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Biomedical subjects

P Viars

Publications and source records attributed to P Viars.

At least 91 records · Page 5Linked to original sources

Diazepam does not improve the mechanical performance of rat cardiac papillary muscle exposed to chloroquine in vitro.

Diazepam has been reported to decrease the cardiac toxicity of chloroquine but the precise mechanism involved remains unknown. Left ventricular papillary muscles from adult Wistar rats were exposed to 10(-4) M chloroquine and assigned to three groups: group I (n = 10) exposed to chloroquine alone; group II (n = 8) exposed to chloroquine and 10(-5) M diazepam; group III (n = 8) exposed to chloroquine and 10(-4) M diazepam. The main mechanical parameters measured were: maximum unloaded shortening velocity (Vmax), maximum lengthening velocity (maxVr), active force normalized per cross-sectional area (AF/s), contraction-relaxation coupling under low load (R1), load sensitivity of relaxation (Isot.A/Isom.A), and peak power output (Emax) determined from Hill's equation of the force-velocity curve. Data are expressed as mean percent of control values +/- SD, for groups I, II, III respectively. No differences between groups I, II, and III were noted for Vmax (87 +/- 13, 82 +/- 9, 86 +/- 7), maxVr (47 +/- 6, 48 +/- 11, 52 +/- 11), AF/s (87 +/- 16, 91 +/- 10, 83 +/- 11), Isot. A/Isom. A (113 +/- 9, 108 +/- 3, 109 +/- 7), or Emax (75 +/- 10, 81 +/- 12, 72 +/- 16). Chloroquine was shown to be a negative inotropic agent since it decreased Vmax, AF/s and Emax, but diazepam did not restore the intrinsic mechanical performance of rat cardiac papillary muscle exposed to chloroquine, therefore 1) the protective cardiovascular effects of diazepam in chloroquine poisoning are not related to an improvement in intrinsic cardiac mechanical properties; 2) inotropic agents are therefore necessary in combination with diazepam for the treatment of severe chloroquine poisoning.

Animals↗

[Ischemia, myocardial infarction and epidural anesthesia in patients with coronary disease].

In patients with coronary artery disease, the beneficial effects of epidural anesthesia are well known and often emphasized. Thus, several studies have shown a decrease in the determinants of myocardial oxygen consumption, and an improvement in regional and global left ventricular performance. The disadvantages of epidural anesthesia in patients with coronary artery disease are also well known, however, rarely reported. These detrimental effects are dominated by a decrease in arterial pressure which in turn may compromise the coronary perfusion pressure and induce myocardial ischemia. These 2 case reports illustrate the occurrence of myocardial complications in relation to epidural anesthesia. These case reports contrast with data from the literature showing a beneficial influence of epidural anesthesia on the myocardium. However, the severity of the coronary artery disease in these 2 reported patients may explain this discrepancy. These case reports pointed out that the decrease in arterial pressure is not the exclusive mechanism by which myocardial ischemia may be observed during epidural anesthesia since an hemodynamically-unrelated ischemic episode is described. The treatment of myocardial ischemia during epidural anesthesia is illustrated by these 2 case reports. A relationship between myocardial ischemia and myocardial infarction is discussed from these observations.

Aged↗

[Baroreflex activity in carotid endarterectomy during general anesthesia].

The baroreceptor reflex was studied in eleven patients, aged 69 +/- 6 years, scheduled for carotid endarterectomy under general anaesthesia. Nine were hypertensive. The anaesthetic protocol was the same for all the patients: premedication with morphine and scopolamine, induction with 5 mg.kg-1 thiopentone, 6 micrograms.kg-1 fentanyl and 0.01 mg.kg-1 pancuronium bromide. All the patients were intubated and ventilated with a mixture of nitrous oxide and oxygen. Fentanyl, 100 micrograms, was routinely given at the time of incision. Baroreflex sensitivity was tested using Smyth's method, with a bolus of 75 micrograms trinitrin and plotting changes in heart rate against those in systolic blood pressure. Electrocardiogram, invasive arterial blood pressure and airway pressure were simultaneously recorded. PaCO2 and PaO2 were measured during arterial clamping. The tests were carried out before clamping, 2 min later and 10 to 20 min after the last injection of fentanyl. In the seven patients for whom clamping lasted more than 15 min, a further test was carried out after administration of 0.4 +/- 0.05 vol% halothane (Datex analyser) for 5 min. During anaesthesia, baroreflex sensitivity was low (1.8 +/- 0.3 ms.mmHg-1). After clamping, there was only a significant change in Pasys, with no changes in heart rate or blood gas values (129 +/- 8 mmHg before clamping; 167 +/- 12 mmHg after clamping; n = 8; p less than 0.01). After halothane administration, the sensitivity slope decreased, but not significantly. Moreover, halothane decreased the R-R intervals (1140 +/- 84 after clamping; 963 +/- 76 under halothane; n = 6; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Comparative evaluation of 2 fiber optic catheters for the continuous measurement of Svo2].

Nineteen intensive care patients with shock and acute respiratory failure were studied using two different fiber-optic catheters used for the continuous measurement of mixed venous blood oxygen saturation (SVO2). In groupe I patients (n = 11), a Swan-Ganz catheter with optic fibres emitting light characterized by three different wavelengths was used (Opticath Oximetrix). In groupe II patients (n = 8), a Sat-one Edwards catheter was used instead (only two different wavelengths). All the patients were studied in the early stages of shock, once all the calibration procedures had been carried out. An increase in FIO2, using PEEP, fluid replacement therapy and vasoactive drugs or diuretics all improved the cardio-respiratory status of each patient. After each new therapeutic procedure, SVO2 was measured in blood samples obtained from these catheters, and from the pulmonary artery (to give the reference value, using an OSM3 Hemoximeter). Over a period of 1.5 to 6 h, 119 measurements were carried out in Group I, and 91 in Group II. The correlation coefficient was higher with the Oximetrix catheter than with the Edwards one (r = 0.970 and 0.855 respectively; p less than 0.001). Moreover, the 24 h spontaneous drift of the former catheter was less than that of the latter (+3.3 +/- 3.1% vs. +9.3 +/- 7%, p less than 0.05). This study showed that a catheter with optic fibres emitting a light with three wavelengths is more accurate than one emitting only two for the measurement of changes in SVO2 in critically ill patients.

Adult↗

[Monitoring of mixed venous oxygen saturation in aortic surgery: value and limits].

This study aimed to determine perioperative changes in mixed venous oxygen saturation (SvO2) in patients undergoing aortic surgery. Continuous SvO2 monitoring was carried out using an Oximetrix pulmonary catheter. Fourteen patients were randomly assigned to 2 groups, group I (n = 7) patients being given a thoracic epidural anaesthetic with a supplementary general anaesthetic, and group II (n = 7) a general anaesthetic as usual. In both groups, SvO2 increased at induction. In group I patients, SvO2 decreased during surgery to less than 60% (n = 2) and less than 70% (n = 4). This fall was corrected by volume loading and intravenous ephedrine. The intraoperative decrease in SvO2 occuring in 2 group II patients was due to a fall in haematocrit in one, and a propranolol infusion in the other. Although patients in group I were all extubated early after the end of surgery (85 +/- 35 min), the lowest value of SvO2 after extubation was always greater than 60%. Patients undergoing aortic surgery under thoracic epidural anaesthesia can be extubated early, without markedly depressing peripheral reserves in oxygen extraction.

Anesthesia, Epidural↗

[Factors influencing mixed venous oxygen saturation in intensive care].

Changes in mixed venous blood oxygen saturation (SvO2) were studied in 2 groups of patients. Group I patients (n = 10) were all hypoxaemic, suffering from acute respiratory failure, requiring that FIO2 be maintained at 1 throughout the study; respiratory and haemodynamic conditions were improved using PEEP and cardiovascular support. On the other hand, Group II patients (n = 13) were non-hypoxaemic patients with circulatory shock in whom FIO2 was gradually increased, and the haemodynamic status was improved using positive inotropic drugs (dopamine, dobutamine, adrenaline, amrinone). All 23 patients had a Swan-Ganz catheter set up for monitoring; all the usual haemodynamic and respiratory parameters were measured. Haematocrit values were kept at the same level throughout the study. Haemodynamic parameters were measured each time a new therapeutic procedure was carried out. No close relationship between SvO2 changes and changes in cardiac index or O2 consumption were found. However, a close relationship existed between changes in SvO2 and changes in O2 extraction (EAO2): SvO2 = -EAO2 + 102 (Group I; r = 0.90, n = 54); SvO2 = -1.2 EAO2 + 103 (Group II; r = 0.93, n = 66). A strong relationship was also found between changes in SvO2 and in FIO2 in each patient of Group II. In the complicated physiological set-up of an intensive care patient, SvO2 reflects oxygen extraction. A fall in SvO2 is related to an altered oxygen demand: oxygen supply ratio. In the most seriously ill patients, there is no relationship between changes in SvO2 and cardiac index.

Adult↗

Changes in ventilation, oxygen uptake, and carbon dioxide output during recovery from isoflurane anesthesia.

Recovery from inhalation anesthesia is often marked by the occurrence of postoperative tremor that resembles shivering, which is known to be associated with an increase in oxygen uptake (VO2), CO2 output (VCO2), and minute ventilation (VE). This study determined the time course of the ventilatory changes observed during the first hour of recovery from isoflurane anesthesia. Ten patients (ASA PS 1) scheduled for minor orthopedic surgery (knee arthroscopy) were included in this study. Anesthesia was induced with thiopental (5 mg/kg) and maintained with 70% N2O and isoflurane (1-2%) in oxygen, allowing spontaneous ventilation. In the recovery room, after N2O had been discontinued, patients were connected to a Beckman Metabolic measurement cart, which allowed a continuous monitoring of VE, VO2, VCO2, and PETCO2. Postoperative tremor was observed in all patients within 7.1 +/- 1.2 min (mean +/- SEM) after isoflurane discontinuation and was associated with a marked increase in the following: VO2, from 173 +/- 26 ml/min at the end of anesthesia to 457 +/- 88 ml/min; VCO2, from 149 +/- 18 ml/min at the end of anesthesia to 573 +/- 98 ml/min; and VE, from 6.8 +/- 0.7 l/min at the end of anesthesia to 16.6 +/- 2.8 l/min (values obtained 20 min after isoflurane discontinuation). In three patients during intense shivering, VO2, VCO2, and VE reached peak values higher than 800 ml/min, 1,300 ml/min and 30 l/min, respectively. This study shows that postoperative tremor following isoflurane anesthesia may be associated with prolonged and large increases in oxygen uptake, CO2 output, and minute ventilation.

Adolescent↗

Anesthesia for creation of a forearm fistula in patients with endstage renal failure.

The effects of local infiltration anesthesia, brachial plexus blockade, isoflurane, or halothane anesthesia on blood flow through the brachial artery and through a newly created forearm arteriovenous fistula (AVF) were compared in 36 patients with endstage renal failure. Brachial artery blood flow was measured at two different times, before anesthesia and during anesthesia but before surgery, using a pulsed Doppler flowmeter. AVF flows were calculated from brachial, radial, and ulnar blood flows at the end of surgery, 2 h after surgery, and 3 and 10 days after the procedure. Mean arterial pressure was lower in patients receiving isoflurane or halothane than in those receiving local anesthesia or brachial plexus blockade (BPB). There was a significant increase in brachial artery blood flow following BPB (43.7 +/- 18.7 to 186.9 +/- 98.2 ml.min-1) during isoflurane anesthesia (46.2 +/- 15.9 to 153.1 +/- 80.5 ml.min-1) and during halothane anesthesia (49.9 +/- 24.1 to 97.6 +/- 62.1 ml.min-1). During anesthesia, the difference in brachial artery blood flow between patients in the BPB and halothane groups was significant. Local anesthesia failed to increase brachial artery blood flow (44.0 +/- 12.7 to 45.6 +/- 11.3 ml.min-1). In the immediate postoperative period, the AVF blood flow was lower in patients in the halothane group than in the other groups, but this difference was only significant when compared with BPB group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Inotropic effect of ketamine on rat cardiac papillary muscle.

The direct effect of ketamine on cardiac muscle was studied using rat left ventricular papillary muscle. At an extracellular calcium concentration [( Ca++]0) of 2.5 mM, rat myocardial contractility is nearly maximum, and a positive inotropic effect was demonstrated by an increase in maximum shortening velocity (Vmax) with ketamine at 10(-5) M but not 10(-4) M. At a [Ca++]0 of 0.5 mM, ketamine 10(-5) and 10(-4) M had a positive inotropic effect as shown by an increase in Vmax (135% +/- 22% and 147% +/- 33%, respectively) and in isometric active force (AF/s) (120% +/- 10% and 152% +/- 44%, respectively). The positive inotropic effect of ketamine was not related to catecholamine uptake inhibition and/or alpha/beta receptor stimulation because it persisted after phentolamine and propranolol and because ketamine had no relaxing effect. Ketamine 10(-5) and 10(-4) M impaired isotonic relaxation, contraction-relaxation coupling under low loading conditions, and the load sensitivity of relaxation, which suggests impairment of the calcium sequestering systems, especially the sarcoplasmic reticulum (SR). Ketamine modified postrest recovery: the first beat (B1) after a 1-min rest period was decreased by ketamine 10(-4) M but not ketamine 10(-5) M. Moreover, the beat-to-beat postrest recovery has been demonstrated to be exponential, and tau, the time constant of the decay was increased by ketamine 10(-4) M (5.4 +/- 0.3 vs. 3.9 +/- 0.2 beats) but not by ketamine 10(-5) M (3.4 +/- 0.4 vs. 3.7 +/- 0.2 beats). These effects on postrest recovery suggest that ketamine impairs SR function. The authors suggest that ketamine had a dual action on rat myocardium: a positive inotropic effect without any relaxing effect, probably related to an increase in calcium influx, and an impairment of SR function. Nevertheless, impairment of SR is only significant at high concentration (10(-4) M) and might overcome the positive inotropic effect only at supratherapeutic concentration.

Animals↗

A prospective study of protected bronchoalveolar lavage in the diagnosis of nosocomial pneumonia.

The value of a new technique of protected bronchoalveolar lavage not requiring bronchoscopy was prospectively evaluated for the diagnosis of nosocomial pneumonia in two groups of critically ill patients. The control group was comprised of 29 patients free of any pulmonary disease whose lungs were ventilated for a mean time of 14 +/- 9 days (mean +/- SD). The pneumonia group was comprised of 30 patients with histologically proven nosocomial pneumonia whose lungs were ventilated for a mean time of 11 +/- 8 days. All patients of the pneumonia group died, and postmortem lung biopsies were taken for bacteriologic and pathologic examination. Twice a week in the control group or within the day preceding death in the pneumonia group, distal bronchial samples were obtained by a technique of protected bronchoalveolar lavage performed at the bedside. Fifty-one distal bronchial samples were bacteriologically analyzed in the control group and 30 in the pneumonia group. The sensitivity of a positive protected bronchoalveolar lavage for diagnosing nosocomial pneumonia was 80%, whereas the specificity was 66%. In 73% of the patients of the pneumonia group, the microorganisms isolated in the protected bronchoalveolar lavage and in the lung culture were partially (16%) or completely in agreement (57%). Among the 43 microorganisms isolated in the lung cultures, 74% were recovered by the protected bronchoalveolar lavage technique. This study shows that the protected bronchoalveolar lavage is an accurate technique for the diagnosis of nosocomial pneumonia. Because the technique is simple, noninvasive, easily repeatable at the bedside, and enables gram staining, it represents an attractive alternative to the fiberoptic bronchoscopy technique using a plugged double-sheathed brush.

Biopsy↗

Respiratory effects of the Jarvik-7 artificial heart.

In five anesthetized patients with a Jarvik-7 artificial heart, pulmonary volume displacements generated by cardiogenic oscillations were measured using an indirect spirometric method. Consequences on gas exchange were also evaluated during a 15-min period of apnea by use of a tracheal insufflation of pure O2 at a constant flow rate of 20 l/min. The Jarvik-7 artificial heart generated a mean pulmonary volume displacement of 105 +/- 29 (SD) ml/heart beat. After 15 min of apnea, arterial PCO2 (PaCO2) significantly increased from 29 +/- 5 to 47 +/- 6 (SD) Torr. PaCO2 increased by 0.8 Torr/min from the 5th to the 15th min of apnea. Mean arterial PO2, mean pulmonary shunt, mean O2 consumption, and mean metabolic production of CO2 did not change significantly during the apnea period. Because cardiac output was kept constant during the study, O2 transport was adequately maintained throughout the apnea period. In patient 1, where the period of apnea was continued for 60 min, PaCO2 progressively increased until the 45th min and then remained stable at 61 Torr during the last 15 min of apnea. This "plateau" corresponded to an alveolar ventilation of 3,907 ml/min, representing 69% of the alveolar ventilation calculated during conventional mechanical ventilation. In conclusion, the Jarvik-7 artificial heart provides a potent respiratory support through the cardiogenic oscillations it generates.

Adult↗