Biomedical subjects
Publications and source records attributed to P Bonnet.
A retrospective study was carried out in 58 patients operated between 1978 and 1983 for cancer of larynx of glottic origin and mainly T1 and T2. Functional results were always of good quality, and the recurrence rate significantly lowered by the use of the Majer-Piquet or C.H.E.P. procedure when compared with results after thyroidectomy. A simplified technique is proposed.
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Liver damage resulting from 4 h exposure to bromobenzene (BB) (146-957 ppm) and 1,2-dichlorobenzene (DCB) (245-739 ppm) as model toxicants was evaluated in rats. The modifications considered were the increases in serum glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SDH) activities and the decreases in centrolobular liver-cell glucose-6-phosphatase (G6-Pase) staining intensity. A linear inverse relationship was established between the logarithmic values of blood enzyme activities and liver G6-Pase staining intensity. In addition, the levels of exposure to each test chemical were found to be linearly related to liver G6-Pase staining intensity and to the logarithmic values of blood enzyme activities.
In male Sprague-Dawley rats, motor and sensory conduction velocities (MNCV and SNCV) of the tail nerve decreased significantly as a result of oral administration of 400 and 200 mg/kg of 2,5 hexanedione (2,5-HD) once daily, 5 days a week for up to 7 and 15 weeks, respectively; and of whole-body exposure to 300 ppm of vinyltoluene for 6 h daily, 5 days a week for up to 21 weeks. Exposure to 100 ppm of vinyltoluene did not cause any significant impairment of tail nerve function throughout the 21-week exposure period. Significant changes in MNCV and SNCV were consistently observed from weeks 4 and 2, respectively, in 2,5-HD-treated rats. Changes resulting from exposure to 300 ppm of vinyltoluene were reported intermittently from week 15. Significant linear relationships were established between the length of treatment with 2,5-HD, length of exposure to 300 ppm of vinyltoluene, and the extent of impairment of tail nerve function. Structural damage to the sciatic nerves was only seen in 2,5-HD-treated rats. It is concluded that vinyltoluene can be regarded as an airborne chemical which leads to the development of a borderline experimental neuropathy at a level of 300 ppm.
Three groups of 10 male Sprague-Dawley rats were exposed daily, 5 days a week for 25 weeks, either to 500 ppm carbon disulfide (CS2), 50 ppm hydrogen sulfide (H2S), or to both of them as a mixture and were periodically examined for sensory and motor tail nerve conduction velocity (SNCV, MNCV). A concomitant control group of 10 rats was used. In addition, rats exposed to 500 ppm CS2, and those simultaneously exposed to 500 ppm CS2 and 50 ppm H2S, were twice examined for 24-h urine excretion of 2-thio-thiazolidine-4-carboxylic acid (TTCA) in the course of the experimental period. Simultaneous exposure to CS2 and H2S had no significant interactive effect on nerve conduction velocities. A significant time-dependent slowing down of MNCV and SNCV occurred as the result of chronic exposure to CS2, including exposure to 500 ppm CS2 and to the mixture of 500 ppm CS2 and 50 ppm H2S, but did not occur after chronic exposure to 50 ppm H2S. With combined exposure to 500 ppm CS2 and 50 ppm H2S, the quantity of TTCA excreted in 24-h urine was not significantly different from that occurring in response to CS2 exposure alone. On the basis of these results it is suggested that chronic exposure to H2S would neither influence CS2-induced peripheral nerve toxicity nor obscure the interpretation of the measurement of urinary TTCA as a biological indicator of CS2 exposure.
Nine patients with Budd-Chiari syndrome (BCS) were treated by a portal systemic shunt. One had thrombosis of the superior mesenteric vein (SMV) and another had complete obstruction of the retrohepatic inferior vena cava (IVC). All other patients had a marked stenosis of the retrohepatic IVC with caval pressure ranging from 12 to 24 mmHg (mean: 17 mmHg). Seven patients had an interposition mesocaval shunt using an autologous jugular vein. The patient with a thrombosed SMV had a portoatrial shunt. The patient with an obstructed IVC had a cavoatrial shunt after an erroneous portacaval shunt had failed to relieve ascites. There were no operative deaths and no major postoperative complications. One patient died 19 months after operation of acute leukemia complicating polycythemia rubra vera. All other patients were alive and well 8 months to 6 years after operation. None of them had encephalopathy. These results suggest several comments: Portal systemic shunts are a good treatment for BCS and have a low operative risk. The mesocaval shunt is an efficient procedure, even when there is stenosis of the IVC with high caval pressure; shunts to the right atrium should be performed only in the case of complete obstruction or inaccessibility of the IVC. The long-term prognosis is excellent, except in patients with potential malignancies. Therefore, portal systemic shunts should be indicated early in patients with symptomatic BCS.
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The authors report 16 cases of tibia vara in children. They insist on: the difficult diagnosis of that pathology at the beginning, the early surgery (simple osteotomy) give a complete restoration, in neglected cases they recommend to elevate the medial condyle of the tibia with bone grafting, a tibial osteotomy and an epiphysiodesis of the lateral tibial condyle and proximal fibula.
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A limited liver resection was performed in two patients with cirrhosis and a hepatocellular carcinoma situated in segment VIII (anterosuperior subsegment of the right lobe). One of the patient had previously bled from esophageal varices. Resection of segment VIII was performed following the anatomical planes of section after complete mobilization of the right lobe of the liver. Both patients were alive and free of recurrence 14 and 30 months after surgery. Hepatocellular carcinomas are thus treatable by limited anatomic liver resection even when they are situated in the vicinity of the major hepatic veins and the vena cava.
Investigation in 16 patients attending the stomatology outpatients clinic over the last 18 years has enabled definition of a particular radioclinical entity that has been named "idiopathic bilateral salivary megacanal". This generally parotid affection occurs in patients between 50 and 60 years, the onset usually being by an episode of sialodochitis. In addition to these inflammatory attacks there is the persistence of a bilateral "salivary ejaculation" from the ostia of the principal glands, sometimes after manual expression of a mucoid plug. Sialography shows dilatation of canals, the appearance being very suggestive for Stensen's duct, which becomes sinuous, enrolled and segmented. Dilatation is bilateral and affects the total length of the duct. The problem arises as to whether etiopathogenicity is from parietal canalar dysplasia or a constitutional anomaly of the nerve plexus comparable with that described in congenital megacolon. The latter hypothesis is plausible but requires confirmation from histopathology. The always benign course of the disease justifies conservative therapy only: oral antibiotics and canal massage several times a day, with a neostomy only when absolutely necessary.
Bepridil is a molecule which, apart from its anti-anginal properties, also has antiarrhythmic effects due to its calcium antagonist action which depresses antero and retrograde AV conduction in the physiological pathways. Conduction in accessory AV pathways is also depressed to a lesser and more variable extent. It also has an anti-ventricular arrhythmic action probably due to an associated membrane-stabilising effect. This drug was used intravenously to treat attacks of reciprocating supra-ventricular tachycardia (SVT) (60 p. 100 conversion to sinus rhythm: 6 out of 10 cases of intra-nodal reentry, 6 out of 10 cases of reentry via an accessory pathway) and also in ventricular tachycardia (VT) (7 conversions in 15 patients within 2 to 9 minutes). It was impossible to induce attacks of SVT after administering the drug in about a third of patients; better results were obtained in intra-nodal SVT (5 cases of effective prevention out of 10) than in SVT involving an accessory pathway (1 case out of 10). It was not possible to reinitiate VT after treatment in 3 out of 6 cases (very aggressive pacing methods, a long QT interval and accelerated idio-ventricular rhythm were responsible for the failures). Oral therapy (400 to 800 mg, usually 600 mg daily in 3 doses) prevented any recurrence of SVT in over half the patients (prevention of intranodal SVT: 80 p. 100; prevention of SVT involving an accessory pathway: 13 p. 100) and in 4 out of 6 patients with VT. Provocative pacing studies after intravenous or oral bepridil provide a good indication of long-term efficacy. The drug is generally well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
Flecainide, a new Vaughan-Williams Class Ic anti-arrhythmic agent, was used in 21 patients with an accessory AV conduction pathway which was apparent in 16 cases (WPW syndrome), latent in 1 case and concealed in 4 cases (block in the anterograde direction). Seventeen patients had spontaneous and inducible arrhythmias; 13 supraventricular tachycardias (SVT) due to orthodromic reentry including the accessory AV pathway and 4 atrial arrhythmias. Intravenous flecainide (2 mg/kg over 5 minute period) terminated the 13 cases of SVT in an average of 3 minutes by depressing then blocking retrograde conduction in the accessory pathway and 3 out of 4 cases of atrial arrhythmias. Conduction in the accessory pathway was blocked in the anterograde direction in 75% of cases and depressed in the rest; it was blocked in the retrograde direction in about half the cases and depressed in the rest. Intravenous flecainide completely prevented the induction or arrhythmias in 13 out of 17 patients (76%). Oral flecainide blocked the accessory pathway in the anterograde direction in 68.7%, and in the retrograde direction in 62% of patients, and prevented arrhythmias during provocative testing in 82% of patients (14 out of 17). With an average follow-up of 20.7 +/- 2.6 months with oral doses adapted to body weight and to the response to IV flecainide only one recurrence of atrial fibrillation was observed, a 100% prevention of spontaneous SVT and 94% prevention of all arrhythmias (16 out of 17 cases). The predictive value for the response to oral therapy of the tests of regularisation of SVT by IV flecainide and of the tests of non-provocation of SVT with oral or IV flecainide was excellent (100%). The cardiac tolerance was very good in these 21 patients (17 of whom had no valvular or myocardial lesion). There were 6 minor cases of general intolerance to oral therapy which were not dose related, only 1 of which required interruption of therapy. Flecainide appears one of the best choices for the treatment of preexcitation syndromes and their related arrhythmias at the present time.
Bioassays of prostacyclin by inhibition of velocity and maximum of both irreversible and biphasic platelet aggregation, and by relaxation of the potassium-contracted isolated superfused rabbit coeliac artery have been undertaken. The use of each parameter is possible within a range of PGI2 concentrations, which have been determined for each of the five parameters studied. The optimal concentrations of PGI2 for a bioassay have also been determined, corresponding to each range.
A decrease in respiratory rate resulting from irritation of upper airways and a decrease in duration of immobility in a 'behavioural despair' swimming test occurred in mice during and following short-term inhalation exposures to some commonly used aliphatic ketones. Linear concentration-effect relationships were obtained that allowed two different median active levels (MALs) to be calculated. MALs that produced a 50% decrease in respiratory rate (RD50) were calculated as indicators of the sensory irritation potency of diisobutyl ketone, mesityl oxide, methyl amyl ketone, methyl isoamyl ketone and methyl propyl ketone. MALs that produced a 50% decrease in immobility (ID50) were determined for acetone, isophorone, mesityl oxide, methyl amyl ketone, methyl isoamyl ketone, methyl isobutyl ketone and methyl propyl ketone. The systematic determination of MALs permits classification of ketones in terms of their relative potencies for eliciting a given effect. The lowest MAL indicates the primary manifestation of toxicity, against which protection should be taken. MALs associated with such critical responses may be useful in the establishment of safe levels of occupational exposure to ketones, a conclusion supported by the linear relationship that was found to exist between MALs and occupational standards.
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