PubMed Health⌕ Search

Biomedical subjects

M Pinaud

Publications and source records attributed to M Pinaud.

At least 19 recordsLinked to original sources
PubMed1992

[Hemodynamic effects of bathing in severe burnt patients].

Repeated water immersion is currently used in France in the treatment of severe burn injury. A prospective study was carried out to assess the haemodynamic effects of immersing such patients in a half sitting position in water, the temperature of which was kept at 35 degrees C. The burn exceeded 50% of body surface area (BSA), with at least 30% being third degree burns. The study was carried out during the first bath, three days after the injury. The patients were immersed up to the clavicles. They were sedated with 2 mg.h-1 of both flunitrazepam and phenoperidine, and were mechanically ventilated. The following haemodynamic parameters were monitored: heart rate, arterial blood pressure (the transducer being level with the arterial catheter), right atrial and pulmonary arterial pressures (the transducer being level with the right atrium, level which had been marked on the chest before immersion and placed two intercostal spaces higher after immersion because of the change in position of the heart). The cardiac output was measured using the thermodilution method. The patient's temperature was monitored with the thermistance of the Swan-Ganz catheter. Values were obtained before immersion, after 15 and 30 minutes of immersion, and 5 minutes after the end of the bath. Nine patients were included, 2 women and 7 men, aged between 24 and 45 years, weighing 73.7 kg on average. Burn size was 78% of BSA (range 64 to 95%). Water immersion was maintained for 34 +/- 3 min. The right atrial, mean pulmonary arterial, and wedge pressures, and the cardiac and systolic indices increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Long-term hypotensive technique with nicardipine and nitroprusside during isoflurane anesthesia for spinal surgery.

Short-term infusion of nicardipine can be used to induce deliberate hypotension but may result in plasma drug accumulation. To assess long-term nicardipine administration for deliberate hypotension in 10 patients in a moderately hemodiluted state who were undergoing spinal surgery, hemodynamics and plasma nicardipine concentrations were concomitantly measured before and 20, 80, and 140 min after starting nicardipine, at drug discontinuation, and 20 and 80 min later. A dose of 6.2 +/- 0.9 mg (mean +/- SEM) of nicardipine was initially required to obtain mean arterial blood pressures at 55-60 mm Hg. Maintenance doses of nicardipine were 3-5 mg/h. The duration of nicardipine administration was 270 +/- 20 min (mean +/- SEM). Hypotension was associated with decreased systemic and pulmonary vascular resistances, increased cardiac index, and decreased arteriovenous difference in O2 contents. Only two patients required homologous blood transfusion. Plasma nicardipine concentrations peaked at 110 +/- 21 ng/mL (mean +/- SEM) and then decreased to 38 +/- 11 ng/mL (mean +/- SEM) without changes in arterial blood pressure. After vasodilator discontinuation, hypotension was observed during a mean time of 43 min (range 27-88 min) despite plasma concentrations less than 20 ng/mL. No relationship was found between plasma nicardipine concentrations and hemodynamics. These findings suggest that an increasing effect of nicardipine over time may occur during prolonged administration. Because the reasons for this hysteresis remain unclear, use of nicardipine infusion during major surgery and anesthesia requires particular caution.

Adult↗
PubMed1991

[Effects of Diprivan on cerebral blood flow, intracranial pressure and cerebral metabolism in head injured patients].

The effects of propofol on cerebral blood flow, intracranial pressure (ICP) and cerebral oxygen consumption (CMRO2) were assessed in ten severely head-injured patients undergoing surgery for limb fractures. The patients, aged between 15 and 40 years, were in deep coma, scored 6-7 on the Glasgow coma score. They were mechanically ventilated and sedated with 1 mg.h-1 phenoperidine. Anaesthesia was carried out with a 2 mg.kg-1 intravenous bolus of propofol, immediately followed by a 150 micrograms.kg-1.min-1 infusion, which lasted for a mean time of 41.4 +/- 7.3 min. Data were collected 5 min before any propofol was given, 15 min after the start of the infusion, and 15 min after its end. A radial artery cannula, a 7.5 Fr thermodilution flow-directed pulmonary arterial catheter, a cerebral intraventricular catheter and a catheter in the jugular venous bulb were used for this purpose. Carotid arterial injection of 133Xenon was used to determine regional cerebral blood flow (rCBF). Anaesthetic blood concentrations of propofol (3 to 5 micrograms.ml-1) were associated with a decrease in all the parameters studied: cerebral perfusion pressure, from 82 +/- 14 mmHg to 59 +/- 7 mmHg (p less than 0.001); rCBF, from 35 +/- 6 ml.100 g-1.min-1 to 26 +/- 5 ml.100 g-1.min-1 (p less than 0.01); ICP from 11.3 +/- 2.6 mmHg to 9.2 +/- 2.5 mmHg (p less than 0.001); CMRO2 from 1.63 +/- 0.38 mlO2 +/- 100 g-1.min-1 to 1.18 +/- 0.38 mlO2.100 g-1.min-1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[Hemodynamic effects of dobutamine in hyperkinetic septic shock treated with norepinephrine].

A prospective study of the haemodynamic effects of dobutamine was carried out in six men and four women suffering from hyperkinetic septic shock, already treated with noradrenaline and dopamine. All ten patients had septic shock, defined as a mean arterial blood pressure of less than 70 mmHg and an urine output under 15 ml.h-1, persisting despite fluid loading, associated with positive blood cultures, increased white blood cell counts, and a septic area. Initial treatment consisted in fluid loading, so as to increase cardiac output whilst keeping pulmonary wedge pressure (Ppw) between 8 and 10 mmHg. Dopamine was then added, up to a dose of 15-20 micrograms.kg-1.min-1, in an attempt to improve coronary and renal blood flows. In patients in whom this failed, the amounts of dopamine were then decreased, down to 3 micrograms.kg-1.min-1, and replaced by noradrenaline. When patients had as steady cardiac index (CI) greater than 3 l.min-1.m-2 and a systemic arterial resistance index (RsaI) of less than 1,800 dyn.s.cm-5.m-2 for more than 60 min, they were included in the protocol. Dopamine was then replaced by increasing doses of dobutamine (0, 5, 7.5, 10, 15 and again 0 micrograms.kg-1.min-1). The usual haemodynamic parameters were measured and calculated once a steady state had been obtained at each dose (within 20 to 30 min). Ppw was kept between 8 and 10 mmHg by fluid loading with a 4% albumin solution. At the beginning of the study, patients had a mean blood pressure of 78 +/- 6 mmHg, a CI of 4.8 +/- 1.5 l.min-1.m-2 and a RsaI of 1,285 +/- 341 dyn.s.cm-5.m-2 RsaI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Comparative effects of diazepam, ranitidine , sodium citrate and enprostil on pH and gastric volume in preanesthetic medication].

A study was designed to assess the efficacy of oral premedication with diazepam or enprostil in preventing the gastric aspiration syndrome in fasted patients scheduled for elective surgery, and to compare the results with those obtained with ranitidine and sodium citrate. The study included 120 consecutive patients undergoing urological or plastic surgery, randomly assigned to four groups of 30. Two hours before anaesthesia, the patients from three groups were given, with 30 ml of water, either 10 mg diazepam, or 150 mg ranitidine, or 35 micrograms enprostil. Those in the fourth group were given 30 ml of 0.5 M sodium citrate, ten minutes before induction. Anaesthesia consisted in the administration of thiopentone, fentanyl, vecuronium and nitrous oxide in oxygen. After endotracheal intubation, a gastric tube was inserted. The stomach fluid content was completely aspirated, and then again 60 and 120 min after induction, as well as at the end of surgery. Age, weight and duration of surgery were comparable in the four groups. Mean pH in the diazepam group was much lower than that in the other groups, both just after induction (2.3 +/- 1.54; p less than 0.001 vs. ranitidine and sodium citrate; p less than 0.01 vs. enprostil) and at the end of surgery (3.2 +/- 2.03; p less than 0.01 vs. ranitidine and sodium citrate; p less than 0.05 vs. enprostil). There was more than 0.4 ml.kg-1 gastric juice in the sodium citrate group.(ABSTRACT TRUNCATED AT 250 WORDS)

Antacids↗
PubMed1991

[Effects of intravenous clonidine on postoperative shivering].

A study was designed to assess the possible effects of intravenous clonidine on postoperative shivering. Fifty patients undergoing spinal fusion under isoflurane anaesthesia were randomly assigned to two groups (n = 25). Patients in one group were given intravenous clonidine (5 micrograms.kg-1 during the first hour, and 0.3 microgram.kg-1.h-1 thereafter) or placebo. Shivering intensity (rated from 0 to 2) and pulmonary artery blood temperature (theta) was recorded every ten minutes for two hours. Haemodynamic and metabolic data were obtained by way of a Swan-Ganz catheter prior to administering the test drug, and then after 1 and 2 hours. On arrival at the recovery room, theta was 36.2 +/- 0.3 degrees C in the clonidine group, and 36.5 +/- 0.2 degrees C in the placebo group. There were no significant differences in shivering between the two groups. Clonidine significantly decreased blood pressure, heart rate, cardiac output and whole body oxygen consumption. The patients in these series were free from any cardiac disease. Further studies are required to assess the possible beneficial effects of clonidine on postoperative oxygen consumption in patients suffering from heart failure.

Adult↗
PubMed1991

Ketamine and midazolam neurotoxicity in the rabbit.

Ketamine and midazolam can produce analgesia following intrathecal administration in rabbits. However, neurotoxicity studies are required before these agents can be considered safe for clinical use. The aim of this study was to evaluate by histologic and blood-brain barrier (BBB) studies whether ketamine or midazolam could be used as an alternative to local anesthetics or opioids to produce spinal analgesia. Forty white New Zealand rabbits were randomly assigned to four groups of 10. In the conscious animal, 0.3 ml 0.9% saline solution, 1% lidocaine, 1% ketamine, or 0.1% midazolam was intrathecally injected intracisternally using a modification of the technique of Yaksh et al. Light and fluorescence microscopy were performed on transverse spinal cord sections by a neuropathologist unaware of the administered agents. All spinal cord section slides were scored within four zones: upper cervical, lower cervical, median thoracic, and lumbar segments. Spinal cord homogeneous lesions with higher scores than those of lidocaine-treated animals were considered abnormal. The BBB study showed evidence of neurotoxicity for ketamine, whereas light microscopy indicated no significant differences in comparison with saline and lidocaine. Midazolam-treated rabbits showed significant changes in both BBB and light microscopy studies. In view of these results, the intrathecal use of midazolam should be avoided in humans. Lesions observed following ketamine suggest the need for further experimental studies of the solvent and different ketamine enantiomers to establish definitively the safety of intrathecal free ketamine in humans.

Animals↗
PubMed1991

Postoperative analgesia by intravenous clonidine.

Clonidine, an alpha 2 adrenoreceptor agonist, has nonopiate antinociceptive properties, which might be an alternative for postoperative analgesia free of opioid-induced side effects. To document the analgesic properties of intravenous clonidine during the postoperative period, 50 ASA physical status 1 patients, immediately after spinal fusion, were randomly assigned to two groups, blindly administered either clonidine (5 micrograms/kg infused the 1st h and then 0.3 microgram-1.kg-1.h-1 during 11 h) or a placebo. A visual analog scale graded from 0 (no pain) to 100 mm was used to assess pain before clonidine or placebo administration (T0), at the end of the loading dose (T1) and then every 2 h (T3, T5, T7, T9, and T11). Morphine (0.1 mg/kg) was administered intramuscularly after each pain measurement if the score was greater than 50 mm. No morphine was given at T0. Hemodynamics, blood gases and plasma clonidine concentrations were measured each time the pain score was measured. The pain score decreased from 42 +/- 5 to 26 +/- 3 mm (mean +/- standard error) in the clonidine group whereas it was unchanged in the placebo group despite a greater morphine requirement (dose for each patient: 3.8 +/- 1 vs. 10.8 +/- 1.2 mg). Clonidine delayed the onset of pain and the first request for morphine injection. Mean arterial pressure decreased to 74 +/- 2 mmHg in the clonidine group (-26 +/- 2 vs. -15 +/- 2% in the placebo group at T11) despite a significant increase in the cumulative fluid volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Clonidine↗
PubMed1991

Effects of oral clonidine premedication and postoperative i.v. infusion on haemodynamic and adrenergic responses during recovery from anaesthesia.

The effects of clonidine, a central alpha 2-adrenoreceptor agonist, on haemodynamic and catecholamine changes were assessed during emergence from anaesthesia, a period which is associated with increased sympathetic nervous discharge, hypertension and tachycardia. According to a double-blind randomized design, 32 patients received either clonidine, preoperatively given by oral route (3.5 micrograms.kg-1) and postoperatively by i.v. infusion (0.3 microgram.kg-1.h-1), or a placebo. Perioperative management was similar in both groups. Measurements were made in the recovery room, before starting clonidine or placebo infusions for evaluation of clonidine premedication, and then during infusion as follows: when core temperature reached 37 degrees C; then 2 h, and 6 h later. Prior to starting infusions, mean blood pressure (88 +/- 15 vs 103 +/- 14 mmHg) (11.7 +/- 2.0 vs 13.7 +/- 1.9 kPa), heart rate (67 +/- 8 vs 87 +/- 17 beats.min-1) and plasma norepinephrine levels (462 +/- 393 vs 615 +/- 361 pg.ml-1) were lower in the clonidine group. Only at the latest measurement (6 h after core temperature reached 37 degrees C) did clonidine elicit significant effects. The values during clonidine infusion compared to placebo were at this time: mean blood pressure (73 +/- 10 vs 86 +/- 13 mmHg) (9.7 +/- 1.3 vs 11.5 +/- 1.7 kPa), heart rate (71 +/- 6 vs 93 +/- 13 beats.min-1) and plasma norepinephrine levels (240 +/- 224 vs 451 +/- 111 pg.ml-1). Our results suggest that: 1) preoperative clonidine may improve the haemodynamic profile associated with anaesthetic discontinuation, but 2) i.v. infusion (0.3 microgram.kg-1.h-1) did not prolong this effect during the early postoperative period in the face of the sympathetic nervous discharge of recovery.

Administration, Oral↗
PubMed1991

Deliberate hypotension with nicardipine or nitroprusside during total hip arthroplasty.

To induce deliberate hypotension during anesthesia, nicardipine was administered to patients undergoing total hip arthroplasty and was randomly compared with nitroprusside. Hemodynamic measurements were performed before and 10, 20, 30, and 60 min after starting to administer either nicardipine (n = 12) or nitroprusside (n = 12) (B, T1, T2, T3, and T4, respectively); at the end of drug infusion (T5); and 10, 20, and 60 min later (T6, T7, and T8, respectively). Plasma renin activity and catecholamine levels were measured at B, T1, T5, T6, and T7. In addition, plasma nicardipine concentration was measured in five patients at T1, T2, T5, T7, and T8. As with nitroprusside, nicardipine administration (1-3 micrograms.kg-1.min-1, after a titration dose of 4.7 +/- 1.5 mg) resulted in hypotension (up to -34% +/- 3%), a decrease in systemic vascular resistances (up to -49% +/- 4%), and increases in heart rate (up to +17% +/- 6%), cardiac index (up to +37% +/- 8%), plasma norepinephrine (up to +63% +/- 17%) and epinephrine (up to +232% +/- 68%) levels, and plasma renin activity (up to +336% +/- 207%). Ten and 20 minutes after discontinuation of the hypotensive drug, nicardipine led to persistent vasodilation and hypotension, which differed significantly from the hypertensive rebound observed after nitroprusside discontinuation, despite a similar increase in plasma renin activity and catecholamine levels. Our results indicate that after the infusion was terminated, the nicardipine-induced vasodilation was opposed to the vasoconstrictive effects of angiotensin II and catecholamines, thus avoiding hypertensive rebound.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Effects of propofol on cerebral hemodynamics and metabolism in patients with brain trauma.

The authors determined the effect of propofol on cerebral blood flow, intracranial pressure, and cerebral arteriovenous oxygen content difference in severely brain-injured patients during orthopedic treatment of fractures of the extremities. The Glasgow Coma Scale score was 6 or 7 at the time of the study. Data were collected in the operating room before and during (5 and 15 min) administration of propofol (2 mg/kg iv bolus immediately followed by a 150 micrograms.kg-1.min-1 infusion) before surgical stimulation. Propofol was infused during 41.4 +/- 7.3 min. After operation, the last set of measurements was made 15 min after propofol was stopped. The study was performed on 10 adults (age range, 15-40 yr) whose lungs were mechanically ventilated (air/O2) and who were sedated (phenoperidine, 1 mg/h), and was conducted using a radial artery cannula; a 7.5-Fr, thermodilution, flow-directed, pulmonary artery catheter; an intraventricular catheter; and a catheter in the jugular venous bulb. The 133xenon intra-internal carotid artery injection technique was used to determine regional cerebral blood flow (rCBF). Anesthetic blood concentration of propofol (3-5 micrograms/ml) was associated with decreases in cerebral perfusion pressure (CPP; from 82 +/- 14 to 59 +/- 7 mmHg; P less than 0.001), rCBF (from 35 +/- 6 to 26 +/- 5 ml.100 g-1.min-1; P less than 0.001), and intracranial pressure (ICP; from 11.3 +/- 2.6 to 9.2 +/- 2.5 mmHg; P less than 0.001). Cerebrovascular resistance and cerebral arteriovenous oxygen content difference were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

[Continuous propofol infusion versus enflurane in children operated on for strabismus. Comparison of the quality of anesthesia and recovery conditions].

In children, the use of a continuous infusion of propofol has not yet been reported. A study was therefore designed to compare the characteristics of anaesthesia and recovery when either propofol or enflurance was used as the main anaesthetic agent. All 42 children (14 girls, 28 boys), ASA I and scheduled for corrective squint surgery under general anaesthesia, received 350 micrograms.kg-1 midazolam and 40 micrograms.kg-1 atropine intrarectally 20 min before induction, which was carried out with 3 mg.kg-1 propofol intravenously in 20 s. The patients were then randomly assigned to two groups, according to the drug used for maintenance: group P (n = 21) received a continuous intravenous infusion of propofol, 18 mg.kg-1.h-1 for the first 30 min and 15 mg.kg-1.h-1 thereafter; group E (n = 21) received 2.5%, then, after 30 min, 2% enflurane. Both groups were given 15 micrograms.kg-1 dextromoramide and 0.09 mg.kg-1 vecuronium. During anaesthesia, the following parameters were monitored: systolic (Pasys), diastolic (Padia) and mean arterial (Pa) pressures, heart rate (fc), the presence or not of an oculocardiac reflex with or without a 20% fall in fc which responded to 10-15 micrograms.kg-1 atropine, the appearance of a cardiac dysrhythmia, duration of anaesthesia and the delay before extubation. Recovery was assessed 1, 2, 4 and 6 h postoperatively by using both clinical and psychomotor criteria, the latter being adapted to children having one or both eyes occluded.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia Recovery Period↗
PubMed1989

[Comparison in healthy volunteers of the systemic beta adrenergic receptor blockade by beta blockader eye drops].

The isoproterenol dose-response curve was used to assess quantitatively the degree of systemic beta-adrenoceptor blockade induced by metipranolol (Bétanol) and betaxolol (Bétoptic) eye drops. The study was carried out in twelve healthy volunteers, aged 22 +/- 1.4 yr. In a randomized double-blind trial, each volunteer received, on separate occasions at least one week apart, one drop in each eye of either placebo (physiological saline) or either of the ophthalmic beta-blockers. The intraocular pressure (Pio), heart rate (fc), arterial systolic (Pasys) and diastolic (Padia) pressures were measured before instillation of the eye drops after 15 to 30 min rest, and 3 h afterwards. The isoproterenol dose-response curve was studied 3 h after instillation of the drops. The CD25 (the amount of isoproterenol needed to increase fc by 25 b.min-1) was obtained by extrapolation on the least square linear regression curve. Both beta-blockers gave a significant fall in Pio compared with placebo, metipranolol more than betaxolol (p less than 0.02). There was also a significantly greater fall in fc with both metipranolol and betaxolol than with placebo. There were no changes in Pasys and Padia. CD25 was significantly increased with both beta-blocker eye drops as compared with placebo (p less than 0.05 for betaxolol; p less than 0.01 for metipranolol), but there was no difference between the two. Systemic absorption after topical application of ocular beta-blockers was thus confirmed for both metipranolol and betaxolol. However, the degree of beta-adrenoceptor blockade was weaker than that observed with other older ocular beta-blockers (timolol and carteolol).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗