PubMed Health⌕ Search

Biomedical subjects

L Lacoste

Publications and source records attributed to L Lacoste.

At least 37 records · Page 2Linked to original sources
PubMed1996

Haemodynamic and ventilatory changes during laparoscopic cholecystectomy in elderly ASA III patients.

PURPOSE: To evaluate the haemodynamic and respiratory changes during laparoscopic cholecystectomy in elderly ASA III patients. METHODS: This clinical descriptive study included 16 patients aged > 75 yr. Anaesthesia was induced with fentanyl and etomidate and maintained with N2O in O2 (50%), fentanyl and isoflurane as needed. Inspired minute volume was kept constant during anaesthesia. Cardiovascular monitoring included a radial artery catheter and a pulmonary artery catheter for measurement of CO, RVEF and SvO2, and calculation of right ventricular end diastolic volume indexed (RVEDVI). Haemodynamic variables, arterial and venous blood gas analyses were collected before and 10 min after anaesthetic induction, 15, 30 and 60 min after insufflation (IAP = 12 mmHg) followed by a 10 degrees head-up tilt, and after exsufflation. RESULTS: The mean age was 81 +/- 4 yr. The main cardiovascular depression was recorded after anaesthetic induction. Peritoneal insufflation resulted in improvement of cardiovascular function with increases in cardiac index (+19%), heart rate (+21%), MAP (+ 19%) and SvO2 (+8%), (P < 0.05) which may be the result of a sympathetic stimulation. No change in preload (RVEDVI) and SVR was recorded. Cardiac index was unchanged during pneumoperitoneum. Laparoscopy was associated with an increase in PaCO2 15 min after CO2 insufflation (from 33.9 to 38.3 mmHg, P < 0.05) and a further elevation after 60 min (44.4 mmHg) without any sign of extra peritoneal diffusion. There was no change in the intra-pulmonary shunt and the Pa-ETCO2 gradient remained stable (mean 7.2 mmHg). CONCLUSION: We conclude that gradual abdominal insufflation to 12 mmHg followed by a limited 10 degrees head-up tilt is associated with cardiovascular stability in elderly ASA III patients.

Aged↗
PubMed1996

A comparison of direct, indirect, and fiberoptic laryngoscopy to evaluate vocal cord paralysis after thyroid surgery.

After thyroidectomy, the anesthesiologist usually performs a laryngoscopy to detect laryngeal edema and nerve palsies. The goal of this study was to compare three different methods of laryngeal examination after tracheal extubation of the patients. For that purpose, between 1990 and 1995, a prospective series of 1608 patients operated for thyroidectomy has been studied. The series was divided into 4 groups. In group I (n = 200), four anesthesiologists have evaluated the efficiency of the immediate postextubation direct laryngoscopy. In group II (n = 100), one anesthesiologist has compared the direct, indirect, and flexible laryngoscopies in every patient in a fixed and timed fashion. In group III (n = 100), the four examiners have evaluated the flexible laryngoscopy at a different timing so as to eliminate the possible temporal relationship of the ease of visualization in group II. In group IV (n = 1208), the four examiners have evaluated flexible laryngoscopy, on a large scale, at any time during the 1-h stay in the recovery room. Special attention was directed to the patients with known cardiovascular diseases. Direct and indirect laryngoscopies were only effective in 76 and 73%, respectively, of the patients, whereas flexible laryngoscopy was effective in 99.6% of them. Flexible laryngoscopy was easy to perform in 96.5% of the patients versus 65 and 55% with direct and indirect laryngoscopies. Finally, variations in monitored cardiovascular parameters were significantly lower with flexible and indirect laryngoscopies than with direct laryngoscopy. These mild variations induced by flexible laryngoscopy were well tolerated by patients with known cardiovascular diseases. Flexible laryngoscopy is the best method for an immediate laryngoscopic examination after thyroidectomy.

Fiber Optic Technology↗
PubMed1996

Delayed forced air warming prevents hypothermia during abdominal aortic surgery.

We have evaluated the efficacy of the delayed forced air warming during abdominal aortic surgery in 18 patients. Patients were allocated randomly to one of two groups: the control group (n = 9) received no intraoperative warming device; the Bair-Hugger group (n = 9) had active skin surface warming with an upper body cover. The device was activated when core temperature decreased to less than 36 degrees C. The reduction in core temperature was 0.6 degrees C during the first hour after induction and 0.4 degrees C during the second hour in both groups. In the control group, core temperature continued to decrease until the end of surgery, whereas in the Bair-Hugger group, the reduction in core temperature stopped after 1 h of warming, and then rewarming began. At the end of surgery, core temperature in the Bair-Hugger group was similar to core temperature before induction, and was higher than core temperature in the control group (P < 0.003).

Adult↗
PubMed1996

Modeled responses to training and taper in competitive swimmers.

This study investigated the effect of training on performance and assessed the response to taper in elite swimmers (N = 18), using a mathematical model that links training with performance and estimates the negative and positive influences of training, NI and PI. Variations in training, performance, NI, and PI were studied during 3-, 4-, and 6-wk tapers. The fit between modeled and actual performance was significant for 17 subjects; r2 ranged from 0.45 to 0.85, P < 0.05. Training was progressively reduced during tapers. Performance improved during the first two tapers: 2.90 +/- 1.50% (P < 0.01) and 3.20 +/- 1.70% (P < 0.01). Performance improvement in the third taper was not significant (1.81 +/- 1.73%). NI was reduced during the first two tapers (P < 0.01 and P < 0.05, respectively), but not during the third. PI did not change significantly during tapers. Thus, the present results show that the model used is a valuable method to describe the effects of training on performance. Performance improvement during taper was attributed to a reduction in NI. PI did not improve with taper, but it was not compromised by the reduced training periods.

Adult↗
PubMed1996

Creatine supplementation does not improve sprint performance in competitive swimmers.

This study was conducted to examine the effects of creatine (Cr) supplementation on sprint swimming performance and energy metabolism. Twenty highly trained swimmers (9 female, 11 male) were tested for blood ammonia and for blood lactate after the 25-, 50-, and 100-m performance in their best stroke on two occasions 7 d apart. After the first trial, subjects were evenly and randomly assigned to either a creatine (5 g creatine monohydrate 4 times per day for 5 d) or a placebo group (same dosage of a lactose placebo) in a double-blind research design. No significant differences in performance times were observed between trials. Post-exercise blood ammonia concentration decreased in the 50- and 100-m trials in the creatine group and in the 50-m trial in the placebo group. The supplementation period had no effect on post-exercise blood lactate. Therefore, creatine supplementation cannot be considered as an ergogenic aid for sprint performance in highly trained swimmers although adenine nucleotide degradation may be reduced during sprint exercise after 5 d of creatine ingestion.

Adult↗
PubMed1996

Ventilatory effects of laparoscopic cholecystectomy.

BACKGROUND: During laparoscopic cholecystectomy the arterial-end-tidal CO2 gradient (Fa-ETCO2) has been variously shown to be unchanged, increased, decreased or even negative. The goal of this study was to evaluate Fa-ETCO2, and to determine the proper contribution of VECO2 and VA in regard to the increase of FETCO2. METHODS: Ventilatory patterns were studied in 15 ASA 1-2 patients (mean age +/- SD: 48.5 +/- 15.0) undergoing laparoscopic cholecystectomy, with intraperitoneal CO2 insufflation limited to 12 mmHg, 15 degrees head-up position, during general anaesthesia and controlled ventilation. The following were studied before, during and after the pneumoperitoneum: FaCO2, FETCO2, nasopharyngeal temperature; dead space ventilation, and expired volumes using the Single Breath Test for CO2. VA was calculated as the alveolar fraction of expired VT multipled by the respiratory frequency. RESULTS: During pneumoperitoneum it is shown that: 1) Fa-ETCO2 either decreases and becomes even negative (n = 8) (P < 0.01), or stays unchanged (n = 7), but never elevates; 2) VECO2 increases (peak value: +22.6%) (P < 0.01); 3) VA is unchanged, and 4) dead space ventilation, determined in 7 patients, remains unchanged. CONCLUSION: We conclude that only exogenous CO2 loading, and not VA, can explain such increase in FETCO2 and FaCO2, in cases of limited CO2 insufflating pressure in ASA 1-2 patients.

Adult↗
PubMed1996

Pharmacokinetics of lidocaine with epinephrine in piglets following epidural anaesthesia.

The time course of arterial plasma lidocaine concentration, following an epidural anaesthesia via the sacrococcygeal or the S4-S5 trans-sacral approach, was studied in nine healthy piglets (7.8 +/- 1.3 weeks). Plasma lidocaine concentrations were measured for up to six hours after administration (5 mg/kg). Peak plasma concentration was 1.83 +/- 0.17 mg/l. Pharmacokinetic parameters determined from an independent compartment model were not different from those observed after an epidural administration of lidocaine via the sacrococcygeal space in children, except for a wide variability in the time taken to reach the maximum concentration (27.3 +/- 7.4 min) and a shorter half-life of elimination (82.8 +/- 7.0 min). The total body clearance of lidocaine was similar in piglets (17.3 +/- 1.6 ml/min/kg) to that in children. The shorter half-life of elimination was therefore attributed to a smaller volume of distribution in piglets (2.0 +/- 0.2 l/kg).

Anesthesia, Epidural↗
PubMed1995

Hyperlipidemia and coronary disease. Correction of the increased thrombogenic potential with cholesterol reduction.

BACKGROUND: Hypercholesterolemia is a risk factor for coronary disease, and platelet reactivity is increased with hypercholesterolemia, suggesting a prethrombotic risk. The aim of this study was to measure mural platelet thrombus formation on an injured arterial wall in a model simulating vessel stenosis and plaque rupture in hypercholesterolemic coronary disease patients before and after cholesterol reduction. METHODS AND RESULTS: Thirty-two patients with stable coronary disease were studied. Platelet thrombus formation and serum lipids were measured in 16 hypercholesterolemic patients (cholesterol > 5.2 mmol/L) before and after a mean of 2.5 months of pravastatin therapy (40 mg/d) and in 16 normocholesterolemic control patients. Thrombus formation was assessed by exposing porcine aortic media to the patient's flowing venous blood for 3 minutes at a shear rate of 754 or 2546 s-1 at 37 degrees C in an ex vivo superfusion chamber. Quantitative morphometric platelet thrombus formation at baseline was higher in the hypercholesterolemic patients at both the high and low shear rates: 4.8 +/- 1.0 and 3.3 +/- 0.7 micron 2/mm, respectively, compared with normocholesterolemic patients: 2.1 +/- 0.5 and 1.6 +/- 0.4 micron 2/mm (both P < .05). In the hypercholesterolemic patients, pravastatin decreased total cholesterol from 6.5 +/- 0.2 to 4.5 +/- 0.2 mmol/L and LDL cholesterol from 4.5 +/- 0.2 to 2.8 +/- 0.1 mmol/L (both P < .05). Platelet thrombus formation at high and low shear rates decreased to 2.0 +/- 0.3 and 1.3 +/- 0.3 micron 2/mm, respectively (both P < .05). CONCLUSIONS: Thus, hypercholesterolemia is associated with an enhanced platelet thrombus formation on an injured artery, increasing the propensity for acute thrombosis. Platelet thrombus formation at both high and low shear rates decreased as total and LDL cholesterol levels were reduced with pravastatin. Cholesterol lowering may therefore reduce the risk of acute coronary events in part by reducing the thrombogenic risk.

Animals↗
PubMed1995

Cigarette smoking acutely increases platelet thrombus formation in patients with coronary artery disease taking aspirin.

BACKGROUND: Smoking is associated with an increased risk of myocardial infarction and sudden death. Platelet activation and thrombosis at sites of vessel stenosis and injury or plaque disruption play a crucial role in these acute coronary events. Thus, the aim of this study was to determine whether cigarette smoking acutely increases platelet thrombus formation on an injured arterial surface at local shear rates typical of a stenotic artery. METHODS AND RESULTS: Twelve habitual smokers with stable coronary disease, on aspirin 325 mg/d, were studied immediately before and 5 minutes after smoking two cigarettes each. Ex vivo platelet thrombus formation on porcine arterial media (simulating deep arterial injury) was measured after exposure to the patient's circulating venous blood for 3 minutes in cylindrical flow chambers at 37 degrees C. The flow chambers were designed to produce shear rates of 754 or 2546 s-1, the latter being typical of the high shear rates produced by vessel stenosis. Plasma catecholamine, thromboxane B2, and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) levels and whole blood platelet aggregation responses to thrombin were also measured before and after smoking. Compared with before smoking, morphometrically measured platelet thrombus formation on arterial media at shear rates of 754 and 2546 s-1 increased by an average of 48% (P = .19) and 64% (P = .014), respectively, after smoking. Plasma epinephrine increased by more than twofold after smoking (P = .026). Plasma thromboxane B2 and 6-keto-PGF1 alpha levels did not change. Smoking also increased whole blood platelet aggregation to thrombin (P < or = .05). CONCLUSIONS: These results suggest that smoking-enhanced platelet thrombosis may be an important contributory mechanism for acute coronary events in smokers that is not prevented by aspirin treatment. Catecholamine release and heightened platelet aggregation response to in vivo agonists may contribute to the prothrombotic effects of smoking.

Adult↗
PubMed1995

Effects of training on performance in competitive swimming.

The relationships between the mean intensity of a training season, training volume and frequency, and the variations in performance were studied in a group of 18 elite swimmers. Additionally, differences between the swimmers who improved their personal record of the previous year during the follow-up training season (GIR, n = 8) and those who did not (GNI, n = 10) were investigated. The improvement in performance during the follow-up season was significantly correlated with the mean intensity of the training season (r = 0.69, p < 0.01), but not with training volume or frequency. The performance improvement during the follow-up season was negatively related to the initial performance level (r = 0.90, p < 0.01). The decline in performance during detraining from the previous year was less for the GIR than for the GNI (6.21 +/- 2.30% vs. 9.79 +/- 2.18%, p < 0.01). The present findings suggest that training intensity is the key factor in performance improvement in a group of elite swimmers. Factors such as previous detraining and initial performance level could jeopardize success in spite of a good adaptation to training.

Adaptation, Physiological↗
PubMed1994

Endothelium-derived nitric oxide attenuates neutrophil adhesion to endothelium under arterial flow conditions.

Nitric oxide (NO) synthesized from cultured endothelial cells inhibits platelet aggregation and adhesion to subendothelial extracellular matrix and may contribute to the thromboresistance of the endothelium. NO has also been shown to inhibit neutrophil aggregation and adherence to postcapillary venules. Whether NO derived from the intact endothelium of an arterial wall can influence platelet and neutrophil adhesion under whole-blood arterial flow conditions was evaluated in this study. Porcine aortic segments with intact endothelium were exposed to flowing porcine arterial blood for 5 minutes at a shear rate of 424 sec-1. Pretreatment of the endothelium with the physiological precursor of NO, L-arginine (2 mmol/L), reduced 111In-labeled neutrophil adhesion by 32% from 10.2 +/- 1.6 to 6.9 +/- 1.3 x 10(3)/cm2 (P < .05), relative to control. This effect was reversed by the inhibitor of NO synthesis, N omega-nitro-L-arginine methyl ester (L-NAME, 5 mmol/L) (8.2 +/- 3.0 versus 8.6 +/- 3.2 x 10(3)/cm2 for control; P = NS). Pretreatment of the endothelium with D-arginine (2 mmol/L) did not influence neutrophil adhesion (8.7 +/- 2.0 versus 8.6 +/- 2.0 x 10(3)/cm2 for control; P = NS). The intact endothelium, which is normally thromboresistant, shows a low basal level of 51Cr activity, corresponding to a platelet adhesion less than 0.5 x 10(6)/cm2, and this thromboresistance was not significantly influenced by L-arginine. These results indicate that NO derived from an intact arterial endothelium under whole-blood arterial flow conditions may be an important modulator of neutrophil interaction with the intact endothelium.

Animals↗
PubMed1993

Methylene blue inhibits the antithrombotic effect of nitroglycerin.

OBJECTIVES: The aim of this study was to examine whether cyclic guanosine monophosphate (GMP) may be involved in the antithrombotic action of nitroglycerin. BACKGROUND: Nitroglycerin has been shown to inhibit platelet function in vitro by stimulating prostacyclin or inhibiting thromboxane A2 production, or both. Nitroglycerin has also been shown to possess potent antithrombotic properties in vivo. However, the mechanism of this antithrombotic effect is unclear. METHODS: Nitroglycerin was infused to produce a 10% decrease in mean arterial pressure in 27 normal pigs by exposing their circulating arterial blood to porcine aortic media in an ex vivo perfusion chamber. Eight pigs received an infusion of nitroglycerin alone; eight received an infusion of methylene blue, a guanylate cyclase inhibitor, followed by nitroglycerin infusion and five pigs received an infusion of nitroglycerin followed by methylene blue and subsequent infusion of cyclic GMP. RESULTS: With nitroglycerin alone, quantitative autologous indium-111-labeled platelet deposition (x10(6) on the aortic media was decreased to 63.9 +/- 10.4% (p = 0.01) of the baseline control platelet deposition. Methylene blue given before nitroglycerin tended to increase platelet deposition relative to baseline and platelet deposition after nitroglycerin was 142 +/- 35% (p = NS) of baseline value. In pigs that received all three agents, nitroglycerin reduced platelet deposition to 42.3 +/- 12.2% of baseline value; this decrease was then attenuated by subsequent methylene blue infusion but was enhanced by cyclic GMP infusion to 16.4 +/- 3.8% of baseline value (p = 0.006 vs. baseline control and p = 0.02 versus methylene blue infusion). CONCLUSIONS: Guanylate cyclase inhibition with methylene blue abolishes the antithrombotic effect of nitroglycerin, which can be enhanced by cyclic GMP.

Animals↗
PubMed1993

Airway complications in thyroid surgery.

Perioperative and postoperative morbidity and mortality were studied in a series of 3,008 thyroidectomies. Compressive symptoms, frequent in substernal and cancerous goiters, were present in 11.0% of the patients, although a low rate of dyspnea (2.7%) was observed. In large goiters, some orotracheal intubations were difficult. In such cases, the transtracheal approach can also be difficult, so failure should be anticipated. Postoperative causes of respiratory obstruction included local hemorrhages, bilateral recurrent nerve palsies, and laryngeal edema. A tracheal collapse was not observed. These respiratory obstructions led to repeat surgery in 11 patients, tracheostomy in 3, and temporary reintubation with steroid therapy in 1. The recurrent laryngeal nerve, which may have been affected preoperatively, was found to be damaged postoperatively in 0.5% of the patients with benign goiters, compared to 10.6% of the patients with thyroid cancer. In this last group a bilateral palsy was observed in 3 cases with prolonged or extensive surgery. After these short-term orotracheal intubations (114 minutes on average), injuries of the airway caused by the endotracheal tube were found in 4.6% of the patients.

Airway Obstruction↗
PubMed1992

Cilazapril and early atherosclerotic changes after balloon injury of porcine carotid arteries.

BACKGROUND: Cilazapril, a converting enzyme inhibitor, has been shown to significantly decrease the extent of intimal smooth muscle cell proliferation after arterial injury in a normotensive rat model. METHODS AND RESULTS: To assess the influence of cilazapril on myofibrotic changes after balloon injury, control (n = 7) or cilazapril-treated (n = 9) (20 mg/kg b.i.d.) normal 3-month-old pigs underwent dilatation angioplasty of the right, and deendothelialization of the left common carotid artery. Carotid arteries isolated at 4 weeks were examined morphometrically with a computerized digitizer after in situ glutaraldehyde fixation. Both in the deendothelialized and dilated arteries, the surface area in square millimeters of the neointima and media were similar in the treated and control animals; therefore, the ratio of neointima to media was again not different. The neointimal changes included a combination of proliferative changes as well as organization of mural thrombus and were equally well distributed in the two groups of animals. At the time that the animals were killed, blood pressure (38.2 +/- 2.1 versus 56.8 +/- 4.8 mm Hg, p = 0.003) and plasma angiotensin converting enzyme activity (5.6 +/- 4.1 versus 182.3 +/- 70.4, p = 0.02) were lower in treated than in control pigs, but aortic media thrombogenicity (as assessed in an ex vivo perfusion flow chamber) and serum lipids were not different between groups. CONCLUSIONS: In pigs, cilazapril did not alter the development of myofibrotic changes after mild or severe balloon injury despite plasma angiotensin converting enzyme activity inhibition.

Angioplasty, Balloon↗
PubMed1990

Effects of nitroglycerin at therapeutic doses on platelet aggregation in unstable angina pectoris and acute myocardial infarction.

The platelet aggregation response to adenosine diphosphate (ADP) and to thrombin was quantified in 10 patients, 5 with unstable angina pectoris and 5 with acute myocardial infarction, before, during and after a 45-minute infusion of nitroglycerin. An impedance aggregometer allowing rapid bedside studies in whole blood was used. The reproducibility of the methods was documented to be within 10%. Doses of nitroglycerin were titrated for a 10 mm Hg decrease in mean arterial blood pressure with mean doses being 1.2 +/- 0.2 (standard error of the mean) micrograms/kg/min. Nitroglycerin decreased the area under the aggregation curve induced by ADP from 43 +/- 3.6 to 30 +/- 6.3 cm2 (p = 0.007) and by thrombin from 8.9 +/- 1.7 to 4.1 +/- 0.9 cm2 (p = 0.003). Peak responses to ADP were decreased from 13.3 +/- 1 to 9.1 +/- 1.7 ohms (p = 0.005) and to thrombin from 9.3 +/- 2 to 5.0 +/- 1.2 ohms (p = 0.003). All patients had greater than or equal to 50% inhibition with 1 agent or the other and the inhibition was greater than 50% with each of the 2 aggregating agents in 6 patients. Analyses performed on blood withdrawn 15 minutes after the discontinuation of nitroglycerin showed a return to baseline before nitroglycerin results. When analyses were delayed and performed on blood preserved at room temperature for 30 minutes, no effect of nitroglycerin could be detected. Thus, bedside platelet aggregation studies document a significant and reversible effect of nitroglycerin at therapeutic doses on platelet function.

Adenosine Diphosphate↗