is reported to reverse the respiratory depression of moderate doses of fentanyl (20 micrograms.kg-1) and still provide good analgesia. We report four patients having abdominal aortic aneurysm repair in which we attempted to reverse the respiratory depression of large doses of fentanyl (50-75 micrograms.kg-1) with nalbuphine (0.3 mg.kg-1, 0.1 mg.kg-1 or 0.05 mg.kg-1). Nalbuphine reversed respiratory depression in all four patients and the respiratory rate increased from 10 to 23 breaths per minute, end-tidal CO2 decreased from 7.0 +/- 0.3 per cent to 5.6 +/- 0.7 per cent, and peak inspiratory pressure after 0.1 seconds increased from 4 +/- 1.4 to 13 +/- 2.6 mmHg. However, hypertension, increased heart rate, and significant increase in analogue pain scores accompanied reversal of respiratory depression. Agitation, nausea, vomiting, and cardiac dysrhythmias also were observed frequently. We do not recommend the use of nalbuphine to facilitate early extubation of the trachea after large doses of fentanyl for abdominal aortic surgery.

Analgesia↗
PubMed1990

Fentanyl is devoid of major effects on coronary vasoreactivity and myocardial metabolism in experimental animals.

Experiments were designed to determine the effects of fentanyl on coronary vascular tone and energetic state of the heart. Both arterial and arteriolar responses were assessed; particular attention was directed to epicardial vessels. Four experimental methods and three animal species were used. Isolated canine coronary artery rings with and without endothelium were suspended in organ chambers, and changes in their tension were measured. Fentanyl (100 ng/ml) had no effect on resting tension of unstimulated rings on a contraction evoked by serotonin 10(-8) to 10(-4) M. In rings with endothelium, the opioid had a minimal depressant effect on the contractile response to phenylephrine. Tension of vessels precontracted with serotonin (3 x 10(-7) M), or phenylephrine (10(-5) M) was unchanged following fentanyl at 10, 30, 70, or 150 ng/ml. Computerized quantitative angiography was used in intact pigs anesthetized with ketamine to determine the effects of fentanyl on coronary artery diameters of vessels with or without endothelium. Intravenous fentanyl 50 and 250 micrograms/kg had no effect on vessel diameters. Isolated perfused rat hearts were used to assess fentanyl effects upon coronary flow and arteriolar tone and upon myocardial energy state. Coronary blood flow was not altered by fentanyl (100 ng/ml) and was unchanged following washout of the drug. The heart maintained a normal energy status prior to and following fentanyl treatment. These data demonstrate that, under the conditions tested, fentanyl is devoid of major effects on the coronary circulation and upon myocardial metabolism.

Animals↗
PubMed1990

Isoflurane and halothane attenuate coronary artery constriction evoked by serotonin in isolated porcine vessels and in intact pigs.

Serotonin is a vasoconstrictor thought to cause coronary artery constriction in humans. The purpose of this study was to determine if isoflurane and halothane each attenuated coronary artery constriction evoked by serotonin in pigs. Both in vitro and in vivo experimental methods were used. Isolated coronary arteries with an without endothelium were studied in organ chambers in the presence and absence of 2.5% concentrations of the anesthetics. In intact pigs serotonin was infused directly into the left anterior descending coronary arteries to induce constriction. The vasodilator effects of 0.5%, 1.25%, and 2.0% isoflurane and halothane were determined using quantitative angiography. Contractile responses of isolated coronary arteries were depressed by the two anesthetics. Maximum contractile responses to serotonin were as follows: rings with endothelium 45 +/- 5% untreated versus 29 +/- 5% with isoflurane 2.5% (difference between dose-response curves, P less than 0.01) and without endothelium 67 +/- 5% untreated versus 51 +/- 6% with isoflurane 2.5% (P less than 0.001); with endothelium 52 +/- 7% untreated versus 28 +/- 7% with halothane 2.5% (P less than 0.001) and without endothelium 65 +/- 5% untreated versus 40 +/- 6% with halothane 2.5% (P less than 0.001). In intact pigs isoflurane and halothane dilated constricted coronary arteries with and without endothelium at all anesthetic concentrations tested, including concentrations as low as 0.5%. Isoflurane 1.25% increased diameter of vessels with endothelium from 1.5 +/- 0.1 mm to 1.7 +/- 0.1 mm (P less than 0.02) and halothane 1.25% increased diameter from 1.6 +/- 0.1 mm to 1.7 +/- 0.1 mm (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The role of coronary angioplasty in patients with associated noncardiac medical and surgical conditions.

Percutaneous transluminal coronary angioplasty was performed in 22 patients with associated significant medical or surgical conditions. It was successful in 22 patients. Two had procedure-related complications: one femoral hematoma and one small myocardial infarction. The patients were divided into a 'medical' group (12 patients) and a 'surgical' group (10 patients). In the medical group, mean coronary artery stenosis decreased from 87 +/- 5% to 20 +/- 13% and mean coronary artery stenosis decreased from 57 +/- 2% to 16 +/- 7%. In the surgical group coronary artery stenosis decreased from 83 +/- 9% to 18 +/- 9% and the gradient from 49 +/- 16 to 16 +/- 6 mmHg. Percutaneous transluminal coronary angioplasty allowed the safe management of underlying conditions in all patients so that medical treatment could be continued and noncardiac surgery performed.

Adult↗
PubMed1989

[Is isoflurane a calcium antagonist?].

The vasodilating and myocardial depressant effects of isoflurane have been allocated to calcium channel blockade. The present study aimed to test this hypothesis by assessing the effect of isoflurane on the contractile response to potassium stimulation of vascular smooth muscle. Seventy two left anterior descending and circumflex coronary artery rings were removed in twelve dogs and mounted in organ chambers filled with Krebs-Ringer bicarbonate solution and aerated with 95% O2-5% CO2. Rings were pretreated with either 3.8% isoflurane (2.5 MAC in the dog) or 10(-8) mol.l-1 nifedipine, a calcium entry blocker. They were stimulated by addition of 10 to 150 mmol.l-1 potassium chloride. At 70 mmol.l-1 K+, the tension generated by the untreated rings was 119 +/- 4.25% of control, while in the isoflurane treated group the tension was 99 +/- 2.4% of control. In the opposite, the tension was 25 +/- 7.11% in the nifedipine treated rings. Likewise, when isoflurane was added to rings preconstricted with 40 mmol.l-1 potassium chloride, no relaxation occurred, while nifedipine produced relaxation. Isoflurane, unlike nifedipine, had a weak effect on ring tension. The calcium-entry blockade effect of isoflurane appeared weak, dose-dependent and virtually absent at clinical concentrations. Therefore, the vasodilation seen with clinical concentrations of isoflurane is mediated by mechanisms other than calcium-entry blockade.

Adult↗