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Biomedical subjects

B Riou

Publications and source records attributed to B Riou.

At least 73 records · Page 4Linked to original sources
PubMed1999

Impaired skeletal muscle performance in the early stage of cardiac pressure overload in rabbits: beneficial effects of angiotensin-converting enzyme inhibition.

Abnormalities of skeletal muscles are frequently observed in patients with congestive heart failure. In these patients, angiotensin-converting enzyme (ACE) inhibitors improve exercise performance. The present study was designed to assess whether skeletal muscle dysfunction develops in the early stage of cardiac overload and if so, whether such functional alterations can be prevented by ACE inhibition. Mechanical performance, cross-bridge (CB) properties, and myosin heavy chain composition were investigated in respiratory and limb skeletal muscles of rabbits with moderate cardiac hypertrophy, and after single therapy with the ACE inhibitor perindopril (PE). After constriction of the aorta, the rabbits were treated during a 10-week period with either PE (1 mg/kg/day; n = 9) or a placebo (PL; n = 15). A third group of sham-operated animals received PL (n = 10). Analyses were performed on isolated diaphragm and soleus strips. Compared with sham-operated animals (shams), peak tetanic tension in PL fell by 40% in diaphragm and 34% in soleus. There were no significant differences in peak tetanic tension and the maximum shortening velocity between PE and shams. In both muscles, the total number of CBs was significantly lower in PL than in shams, but did not differ between shams and PE. The elementary force per CB did not differ between groups. In both muscles, the myosin heavy chain composition did not differ between groups. The study demonstrated that intrinsic performance of diaphragm and soleus muscles was affected early in the development of chronic pressure overload. Single therapy with PE tended to preserve muscle strength, essentially by limiting the loss of CBs.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Administration of desmopressin in brain-dead donors and renal function in kidney recipients.

BACKGROUND: Diabetes insipidus is common among brain-dead donors and may lead to decreased graft function. The use of desmopressin to limit the consequences of diabetes insipidus is controversial. We assessed the effects of desmopressin administered to brain-dead donors on early and long-term graft function in kidney recipients. METHODS: In a randomised controlled study, 97 brain-dead donors received desmopressin as 1 microg bolus every 2 h when diuresis was more than 300 mL/h (desmopressin group n=49) or no desmopressin (control group n=48). In 175 kidney recipients (controls n=89, desmopressin group n=86) we measured serum concentrations of creatinine and haemodialysis requirements to assess early renal function in the first 15 days after transplantation. We assessed long-term results of transplantation (median time 45 months) for a homogeneous subgroup of 95 recipients (48 in the desmopressin group). FINDINGS: We found no significant differences between the two groups of brain-dead donors, except for final diuresis, which was lower in the desmopressin group than among controls. Haemodialysis requirement in controls and the desmopressin group (20 vs 23%, p=0.63) and serum creatinine concentrations (decrease from 903 micromol/L to 206 micromol/L vs 814 micromol/L to 193 micromol/L, p=0.14) did not differ significantly in the first 15 days after transplantation. Long-term graft survival was similar in the two groups (88 vs 87%). INTERPRETATION: Desmopressin can be given to brain-dead donors to limit the harmful effects of diabetes insipidus without any substantial effects to graft function in recipients.

Adult↗
PubMed1998

[Principles of tests of hypotheses in statistics: alpha, beta and P].

Modern clinical research requires control of statistical methods. We reviewed 120 original manuscripts which were submitted to the Annales françaises d'anesthésie et de reanimation and analyzed their statistical methodology. Most of them contained errors (inappropriate numerical expression of the data, uncontrolled alpha risk, lack of power, use of inadequate statistical tests) and only 9 (7%) were considered as adequate. Therefore it is useful to come back to the methodology of hypothesis testing. An hypothesis test helps to decide between two hypothesis, the null hypothesis (H0) and the alternative hypotheses (H1) that we intend to demonstrate. The decision of the choice between H0 and H1 is associated with two probabilities: the alpha risk which is the probability to reject H0 whereas H0 is true, and the beta risk which is the probability not to reject H0 whereas H1 is true. Because the alpha risk is considered to be very important, it should be verified that the actual risk corresponds to the risk initially retained. The P value is the probability to observe a difference as great as that noted. The P value should be assessed according to its environment: the clinical relevance of a result should be assessed according to the amplitude of the difference and its confidence interval. When the null hypothesis is not rejected, the power of the test is essential. Power calculation is essential in clinical research trials. The number of patients included depends on four elements: the response to the control treatment, the expected response to the new treatment, the level of significance, and the power. The following items should be checked to choose the appropriate test: assess the kind of variable, verify the requirements for application of the test (type of the variable distribution, sample size, particular conditions such as equality of variance, dependence or independence of the variables), determine if data come from paired samples or if multiple comparisons are performed. Statistical analysis has become more easy with computers, however a precise knowledge of statistics remains essential. Advice from a statistician is often useful especially when obtained a priori and not a posteriori.

Analysis of Variance↗
PubMed1998

Comparison of the effects of sevoflurane, isoflurane and halothane on rat myocardium.

The effects of sevoflurane on myocardial contraction and relaxation are poorly understood. Therefore, we studied the effects of equianaesthetic concentrations (0.5, 1, 1.5, 2 and 2.5 MAC) of sevoflurane, isoflurane and halothane on inotropic and lusitropic (myocardial relaxation) variables, and post-rest potentiation in rat left ventricular papillary muscles in vitro. Sevoflurane and isoflurane caused comparable concentration-dependent negative inotropic effects which were significantly lower than those induced by halothane (P < 0.05). Sevoflurane and isoflurane did not modify lusitropic variables under low or high load, whereas halothane showed a negative lusitropic effect at high concentrations. Halothane suppressed post-rest potentiation, whereas isoflurane and sevoflurane did not. Post-rest recovery was unaffected by halothane, isoflurane or sevoflurane at any concentration. Thus in rat myocardium, sevoflurane and isoflurane caused comparable negative inotropic effects, had no significant lusitropic effects and did not alter post-rest potentiation, suggesting that they did not significantly modify the functions of the sarcoplasmic reticulum.

Anesthetics, Inhalation↗
PubMed1998

Effects of dantrolene on the diaphragm muscle of the normal and myopathic hamster.

Dantrolene is the only known effective treatment for malignant hyperthermia. However, its effects on the myopathic diaphragm remain unknown. The effects of dantrolene 10(-8) to 10(-4) mol litre-1 on diaphragm muscle strips in normal (n = 12) and myopathic hamsters (n = 13) were investigated in vitro in response to tetanic stimulation. We studied contraction under isotonic and isometric conditions. Data are presented as mean (SD) percent of baseline. Dantrolene induced a negative inotropic effect in normal and myopathic hamsters but no significant difference was observed between groups (active force at 10(-4) mol litre-1; 34 (7) vs 32 (11)%; ns). We conclude that dantrolene induced a comparable negative inotropic effect on diaphragm muscle in normal and myopathic hamsters.

Animals↗
PubMed1998

Mechanics, energetics, and crossbridge kinetics of rabbit diaphragm during congestive heart failure.

Crossbridge (CB) properties were investigated in isolated diaphragm of rabbits during congestive heart failure (CHF, n=9) induced by chronic volume and pressure overload. This model induced cardiac hypertrophy and heart failure. Controls (C) were prepared (n=14). Compared to C, peak tension in CHF fell by 57% in twitch and by 40% in tetanus; Vmax declined by 47% in twitch and by 48% in tetanus. Our study provided an analytical means of calculating from A. F. Huxley's equations the rate constants for CB attachment and detachment, CB single force (II), CB number per mm3 (m'), peak mechanical efficiency (Effmax), and turnover rate of myosin ATPase (kcat); m', II, and Effmax were lower in CHF than in C in both twitch and tetanus. The marked decline in m' and II accounted for the fall in diaphragm strength. In the overall population of C and CHF, Effmax was linearly related to II. Conversely, there was no relationship between Vmax and kcat. Dissociation between Vmax and kcat might be explained by the crucial role attributed to two apparently nonconserved surface 'loops' on the motor domain of myosin head.

Animals↗
PubMed1998

Modifications of the inotropic responses to alpha- and beta-adrenoceptor stimulation by propofol in rat myocardium.

UNLABELLED: Propofol induces cardiovascular depression but without significant effect on intrinsic myocardial contractility in many species. However, its interactions with adrenoceptor stimulation are unknown. We studied the effects of propofol (1 and 10 microg/mL) and its solvent on the inotropic response induced by phenylephrine (10(-8)-10(-4) M) or isoproterenol (10(-8)-10(-4) M) in rat left ventricular papillary muscles in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, calcium 0.5 mM, stimulation frequency 12 pulses/min). We also studied the lusitropic effects in isotonic and isometric conditions. In control groups, phenylephrine (127% +/- 3% of baseline; P < 0.05) and isoproterenol (169% +/- 11% of baseline; P < 0.05) induced a positive inotropic effect. Propofol (10 microg/mL) completely abolished the positive inotropic effect of phenylephrine (100% +/- 3% of baseline; P = not significant). In contrast, at the lowest concentration (1 microg/mL), propofol did not modify the positive inotropic effect of phenylephrine. Propofol did not modify the inotropic effect of isoproterenol. Propofol (10 microg/mL) enhanced the positive lusitropic effect of isoproterenol under low-load (P < 0.05) but not under high-load conditions. IMPLICATIONS: A high concentration of propofol abolished the positive inotropic effect of alpha- but not beta-adrenoceptor stimulation and enhanced the positive lusitropic effect of beta-adrenoceptor stimulation.

Adrenergic alpha-Agonists↗
PubMed1998

Interaction of isoflurane and sevoflurane with alpha- and beta-adrenoceptor stimulations in rat myocardium.

BACKGROUND: Halothane potentiates the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but impairs the positive lusitropic effect of beta-adrenoceptor stimulations. However, the interactions of isoflurane and sevoflurane with alpha- and beta-adrenoceptor stimulation have not been entirely defined. METHODS: The effects of 1 minimum alveolar concentration isoflurane and sevoflurane on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) or isoproterenol (10(-8 to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (Krebs-Henseleit solution, 29 degrees C; pH, 7.4; 0.5 mM calcium; stimulation frequency, 12 pulses/min). The positive lusitropic effects of alpha- and beta-adrenoceptor stimulations were studied under isotonic and isometric conditions. Data are mean percentages of baseline +/- SEM. RESULTS: In control groups, phenylephrine (134 +/- 8%; P < 0.05) and isoproterenol (171 +/- 7%; P < 0.05) induced a positive inotropic effect. Isoflurane enhanced the positive inotropic effects of phenylephrine (185 +/- 10%; P < 0.05) and of isoproterenol (203 +/- 11%; P < 0.05). Sevoflurane enhanced the positive inotropic effects of phenylephrine (187 +/- 10%; P < 0.05) and of isoproterenol (228 +/- 11%; P < 0.05). These potentiations were similar to those previously reported with halothane. Isoflurane and sevoflurane did not modify the positive lusitropic effects under low and high loads of isoproterenol. CONCLUSION: Although isoflurane and sevoflurane have moderate negative inotropic effects, they potentiated the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but did not modify the positive lusitropic effects of beta-adrenoceptor stimulation.

Anesthetics, Inhalation↗
PubMed1998

Ketorolac and enoxaparin affect arterial thrombosis and bleeding in the rabbit.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with hemostasis during the perioperative period, and the combination of NSAID and enoxaparin could increase this effect. The aim of this prospective, blinded experimental study was to assess these effects using a model of arterial thrombosis and bleeding in the rabbit. METHODS: After anesthesia was induced and monitors placed, the common carotid arteries were exposed, and 60% stenosis of the right common carotid artery was produced. Twenty minutes later, a compression injury of the artery was produced that triggered a series of cyclic episodes of thrombosis and clot lysis. This was manifested as cyclic flow reductions (CFR; measured with an electromagnetic flow meter). After the first flow reduction was noted, the rabbits were immediately and randomly assigned to one of four groups (n = 10 each) that received intravenous infusions: control, ketorolac (2 mg/kg), enoxaparin (0.5 mg/kg), and ketorolac plus enoxaparin (2 mg/kg and 0.5 mg/kg, respectively). The number of CFRs that occurred in the subsequent 20-min period was used as a measure of treatment effect. The contralateral common carotid artery was exposed, and both stenosis and injury were produced. The ability of the administered drug to prevent thrombosis was assessed as the number of CFRs that occurred during the first 20-min period after vessel injury. In addition, both before and after group assignment and drug injection, bleeding times were noted and a platelet aggregation test was performed. Laparotomy was followed by a spleen section, and the extent of the wound and the amount of splenic bleeding were measured. RESULTS: The treatment effect was indicated by the median number of CFRs, which was 5.5 in the control group, 1 in the ketorolac group, 2 in the enoxaparin group, and 0 in the ketorolac + enoxaparin group. The prevention effect was indicated by the median number of CFRs, which was 4 in the control group, 0 in the ketorolac group, 2 in the enoxaparin group, and 0.5 in the ketorolac + enoxaparin group. Bleeding time was significantly lengthened in the enoxaparin and in the ketorolac + enoxaparin groups. Splenic and wound bleeding was greater in the ketorolac group. Platelet aggregation was completely inhibited in the ketorolac and the ketorolac + enoxaparin groups. CONCLUSIONS: Ketorolac had an important antithrombotic activity. The association of enoxaparin with ketorolac seemed to lengthen the bleeding time observed with ketorolac.

Animals↗
PubMed1998

Myocardial effects of desflurane in hamsters with hypertrophic cardiomyopathy.

BACKGROUND: The effects of desflurane on myocardial contraction and relaxation in diseased myocardium have not been completely understood. METHODS: The effects of desflurane (1.8 to 9.4 vol%) in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C, pH 7.40, Ca2+ 2.5 mM; stimulation frequency, 3/min) under low (isotony) and high (isometry) load. Data are mean percentages of baseline +/- SD. RESULTS: Desflurane induced no significant inotropic effect in healthy muscles (maximum unloaded shortening velocity and isometric active force at 9.4 vol%: 97 +/- 9% and 92 +/- 20%, respectively). In contrast, in cardiomyopathic muscles, desflurane induced a moderate negative inotropic effect (maximum unloaded shortening velocity and active force at 9.4 vol%: 84 +/- 19% and 75 +/- 25%, respectively). The negative inotropic effect was more pronounced than that in healthy muscles under low (P < 0.05) but not high load, and even when concentrations were corrected for minimum alveolar concentrations in each strain. Adrenoceptor blockade or pretreatment with reserpine did not modify the inotropic effect of desflurane, suggesting the absence of intramyocardial catecholamine release. However, tyramine also did not induce any significant catecholamine release in hamster myocardium. In both strains, desflurane induced no significant lusitropic effect under low or high load. CONCLUSIONS: Desflurane had no inotropic effect in healthy muscles and a moderate negative inotropic effect in cardiomyopathic muscles. The absence of desflurane-induced intramyocardial catecholamine release was related to hamster myocardium characteristics.

Adrenergic Uptake Inhibitors↗
PubMed1998

Comparison of the haemodynamic actions of desflurane/N2O and isoflurane/N2O anaesthesia in vascular surgical patients.

BACKGROUND: The purpose of this study was to compare heart rate and arterial blood pressure response to desflurane/N2O vs isoflurane/N2O anaesthesia in a randomized clinical trial performed in patients before vascular surgery. METHODS: To evaluate associated changes in the autonomic nervous system with maintenance of anaesthesia, we used power spectral analysis (PSA) of heart rate and blood pressure and measured plasma catecholamine concentrations. Twenty-five patients whose trachea had been intubated after propofol induction were given either desflurane or isoflurane at 1 and 1.5 MAC in N2O (60%) in a random manner. RESULTS: At an anaesthetic depth of up to 1.5 MAC, arterial blood pressure, indices of sympathetic activity derived from PSA, decreased with both anaesthetics, while heart rate and plasma catecholamine concentrations did not significantly change. Plasma renin activity significantly increased at 1.5 MAC anaesthesia in both groups. CONCLUSIONS: We conclude that sympathetic hyperactivity previously reported during desflurane anaesthesia in healthy volunteers is not frequent in clinical practice in elderly vascular surgical patients under desflurane/N2O anaesthesia, since it occurs at an anaesthetic depth which cannot be reached in these patients because of the lowering arterial blood pressure effects of desflurane, which are similar to those of isoflurane.

Adult↗
PubMed1997

[Assessment of a new light guide (Trachlight) for tracheal intubation].

OBJECTIVE: To assess the learning curve of a new lighwand device, Trachlight (Laerdal), for blind orotracheal intubation in patients without foreseen difficulty in airway management. STUDY DESIGN: Open, prospective, clinical study. USERS: Twelve persons practicing anaesthesia (specialists, trainees, nurses) underwent videotape learning and manikin training with ten successful intubation manoeuvres required with the device. METHODS: Each person had to carry out a tracheal intubation in ten consecutive patients undergoing scheduled surgery and without history or clinical sign of difficults airway management. RESULTS: One hundred and twenty patients were included. The overall success rate with the Trachlight was 87%. An easy learning curve was obtained as demonstrated by the low failure rate in the first three patients, and by the success rate on the first or second attempt in the last four patients. There was no significant difference in failure rate with or without muscle relaxation (10 vs 20%, NS). Finally, all failures with the Trachlight were followed by successful intubation using direct laryngoscopy, and no traumatic complications were recorded with the device. CONCLUSION: Trachlight is a new lightwand device enabling blind tracheal intubation with a easy learning curve in patients without difficulty in airway management, even for non-selected operators.

Adult↗
PubMed1997

Comparison of the effects of ketamine-midazolam with those of fentanyl-midazolam on cortical somatosensory evoked potentials during major spine surgery.

Cortical somatosensory evoked potentials (CSEP) allow monitoring of spinal cord function during surgery. Ketamine has been shown to enhance CSEP amplitude, but there is no previous study comparing its effects with those of other anaesthetic regimens. Therefore, we have compared the effects of ketamine with those of fentanyl, both combined with midazolam, on CSEP monitoring during major spine surgery. Twenty patients with normal preoperative CSEP were allocated randomly to a ketamine or fentanyl group. Anaesthesia was induced with ketamine 3 mg kg-1 or fentanyl 6 micrograms kg-1 i.v., and midazolam 0.3 mg kg-1 i.v in both groups, and maintained with continuous i.v infusion of ketamine 2 mg kg-1 h-1 or fentanyl 3 micrograms kg-1 h-1, combined in both groups with midazolam 0.15 mg kg-1 h-1 and 60% nitrous oxide in oxygen. CSEP were elicited by tibial posterior nerve stimulation and measured P1 and N1 latencies, and P1-N1 amplitude, CSEP were recorded before and after induction, at 15 min, 1 and 2 h after induction, during skin closure and after removal of nitrous oxide. Both groups were comparable in characteristics, duration of surgery, mean arterial pressure and temperature. CSEP latencies were not significantly affected in either group. CSEP amplitude decreased significantly over time in the fentanyl group (from mean 2.02 (SEM 0.41) to 0.95 (0.17) microV, P < 0.05), but not in the ketamine group (from 1.33 (0.36) to 1.05 (0.31) microV, ns). Nevertheless, we did not observe any significant differences in amplitudes or latencies between the two groups. The delay in obtaining the first voluntary postoperative motor response was significantly greater in the ketamine group (170 (54) vs 55 (17) min, P < 0.01). Both ketamine and fentanyl allowed us to obtain reliable CSEP during major spine surgery, and there were no significant difference between these two anaesthetic regimens for CSEP monitoring, but a longer delay for voluntary postoperative motor assessment was observed in the ketamine group.

Adult↗
PubMed1997

Lumbar muscle rhabdomyolysis after abdominal aortic surgery.

Lumbar muscle rhabdomyolysis has been very rarely reported after surgery. The aim of this study was to determine its incidence and main characteristics in a large population undergoing abdominal aortic surgery. Over a 21-mo period, 224 consecutive patients, 209 male and 15 female, mean age 65 +/- 10 yr, underwent abdominal aortic surgery (aortic aneurysm in 142 patients and occlusive aortic degenerative disease in 82 patients). Surgical incision was a midline incision with exaggerated hyperlordosis in 173 patients and a flank incision with a retroperitoneal approach in 51 patients. Postoperative rhabdomyolysis was diagnosed in 20 patients. In these patients, 9 (4%) experienced severe low back pain, and lumbar muscle rhabdomyolysis was confirmed by tomodensitometry (n = 6) or muscle biopsy (n = 3). The remaining 11 patients had lower limb muscle rhabdomyolysis. Rhabdomyolysis occurred after surgery of longer duration, which involved more frequent visceral artery reimplantation, with longer duration of aortic clamping and greater intraoperative bleeding. Lumbar rhabdomyolysis occurred in younger patients who were more frequently obese. On first postoperative day, the mean creatine kinase (CK) value was greater in lumbar rhabdomyolysis than in lower limb rhabdomyolysis (17,082 +/- 15,003 vs 3,313 +/- 3,120 IU/L, P < 0.05). Acute renal failure and postoperative death did not occur in patients with lumbar muscle rhabdomyolysis. Lumbar rhabdomyolysis was not a rare event after abdominal aortic surgery (4%). This syndrome was characterized by postoperative low back pain of unusual severity, which required analgesic therapy, and induced a very high increase in CK with typical findings at tomodensitometry or muscle biopsy but was not associated with postoperative renal failure.

Acute Kidney Injury↗
PubMed1997

Risk factors for acute postoperative renal failure in thoracic or thoracoabdominal aortic surgery: a prospective study.

UNLABELLED: Acute postoperative renal failure is a common complication of thoracic aorta, thoracoabdominal aorta, or aortic arch surgery. To identify variables associated with acute postoperative renal failure, we prospectively studied 475 consecutive patients undergoing thoracoabdominal aortic surgery over a 12-yr period, including those requiring emergent surgery. One hundred twenty-one (25%) patients developed acute postoperative renal failure, and 39 (8%) required hemodialysis. Using multivariate analysis, acute postoperative renal failure was significantly associated with the following variables: age >50 yr (odds ratio [OR] 2.90 [95% confidence interval 1.52-5.53]), preoperative serum creatinine >120 micromol/L (OR 2.76 [1.70-4.48]), duration of left kidney ischemia >30 min (OR 2.01 [1.27-3.17]), packed red cells administration >5 units (OR 2.04 [1.24-3.37]), and Cell-Saver administration >5 units (OR 2.31 [1.34-1.96]). Reimplantation of visceral, renal arteries and the Adamkievicz artery; duration of visceral, spinal, and right kidney ischemia; requirement for fresh frozen plasma; administration of aprotinin; extracorporeal circulation; and procedures with circulatory arrest and profound hypothermia were not predictive of postoperative renal failure. In addition, age >50 yr (OR 5.59 [1.31-23.91]), requirement for packed red blood cells >5 unit (OR 3.91 [1.58-9.67]), and preoperative serum creatinine concentration >120 micromol/L (OR 2.26 [1.13-4.53]) were independent factors for acute renal failure requiring hemodialysis. In conclusion, acute renal failure is often observed after thoracic aortic surgery. Numerous predictive factors must be considered when evaluating the etiology of this complication. IMPLICATIONS: Acute postoperative renal insufficiency is a common complication of thoracic aortic surgery. This study found that age >50 yr, preoperative renal dysfunction, duration of renal ischemia, and amount of blood transfusion are significant predictors of this complication.

Acute Kidney Injury↗