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Biomedical subjects

S H Gilani

Publications and source records attributed to S H Gilani.

35 records · Page 2Linked to original sources

Cardiac myopathies in neonatal lambs: histological and histochemical studies.

White muscle disease (WMD), a selenium-responsive cardiac myopathy in neonatal lambs has been described from southern Iran. 15 lambs in terminal condition were referred to our lab. All the lambs were observed with the affected hearts. The lambs examined were between the postnatal ages of 1 week and 3 months. Gross changes included chalky-white appearance of entire endocardium of right ventricle and subendocardial plaques in the interventricular septum and left ventricular wall. Histologically the affected myofibrils showed swelling, acidophilia, fragmentation, segmental and patchy myonecrosis, round muscle cell nuclei, loss of sarcoplasm and sarcolemmal collapse. Purkinje fibers were relatively unaffected. Histochemical studies including Von Kossa and other stains indicated marked deposition of calcium salts in the cytoplasm of the damaged myofibrils. Calcium salts appeared as uniform, fine granules in relation to individual fiber striations. It appears that rapid accumulation of calcium into the damaged cells possibly interferes with the mitochondrial activity. As mitochondria bind excessive calcium, their capacity to respire and phosphorylate is depressed thus causing myocardial necrosis. The cardiac myopathy noted in our investigation is probably due to selenium deficiency in the soil of southern Iran. When selenium was given, it resulted in the fast recovery of the affected neonatal lambs. Moreover, no further cases of this disease (WMD) were reported after such treatments.

Animals↗

Disposition of 14C-nicotine in the fertilized chick egg.

14C-Nicotine-HCl (4.5 mg) was injected into the air space of chick eggs after one day of incubation and the distribution of radioactivity measured on days 3, 5, 7 and 12. By day 3, 98% of the dose had passed from the air space into the egg, proper. The quantity of nicotine in the yolk was highest on day 3 (74% of dose) and decreased steadily until day 12 (52%). The quantity in the albumen increased from 16% on day 3 to a maximum on day 7 and remained constant at 34% until day 12. The embryo contained 0.03% of the nicotine on day 3, and this level increased to 5% by day 12. Nicotine in the allantois increased throughout the study period (0.01% on day 3 to 3% on day 12). Although only 5% of the dose was present in the embryo, the highest concentrations within these components of the embryo ranged from a minimum of 0.85 microng nicotine/mg dry wt in the heart to a maximum of 2.00 microng nicotine/mg dry wt in the carcass. These levels within the embryo were two to five times higher than the greatest concentrations in the yolk and albumen. The dynamics of nicotine passage from the air space into other components of the fertilized chick egg were clarified. Whereas the conventional expression of teratogenic doses of drugs in chick eggs (i.e., ppm of egg weight) assumes that the compound is distributed uniformly, this study indicates that such expressions are inaccurate.

Animals↗

The effect of propranolol upon chick embryo cardiogenesis.

The teratogenic effects of propranolol HCl on cardiac development were studied in chick embryos of days 3 and 4 of incubation. Propranolol was injected into the yolk sac at doses ranging from 0.05 to 0.6 mg per egg. All the treated and control embryos were examined on day 7. The LD50 for the embryos treated on the 3rd and 4th day was 0.15 and 0.35 mg per embryo, respectively. Cardiac anomalies such as aortic stenosis ventricular septal defects and common truncus arteriosus were observed. Other malformations included atrial septal defects, thin atrial wall and defects of the pulmonic, aortic and atrioventricular valves. The incidence of cardiac anomalies in the controls was very low. Propranolol was observed to slow the heart rate in the experimental embryos. It is suggested that slowing of heart rate at the early stages of heart development caused aberrant bloodstream flow patterns which probably resulted in the genesis of cardiac anomalies. The results of this study indicate that propranolol has teratogenic effects on chick embryo cardiogenesis.

Abnormalities, Drug-Induced↗

Nicotine effects on the acid mucopolysaccharide content of chick embryo cardiac jelly.

Histochemical studies were made on the developing chick embryo heart to determine the effects of nicotine on acid mucopolysaccharide content during the critical stages of the cardiac morphogenesis. Two-day old embryos were injected with the dosages of nicotine ranging from 1.5 to 3 mg per embryo. The embryos were studied on the 3rd and 4th days of incubation. For an evaluation of acid mucopolysaccharides, the staining procedures of Mowry (1958) and Saunders (1964) were employed. It was found that nicotine decreases the content of acid mucopolysaccharide in the developing cardiac jelly. In the control embryos, the cardiac tissues picked up very intense coloration. At lower dosages (Group A; 1.5 mg/egg), the staining response of the treated heart tissues containing acid mucopolysaccharides was moderate as compared to the control embryos. At higher dosages (Group B; 3 mg/egg), the cardiac tissues were faintly colored as compared to the embryos of Group A. It is possible that the cardiac lesions previously reported in the chick embryos following the administration of nicotine (Gilani, 1971) are due to the reduction of the amount of acid mucopolysaccharides in the developing cardiac jelly--a susceptible period of the genesis of heart.

Animals↗

Fine structural changes in embryonic chick heart ventricle induced by lead poisoning.

The embryonic chick heart ventricle of day 11 was studied electron microscopically to learn the structural changes that develop in lead poisoning. The chick embryos were administered with 0.015 mg/egg of lead acetate at day 2. The most pronounced changes observed in the ventricle were: malformed mitochondria, disorganized, short and scanty myofibrils and abundance of swollen vacuoles. The ultrastructure of the ventricle from the control chick embryos was normal. The most frequent change noted in the ventricular tissue was an alteration in the myofibrils. This study indicates that electron microscopic changes can be induced in the embryonic chick heart ventricle by lead poisoning.

Animals↗

Abnormal embryogenesis induced by thiopental.

The effects of thiopental on chick embryos were analyzed in the present study. Thiopental was dissolved in saline and injected into embryonating chicken eggs at doses ranging from 0.2 to 4.0 mg per egg. The injections were made into the air sacs of eggs after two to four days of incubation. Control eggs were injected with an equivalent volume of saline (0.1 ml per egg). In all 1080 chicken eggs were used for this study. All embryos were examined on day 7. The LD50 for eggs injected on days 2, 3 and 4 was 2.1, 1.9, and 4.1 mg per egg, respectively. The principal malformations observed were exencephaly, anencephaly, twisted limbs, twisted neck, microphthalmia, everted viscera, and hemorrhage above the left eye and in both cerebral hemispheres. The results of the present study indicate that thiopental has a tendency to cause malformations in the chick embryos tested.

Abnormalities, Drug-Induced↗

Teratogenicity of cytochalasin D in chick embryos.

The effects of cytochalasin D on chick embryos were analyzed in the present study. Cytochalasin D was dissolved in DMSO and injected into embryonating chicken eggs at dosages ranging from 0.001 to 0.014 mg per egg. The injections were made into the air sacs of eggs at days 0, 1, 2 and 3 of incubation. The volume of each injection was 0.1 ml per egg. In all, 864 chicken eggs were used for this study. All embryos were examined on day eleven. The following malformations were observed: exencephaly, microphthalmia, everted viscera, body hemorrhage, edema, anophthalmia and a reduced body size. The dose-response relationship was observed in all of the groups tested. The results of the present study indicate that cytochalasin D is embryolethal and has some tendency to cause malformations in the chick embryos tested.

Abnormalities, Drug-Induced↗