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Biomedical subjects

B Riou

Publications and source records attributed to B Riou.

At least 19 recordsLinked to original sources
PubMed1995

Circulating cardiac troponin T in potential heart transplant donors.

BACKGROUND: Brain death may induce myocardial dysfunction, the mechanisms of which are not yet fully understood. Circulating cardiac troponin T is considered a highly sensitive and specific marker of myocardial cell injury. METHODS AND RESULTS: We prospectively measured circulating cardiac troponin T in 100 brain-dead patients and measured the left ventricular ejection fraction area (LVEFa), using transesophageal echocardiography. Sixty-one patients had normal LVEFa, 25 had moderate decrease in LVEFa (30% to 50%), and 14 had severe decrease in LVEFa (< or = 30%). Circulating cardiac troponin T concentrations were significantly higher (1.68 +/- 1.03 micrograms/L-1, P < .01) in patients with a severe decrease in LVEFa than in the two other groups (0.42 +/- 0.43 and 0.12 +/- 0.16 microgram/L-1, respectively), and there was a significant correlation between LVEFa and cardiac troponin T concentration (p = -0.59, P < .0001). An elevated circulating cardiac troponin T concentration (> or = 0.5 microgram/L-1) was more accurate (sensitivity, 1.00; specificity, 0.84) in predicting a severe decrease in LVEFa than an elevated CKMB value or an increased CKMB/CK ratio. CONCLUSIONS: An elevated circulating cardiac troponin T was associated with a severe decrease in LVEFa in brain-dead patients, suggesting that severe and potentially irreversible myocardial cell damage occurred. In contrast, CKMB determination was not useful. Since the quality of the donor's heart is considered an important prognosis factor in heart transplantation, the determination of circulating cardiac troponin T concentration could be useful to the heart transplantation team.

Adult↗
PubMed1995

Plasma ionized calcium in brain-dead patients.

BACKGROUND: The mechanism of brain death-induced myocardial dysfunction remains debatable. Hypocalcemia is known to induce reversible myocardial dysfunction. However, the incidence of hypocalcemia and its effect on myocardial function during brain death is unknown. METHODS: In 54 consecutive brain-dead patients, we measured plasma total and ionized calcium concentrations, QT and corrected QT intervals, and left ventricular ejection fraction area (LVEFa), using transesophageal echocardiography. RESULTS: 49 (91%) of brain-dead patients had a decrease in total plasma total calcium concentration but only 19 (35%) had a decrease in plasma ionized calcium. Corrected total plasma calcium failed to predict ionized calcium concentration and QT intervals were not significantly different in normo and hypocalcemic patients. The LVEFa was not significantly different between normo and hypocalcemic patients (53 +/- 13 versus 50 +/- 20%), and no correlation was found between LVEFa and ionized calcium (R = 0.02, NS). Hypocalcemic patients required greater doses of dopamine (8.2 +/- 5.2 versus 5.0 +/- 3.4 micrograms.kg-.min-1, p < 0.02) to maintain arterial pressure. Hypocalcemia was associated with a higher volume loading and a lower plasma protide concentration which reflected hemodilution. CONCLUSION: A decrease in plasma ionized calcium is not frequent, rarely severe, and probably not the main mechanism of myocardial dysfunction in brain-dead patients. Hypocalcemic patients required higher doses of dopamine, suggesting a decrease in systemic resistance. Only direct measurement of ionized calcium can assess plasma calcium ion status in brain-dead patients.

Adult↗
PubMed1995

[Comparison of the effects of ketorolac and aspirin on hemostasis in the rabbit].

OBJECTIVE: Comparison of ketorolac with aspirin and placebo for the antithrombotic activity using the Folts' model of experimental arterial thrombosis and the perioperative blood loss. STUDY DESIGN: Experimental randomized blinded study anaesthetized, tracheotomized and mechanically ventilated. Carotid blood flow variations were detected by a probe directly inserted around the artery and monitored by an electromagnetic flowmeter. A segment of the exposed carotid artery was de-endothelialized by gently squeezing the artery with a needle holder forceps, and an external constrictor was placed around it (stenosis 60%), to induce cyclic flow reductions (CFR). During 20 min, CFR rate was assessed. Animals were then randomized in 3 groups of 9: ketorolac (K) 1 mg.kg-1, aspirin (A) 10 mg.kg-1 or saline (S), injected intravenously (peripheral ear vein). After drug administration, CFR rate was assessed over 20 min, to determine the potential antithrombotic activity of the drug (curative phase). Thereafter, the opposite carotid artery was injured and stenosed and the occurrence of CFR was assessed over 20 min (preventive phase). The amount of blood loss of a xipho-pubic laparotomy with a spleen section was also measured 30 min after drug administration. RESULTS: In all untreated animals, CFRs developed with a mean rate of 4 cycles/20 min. Aspirin completely abolished CFR during the curative phase in all rabbits, except in one. No effect was observed during this phase with ketorolac or saline. During the preventive phase, a partial inhibition of CFRs was induced by ketorolac and aspirin. Peri-operative bleeding was not increased significantly by ketorolac or aspirin. Postinjection bleeding-time did not differ between the three groups. CONCLUSIONS: Ketorolac (1mg.kg-1) has not a strong antithrombotic activity. Ketorolac and aspirin do not increase peri-operative blood loss, and therefore do not seem to strongly interfere with haemostasis in the rabbit.

Animals↗
PubMed1995

[Combination of propofol-sufentanil on somatosensory evoked potentials in surgery of the spine].

OBJECTIVES: Most anaesthetics depress cortical somatosensory evoked potentials (CSEPs). However, the modification of CSEPs during total intravenous anaesthesia using propofol remaining still unknown, justified this trial. TYPE OF STUDY: Open, prospective, clinical study. METHODS: Nine consecutive patients requiring CSEPs monitoring for spine surgery, were studied. Anaesthesia was induced with propofol (2.5 mg.kg-1 then 10 mg.kg-1.h-1) and sufentanil (0.50 micrograms.kg-1 then 0.25 micrograms.kg-1.h-1). Maximum positive (P40) and negative (N50) waweform latencies, and the peak to peak amplitude of CSEPs (posterior tibial nerve stimulation, cortical recording), were recorded before induction, 30 min, 1 and 2 h after induction, and at the end of surgery. Data are means +/- SD. RESULTS: Duration of anaesthesia was 260 +/- 73 min. Propofol induced significant lengthening of CSEPS (P40: from 37 +/- 10 up to 41 +/- 11 ms; N50: from 45 +/- 11 up to 51 +/- 14 ms), and a significant decrease in amplitude (from 1.9 +/- 0.9 down to 0.8 +/- 0.4 microV), but these changes were stable from 30 min after the induction to the end of spine surgery. A motor response was obtained 29 +/- 14 min after the end of anaesthetic administration. CONCLUSIONS: Total intravenous anaesthesia with propofol and sufentanil induces a small but stable lengthening of CSEPs latency and a stable decrease of its amplitude, which enable an appropriate monitoring of CSEPs during spine surgery.

Adult↗
PubMed1995

Cardiovascular consequences of severe hypophosphataemia in brain-dead patients.

Hypophosphataemia is known to induce reversible myocardial dysfunction, but the incidence of hypophosphataemia and its effect on myocardial function during brain death are unknown. In 90 consecutive brain-dead patients, we measured plasma concentrations of phosphate and left ventricular ejection fraction area (LVEFa), using transoesophageal echocardiography. In 15 severely hypophosphataemic (< 0.40 mmol litre-1), consecutive, brain-dead patients, haemodynamic status, LVEFa, and oxygen delivery and consumption were assessed before and after phosphorus loading (0.30 mmol kg-1). In 10 other brain-dead patients, urine elimination of phosphates was measured. Only 30 (33%) brain-dead patients had normal plasma phosphate concentrations, 22 (24%) had mild hypophosphataemia (0.40-0.80 mmol litre-1) and 38 (42%) had severe hypophosphataemia (< 0.40 mmol litre-1). There were no significant differences in LVEFa between these three groups (mean 53 (SD 16), 55 (12) and 51 (17)%, respectively) and no significant correlation between LVEFa and plasma phosphate concentration (r = 0.04). In 15 severely hypophosphataemic patients, phosphorus loading increased plasma phosphate concentration from 0.30 (0.10) to 1.06 (0.41) mmol litre-1, but did not modify haemodynamic status, LVEFa or oxygen delivery and consumption. In 10 other patients, urine phosphorus elimination was 16.8 (23.3) mmol/24 h while plasma phosphate concentration was at its highest level (0.80 (0.37) mmol litre-1), and only one of these patient had a slightly elevated phosphaturia. In conclusion, hypophosphataemia frequently occurs after brain death but has no significant cardiovascular consequences, suggesting that it is related to intracellular transfer and not phosphorus depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Myocardial effects of propofol in hamsters with hypertrophic cardiomyopathy.

BACKGROUND: Propofol is a short-acting intravenous induction agent that induces cardiovascular depression but without significant effect on intrinsic myocardial contractility in various species. However, its effects on diseased myocardium remain unknown. METHODS: The effects of propofol (1, 3, and 10 micrograms.ml-1) on the intrinsic contractility of left ventricular papillary muscles from normal hamsters and those with hypertrophic cardiomyopathy (strain BIO 14.6, aged 6 months) were investigated in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca++ 2.5 mmol.l-1, stimulation frequency 3/min). RESULTS: Cardiac hypertrophy (143 +/- 13%, P < 0.001) was observed in cardiomyopathic hamsters. The contractility of papillary muscles from hamsters with cardiomyopathy was less than that of controls, as shown by the decrease in maximum shortening velocity (-29%, P < 0.03) and active isometric force (-51%, P < 0.001). Propofol did not induce any significant effect on contraction, relaxation, and contraction-relaxation coupling under low and high loads in normal hamsters. The effects of propofol were not significantly different between normal hamsters and those with cardiomyopathy. A slight but significant increase in maximum unloaded shortening velocity was observed in cardiomyopathic hamsters at 3 micrograms.ml-1 (4 +/- 6%, P < 0.05) and 10 micrograms.ml-1 (7 +/- 6%, P < 0.05). CONCLUSIONS: Propofol did not modify intrinsic myocardial contractility in normal hamsters, and no significant differences were observed between normal and cardiomyopathic hamsters. These results may be useful because, unlike propofol, most anesthetics decrease myocardial contractility. Nevertheless, indirect cardiac effects of propofol may be more important than its direct cardiac effects in patients with impaired cardiac function.

Animals↗
PubMed1995

In vitro effects of eltanolone on rat myocardium.

BACKGROUND: Eltanolone is a new short-acting intravenous induction agent. However, its effects on intrinsic myocardial contractility remain unknown. METHODS: The effects of eltanolone and its solvent (soya bean emulsion) on the intrinsic contractility of rat left ventricular papillary muscles were investigated in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca2+ 0.5 mM, stimulation frequency 12 pulses/min). We studied contraction; relaxation; contraction-relaxation coupling under high and low loads; and postrest potentiation. RESULTS: Eltanolone (0.1, 0.3, 1, 3, and 10 micrograms.ml-1) induced no significant inotropic effect, as shown by the lack of changes in maximum unloaded shortening velocity and active isometric force. Eltanolone did not significantly modify the contraction-relaxation coupling under low load, suggesting that it did not modify calcium uptake by the sarcoplasmic reticulum. Eltanolone did not significantly modify the contraction-relaxation coupling under high load, suggesting that it did not modify calcium myofilament sensitivity. Eltanolone decreased the postrest potentiation in a concentration-dependent manner (from 150 +/- 14% to 118 +/- 9% at 10 micrograms.ml-1, P < 0.001), suggesting a decrease in the maximum capacity of calcium release by the sarcoplasmic reticulum, whereas its solvent did not. However, eltanolone did not slow postrest potentiation recovery, as shown by the absence of significant changes in the recovery slope, tau (4.5 +/- 1.4 vs. 3.8 +/- 1.0 beats; difference not statistically significant). CONCLUSIONS: Eltanolone induced no significant inotropic effect on rat myocardium. It induced a decrease in the calcium release function of the sarcoplasmic reticulum, but this effect was not sufficiently important to modify the inotropic properties.

Anesthetics, Intravenous↗
PubMed1995

Systemic gas embolism complicating pulmonary contusion. Diagnosis and management using transesophageal echocardiography.

Systemic air embolism has been frequently reported after penetrating thoracic trauma. In blunt thoracic trauma, systemic air embolism has been rarely diagnosed, and then only after an invasive procedure such as thoracotomy. Transesophageal echocardiography has been recently introduced for the early assessment of trauma patients and is considered a sensitive noninvasive procedure to diagnose air embolism. We report three cases of systemic air embolism in patients with pulmonary contusion secondary to a blunt thoracic trauma requiring controlled ventilation. Transesophageal echocardiography was performed for evaluation of hemodynamic instability, and it showed air bubbles in the left atrium and left ventricle during the insufflation phase, which disappeared during apnea. A decrease in airway pressure (release of PEEP, low tidal volume, high frequency jet ventilation) significantly reduced the systemic air embolism. We concluded that systemic air embolism can occur after blunt thoracic trauma, and transesophageal echocardiography enables a rapid and accurate diagnosis that may be useful for therapeutic management.

Adult↗
PubMed1995

Contraction, relaxation, and economy of force generation in isolated human diaphragm muscle.

Contraction, relaxation, and energetics of normal human diaphragm strips (n = 10) were investigated over the whole load continuum in both twitch and tetanus modes. For a given level of isotonic total force and over a large part of the contraction phase, instantaneous velocity was shown to be a unique function of instantaneous length, regardless of time and initial length. In afterloaded tetanic contractions and over a wide range of loads, the peak lengthening velocity (VL) linearly decreased when maximum extent of muscle shortening (delta L) decreased. Stimulation mode modulated the VL versus delta L relationship, the slope of this linear regression being greater in tetanus than in twitch. Conversely, over a wide range of load, an increase in load linearly accelerated the peak rate of force decay, regardless of the stimulation mode. The energetics of human diaphragm muscle was evaluated in terms of both mechanical activity and economy of force generation. Maximum mechanical work (Wmax) differed significantly according to the stimulation mode, and the relative force at which Wmax occurred was higher in tetanus than in twitch (p < 0.05). The G curvature of the P-V hyperbola and maximum mechanical efficiency were significantly higher in tetanus than in twitch. This strongly suggests that the economy of force generation is higher in tetanus contractions than in twitch.

Adult↗
PubMed1994

Cardiotoxicity of colchicine in the rat.

OBJECTIVES: Colchicine poisoning may be lethal and a decrease in cardiac function has been reported in several case reports, but the precise cardiotoxicity of colchicine remains unknown. DESIGN: The experimental in vitro study assessed the intrinsic contractility of left ventricular papillary muscle in rats, 24 h after administration of intraperitoneal colchicine or saline. RESULTS: The administration of colchicine (2 or 4 mg.kg-1) in adult Wistar rats markedly impaired intrinsic myocardial contractility, as shown by a decrease in maximum shortening velocity (-32 and -61%, respectively), active isometric force (-47 and -65%, respectively), and peak power output (-57 and -69%, respectively) of left ventricular papillary muscle. Colchicine impaired isotonic relaxation and load dependence of relaxation, suggesting a decrease in sarcoplasmic reticulum function. Conversely, colchicine significantly accelerated isometric relaxation, suggesting a decrease in calcium myofilament sensitivity. Myothermal economy was markedly impaired only in some rats (3/10 in each group), in which the negative inotropic effect of colchicine appeared to be more particularly pronounced. CONCLUSION: The results indicate that the administration of high doses of colchicine induced intrinsic cardiotoxic effects. Due to its amplitude, such cardiotoxic action may participate in the fatal outcome of acute colchicine poisoning.

Acute Disease↗
PubMed1994

Ventilatory effects of active compression-decompression in dogs.

STUDY OBJECTIVE: To determine the ventilatory effect of active compression-decompression CPR and to compare it with two other techniques, standard manual cardiac massage and mechanical cardiac massage. DESIGN: Prospective, randomized laboratory investigation. PARTICIPANTS: Mongrel dogs. INTERVENTIONS: Nine adult mongrel dogs were anesthetized, intubated, and mechanically ventilated. They were instrumented to measure arterial pressure, esophageal pressure, airway pressure, end-tidal carbon dioxide concentration, and minute ventilation. RESULTS: After induction of ventricular fibrillation, three sequences of cardiac massage were performed randomly during mechanical ventilation, standard cardiac massage, mechanical cardiac massage, and active compression-decompression technique. The animals then were disconnected from the ventilator, and the three sequences were performed again. Active compression-decompression created negative minimum esophageal pressures and significantly decreased the minimum airway pressure as compared with the other techniques. Whatever the ventilatory condition, minute ventilation was increased dramatically during active compression-decompression. CONCLUSION: In this model of cardiac arrest, an important increase in minute ventilation was observed during active compression-decompression. This effect was significantly greater than the increases observed with other techniques of cardiac massage and was related to the negative pressure generated by active decompression.

Airway Resistance↗
PubMed1994

[Cardiovascular effects of Diprivan].

Propofol is a greater cardiovascular depressant agent than barbiturates (thiopentone, methohexitone). It is agreed that propofol changes the ventricular load as a result of its vasodilating effects, and that it depresses the sympathetic nervous system and the baroreflex, which result in a moderate bradycardia. The direct effects of propofol on the myocardium remain controversial. Propofol has no significant direct effect on intrinsic myocardial contractility and the decrease in cardiac output is related to anaesthesia on the one hand and to changes in ventricular load and the activity of the cardiac autonomic nervous system on the other hand. It is therefore understandable that the overall depressant effect of the cardiovascular system is amplified in patients whose ventricular function is closely dependent upon ventricular load and/or the activity of the sympathetic nervous system, and that the association with drugs causing bradycardia must be avoided. The logical therapeutic solution to propofol related cardiovascular depression, when deemed necessary, consists of vascular fluid loading and/or the administration of a vasoconstrictor.

Animals↗
PubMed1994

[Bilateral sensorineural hearing loss after general anesthesia].

A bilateral sensorineural (perceptive) deafness occurred in a 12-year-old girl, following laparoscopic appendicectomy under general anaesthesia not comprising nitrous oxide and low insufflation pressures and a normal haemodynamic status. There was neither a personal nor a familial history of hearing disturbances nor a preoperative intake of ototoxic drugs. The initial loss of 50 dB has been substantiated by evoked auditive potentials. The treatment consisted of hyperbaric oxygenotherapy and vasodilators. The girl recovered completely. Finally the etiology of this complication remained unrecognized. Possibly the CO2 insufflated into the abdominal cavity could be considered. However, its causative effect remains to be proven.

Anesthesia, General↗
PubMed1994

Intraoperative autologous transfusion in emergency surgery for spine trauma.

Although numerous studies have reported the use of intraoperative blood salvage in elective spine, cardiac, and vascular surgery, very few have assessed its efficiency during emergency surgery after spine trauma. We therefore retrospectively analyzed 238 cases of patients with spine trauma who had emergency surgery. Three variables were significantly associated with the risk of perioperative blood transfusion: thoracolumbar spine injury, a preoperative hematocrit < 35%, and an Injury Severity Score > 20. Among the 118 patients who received blood transfusions, 53 benefitted from intraoperative blood salvage using the Cell-Saver apparatus (Cell-Saver group) and 65 did not (control group). The Cell-Saver enabled a 47% reduction in homologous blood requirements (743 +/- 1191 mL vs. 1403 +/- 1453 mL, p < 0.008) and a 45% reduction in the number of patients who received homologous blood (45% vs. 82%, p < 0.001). Between these two groups, no significant differences were observed in the evolution of hematocrit, platelet count, and hemostasis values, but a slight increase in postoperative blood loss was noted in the Cell-Saver group (465 +/- 383 mL vs. 301 +/- 292 mL, p < 0.01). In conclusion, the efficiency of intraoperative blood salvage in emergency surgery for spine trauma is high and similar to that previously reported in elective spine surgery. The cost-effectiveness of this technique may be improved by appropriate selection of the patient.

Adolescent↗
PubMed1994

Pharmacokinetics of hydroxocobalamin in dogs.

Hydroxocobalamin is a powerful cyanide antidote that prevents sodium nitroprusside-induced cyanide toxicity. The pharmacokinetics of an i.v. bolus of hydroxocobalamin (70 and 140 mg/kg) were studied in conscious dogs (n = 6). Plasma hydroxocobalamin concentrations were measured using derivative spectrophotometry. The pharmacokinetics were compatible with a two-compartment model with a first-order distribution and elimination rate, and pharmacokinetic parameters were not different between the two doses, except for the elimination half-life. At 70 mg/kg, which is the recommended dose in acute cyanide poisoning, the elimination half-life was 7.36 +/- 0.79 h, the volume of distribution was 0.49 +/- 0.10 L/kg, and the total clearance 0.58 +/- 0.11 L/h. At high doses, hydroxocobalamin has a short elimination half-life and a limited volume of distribution that exceeds blood volume. These results could be useful in elaborating guidelines for the administration of hydroxocobalamin, when repetitive bolus and/or continuous infusion is required.

Animals↗