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Biomedical subjects

L Bertrix

Publications and source records attributed to L Bertrix.

At least 37 records · Page 2Linked to original sources
PubMed1987

[Coagulopathy and anemia caused by anticonvulsants].

Long-term antiepileptic polytherapy regularly induces some slight impairment of haemostasis without clinical manifestations, but serious clinical disorders may appear, even in the absence of over-dosage. In the case reported here the patient was undergoing surgery for correction of scoliosis. Preoperative laboratory tests only showed a slight decrease of fibrinogen and a moderate lengthening of thrombin time; there was no anaemia. Immediately after the incision a severe haemorrhagic syndrome occurred. It was treated with a massive transfusion and administration of some blood coagulation factors, but bleeding was so profuse that surgery was abandoned. Later, the patient developed acute thrombocytopenia, progressive decrease of Quick time and of plasma blood coagulation factors, and anaemia due to folate deficiency. Awareness of these disorders should lead to prophylactic measures.

Adolescent↗
PubMed1987

[Diaphragmatic hernia: the role of perioperative resuscitation].

Twenty-nine newborn infants with diaphragmatic hernia have been received in a neonatal intensive care unit over a seven year period. In three cases, clinical signs appeared after the first day: they all survived. Six infants died before surgery: five of them had major pulmonary hypoplasia. Surgery was performed in twenty cases: nine of these infants died. Death occurred during the first twelve post-surgical hours in six cases with major pulmonary hypoplasia. Fourteen infants were followed from 6 to 24 months; two developed post-anoxic hydrocephaly with poor neurological development in one case. A pH above 7.1 and an adequate hemodynamic status obtained before surgery are simple criteria of a good prognosis. When these criteria are not obtained, prognosis is poor as they are in favor of major pulmonary hypoplasia.

Hernia, Diaphragmatic↗
PubMed1987

Electrophysiological study in the dog of the risk of cardiac toxicity of bupivacaine.

The risk of toxic effects on the heart of bupivacaine following several kinds of locoregional anaesthesia has been investigated in the dog in situ heart by determining conduction time and effective refractory period in the various parts of the conduction system and the ventricular muscle, as well as the discharge rate of the sinus node. Bupivacaine, i.v. infused at 3 rates, 0.2, 0.3 and 0.4 mg X kg-1 X min-1, proved to have depressant effects on conduction, automatism and excitability. It slows down conduction in all the parts of the myocardium, considerably at high stimulation frequencies, but always much more in the His-Purkinje system and the ventricular contractile fibres than in the atrioventricular node, because it tends to block the sodium rather than the calcium or potassium channel. Its effect remain more moderate, indeed, on sinus automatism and atrial and mainly ventricular refractoriness. Its danger lies, therefore, in the inhibition of conduction, with atrioventricular or His bundle branch block, but more frequently reentrant arrhythmias, likely to result in ventricular fibrillation. However: these alterations are observed with very high plasma levels (about 4 to 9 micrograms X ml-1), much higher than usual peak concentrations following spinal anaesthesia (0.10 micrograms X ml-1) or even epidural anaesthesia or brachial plexus block (1.20 micrograms X ml-1); reversal of these alterations occurs rapidly (reduction by 50% within 30 min for instance), when they have not led to ventricular fibrillation or they have not been associated with circulatory collapse.

Action Potentials↗
PubMed1986

[Peranesthetic monitoring of ventilation in children: value of capnometry].

Continuous measurement of the end-expiratory partial pressure of carbon dioxide (PETCO2) during anaesthesia has been proposed for non-invasive monitoring of arterial PCO2 (PaCO2). The values and the stability of the difference (PaCO2-PETCO2) during anaesthesia were studied for two ventilatory settings in eight children with healthy lungs and normal cardiac function undergoing minor surgery. PaCO2 values were all within a physiological range (30.2-43.6 mmHg). PaCO2-PETCO2 values ranged from 0.2 to 9.9 mmHg. With either mode of ventilation, there was no significant variation in PaCO2-PETCO2. It is concluded that estimation of PaCO2 was reliable during anaesthesia when haemodynamic and ventilatory states were stable, but a first determination of the PaCO2-PETCO2 gradient remained necessary for each child.

Anesthesia, General↗
PubMed1986

Protection against ventricular and atrial fibrillation by sotalol.

Sotalol is not only a beta blocker but a class III antiarrhythmic drug. Its possible antifibrillatory activity was therefore investigated in both the ventricles and atria of dog heart in situ, since vulnerability to fibrillation is not the same in both these parts of the myocardium. Fibrillation threshold was measured concurrently with the duration and amplitude of monophasic action potential, the effective refractory period, the conduction time in the contractile fibres, and after fibrillation had been triggered the fibrillation rate. Variables were measured at 5 and 10 min after sotalol had been given intravenously in closed chest dogs in three doses (1, 1, and 2 mg X kg-1) at 15 min interval. Sotalol produced a rise in fibrillation threshold that occurred simultaneously with a prolongation in monophasic action potential duration and effective refractory period of the contractile fibres and a slowing in fibrillation rate, whereas conduction time was not affected. The changes appeared, however, to be less pronounced in the ventricles than in the atria, in which vulnerability to fibrillation, normally increased by vagal tone, had been previously enhanced by acetylcholine. Sotalol antagonised the changes due to acetylcholine. In both the atria and the ventricles the first dose (1 mg X kg-1), which produced plasma concentrations of approximately 2 micrograms X ml-1 10 min after injection, produced a submaximal effect. Nevertheless, subsequent administrations increased the beneficial effects but not in proportion to the dose and plasma concentrations.

Action Potentials↗
PubMed1985

Biphasic effect of a gradual rise in plasma calcium concentration on vulnerability to fibrillation.

The possible potentiation by a rise in plasma calcium concentration of the effects of acetylcholine (ACh) on the atrial myocardium was investigated, mainly with a view to define the increase in vulnerability to fibrillation by hypercalcaemia. The effective refractory period (ERP) of the atrial myocardium, the atrial fibrillation threshold (AFT) and the atrial fibrillation rate (AFR) were measured repeatedly before and during the intravenous infusion of calcium at the rates of 0.025, 0.050 and 0.100 mmol . kg-1 . min-1 in dogs whose heart was, in addition, submitted to a cholinergic influence. 1. As long as the rise in plasma calcium concentration did not reach 100% approximately, this influence was enhanced considerably: in particular, ACh shortened ERP and raised AFR to a much larger extent, so that it resulted in fibrillation with a minor electrical stimulation. 2. When the rise in plasma calcium concentration exceeded 100%, hypercalcaemia became inhibitory of the effects of ACh, with a reversal in the modification of all the parameters, AFT especially, and, finally, prevention or even conversion to sinus rhythm of fibrillation.

Acetylcholine↗
PubMed1985

Efficacy of disopyramide in comparison with verapamil and propranolol in the prevention of acetylcholine-induced atrial fibrillation in the dog.

The efficacy of verapamil and propranolol was studied in comparison with disopyramide on the atrial fibrillation experimentally induced in the dog heart in situ by electrical stimulation combined with intra-aortic injection of acetylcholine (ACh). After reducing the amplitude and duration of the monophasic action potential (MAP) and the duration of the effective refractory period (ERP) of the atrial contractile fibres, ACh lowered the fibrillation threshold (FT), and, when fibrillation had been elicited, it accelerated the fibrillation rate (FR). Verapamil and propranolol failed to prevent atrial fibrillation: they did not counteract any of the alterations in the electrophysiological properties of the atrial contractile fibres due to ACh. In contrast, disopyramide, at doses within the therapeutic range, prevented fibrillation. The fibrillation threshold, which fell from 50 mA to 1 mA in the presence of ACh, was restored to control values by disopyramide. Disopyramide also antagonized the reduction in amplitude of MAP caused by ACh before the triggering of fibrillation and the reductions by ACh of the durations of MAP and ERP. Disopyramide first slowed FR, in association with an increase in amplitude of fibrillation waves and a tendency to synchronous activity, and ultimately terminated the fibrillation.

Acetylcholine↗
PubMed1984

Potentiation by hypokalemia of the effects of acetylcholine on the canine heart in situ.

In the heart in situ of vagotomized dogs, atrioventricular conduction was studied by the His bundle potential recording, sinus rate continuously registered and the effective refractory period (ERP) of the atrial muscle measured by the extrastimulus method. The modifications induced by the acute lowering of plasma potassium concentration from 3.5 to 2.0 mmol/l obtained by hemodialysis appeared to be similar to those due to parasympathetic stimulation and the effects of hypokalemia and acetylcholine (ACh) on the atrioventricular (A-V) and sinoatrial nodes as well as on the atrial contractile tissue gave rise to potentiation. Intraaortically injected near coronary ostia in a dose lower than liminal dose, ACh enhanced to a large extent all the phenomena elicited by hypokalemia, since the variations respectively observed under the influence of hypokalemia alone and the combination of hypokalemia and ACh were as follows: lengthening of conduction time in the A-V node by 100 and 180%, reduction of sinus rate by 10 and 20%, shortening of the atrial ERP by 20 and 40%.

Acetylcholine↗
PubMed1983

Enhancement by Ca2+ ions of cholinergic effects on the canine heart in situ.

The effects of Ca2+ ions were studied on the canine heart in situ, submitted to vagal influence or not. In addition to heart rate, conduction time was determined separately in atrial muscle, atrioventricular node and His-Purkinje system by means of His bundle potential recording and the effective refractory period (ERP) measured in atrioventricular node, atrial and ventricular muscle according to the extrastimulus method. In the presence of acetylcholine (ACh) released by vagal endings, an increase in plasma calcium concentration from 2.40 to 4.12 mmol/l, acutely induced by the infusion of calcium chloride, elicits the following alterations: slowing down of sinus rate, lengthening of conduction time in atrioventricular node without change of this time in atrial muscle and His-Purkinje system, prolongation of atrioventricular node ERP, but notable decrease of atrial muscle ERP and slight decrease of ventricular muscle ERP. These effects are similar to those of ACh:Ca2+ ions probably enhance the responsiveness to ACh.

Acetylcholine↗
PubMed1983

Blockade by verapamil of cholinergic effects on atrial specialised tissue in the anaesthetised dog.

The effects of verapamil were studied in anaesthetised dogs administered dextromoramide intrathecally to provide background vagal tone. Measurements were made of spontaneous heart rate, and, in paced hearts, of conduction times in atrial muscle, the atrioventricular node (A-V node) and His-Purkinje system by means of His bundle potential recording. The effective refractory period (ERP) of A-V node was measured by the extrastimulus method. In atropinised and vagotomised animals, verapamil reduced sinus rate and increased A-V nodal conduction time. In dogs high vagal tone after dextromoramide, however, verapamil increased sinus rate and reduced A-V nodal ERP. After dextromoramide alone, A-V block was observed at an atrial pacing rate of 150 beats X min-1, but after verapamil 1:1 A-V conduction was restored. The decrease in conduction velocity in the A-V node due to ACh was neither attenuated nor enhanced by verapamil.

Acetylcholine↗
PubMed1983

Study of the ventricular antifibrillatory effects of calcium channel blocking agents in comparison with lidocaine on canine normal heart in situ.

The ventricular antifibrillatory effects of two calcium channel blocking agents have been studied by determining fibrillation threshold several times in the course of an experiment on dogs placed under total cardiopulmonary by-pass to avoid the impairment of the myocardium properties subsequent to the interruption of blood circulation. These drugs were used in therapeutic or even higher doses (verapamil 0.40 mg.kg-1, diltiazem 0.60 mg.kg-1). They failed to modify fibrillation threshold significantly, and did not influence fibrillation rate or the effective refractory period of contractile fibres. Lidocaine, on the contrary, under the same experimental conditions, induced a dose-dependent rise in fibrillation threshold of up to nearly 200%, correlated to a fall in fibrillation rate and a prolongation in effective refractory period.

Animals↗
PubMed1979

[Meconial peritonitis. Recordings about six observations. Diagnostic and prognostic value of calcifications. Therapeutic given off (author's transl)].

The authors report six cases of meconium peritonitis with intra-abdominal calcifications; surgical intervention was successful in four. In five patients, fibrocystic desease of pancreas was eliminated. Presenting this report, it is their intention to underline the good prognosis of calcifications which generally eliminate the meconium ileus.

Calcinosis↗
PubMedDate not supplied

Possible role of drug interactions in bupivacaine-induced problems related to intraventricular conduction disorders.

Clinically, bupivacaine has depressant effects on intraventricular conduction that may lead to serious atrioventricular blocks or reentrant arrhythmias at plasma levels below those required to produce these effects experimentally (2-3 micrograms/ml instead of 8-10 micrograms/ml). The difference could be due to drugs present in the blood at the time of regional anesthesia that similarly inhibit conduction. This hypothesis was examined in 30 anesthesized, closed-chest dogs by measuring conduction time in the ventricular contractile fibers as well as effective refractory period under pacing at a constant, relatively high (180 beats/minute) rate. Changes in sinus rate were limited, as well as changes in ventricular effective refractory period and blood pressure regardless of the drug tested. In contrast, cibenzoline, disopyramide, and propranolol increased conduction time and lengthened QRS duration. Clomipramine appeared to prolong conduction time and widen QRS only moderately in therapeutic doses, whereas verapamil did not manifest noticeable effects on conduction. Caution is therefore recommended in regional anesthesia with bupivacaine in subjects being treated with cardiovascular drugs, such as cibenzoline, disopyramide, and propranolol and their congeners, or even by tricyclic antidepressants.

Animals↗