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Biomedical subjects

M Tariq

Publications and source records attributed to M Tariq.

138 records · Page 8Linked to original sources
PubMedDate not supplied

Tolerance to beta,beta'-iminodipropionitrile (IDPN)-induced neurobehavioural and vestibular toxicity in diabetic rats.

The present investigation was undertaken to study the neurotoxic effects of beta,beta'-iminodipropionitrile (IDPN) in normal, diabetic and insulin-treated diabetic rats. Sprague-Dawley male rats were divided into five groups: control, IDPN, diabetes, diabetes plus IDPN and diabetes plus insulin plus IDPN. The diabetes was induced with a single i.p. injection of streptozotocin (50 mg kg(-1)). One month after the induction of diabetes, the rats were treated with IDPN (100 mg kg(-1), i.p.) daily for 11 days. One of the diabetic groups treated with IDPN also received daily injection of insulin (25 U kg(-1), s.c.), 1 h before IDPN. The rats were observed daily for abnormal head movements and circling. The grip strength of the forelimbs was also measured. In the IDPN group the dyskinetic symptoms appeared on the 8th day, whereas the onset of dyskinesia was on the 12th day in IDPN-treated diabetic rats. The incidence and severity of dyskinesia were significantly higher in IDPN-treated normal (non-diabetic) rats as compared to IDPN-treated diabetic rats. The treatment of diabetic rats with insulin normalized striatal dopamine (DA) turnover but partially reversed diabetes-induced protection against IDPN dyskinesia. There was severe degeneration of sensory hair cells in crista ampullaris of IDPN-treated normal rats, whereas the diabetic rats showed significant protection against IDPN-induced vestibular hair cell degeneration. In conclusion, our study clearly demonstrates that diabetic rats are resistant to IDPN-induced neurobehavioural and vestibular toxicity. The results also show that diabetes-induced protection against IDPN-induced dyskinesia can be partially reversed by insulin. The mechanism behind the decreased vulnerability of diabetic animals to IDPN remains to be resolved. Further studies are warranted to investigate this paradoxical phenomenon.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Effect of Salvia haematodes on sexual behaviour of male rats.

The effect of an ethanolic extract of Salvia haematodes roots was studied on the sexual behaviour of male rats. In the initial experiments, male sexual responses were assessed by recording penile erection, licking and grooming of genitals and copulatory movement in absence of females. In the second set, copulatory behaviour was observed by caging males with a receptive female brought into estrus with s.c. injection of estradiol benzoate and progesterone. The frequencies of mounting and intromission and latency of the ejaculation were recorded. The results show that the extract (500 mg/kg, orally) produced a significant increase in episodes of penile erection. The drug was found to enhance the orientation of males towards the female by increased anogenital investigatory behaviour and enhanced licking and grooming of the genitals. The extract also increased the ejaculation latency. These findings support the folk use of this plant as aphrodisiac and for the treatment of premature ejaculation.

Animals↗
PubMedDate not supplied

Proglumide, a cholecystokinin receptor antagonist, exacerbates beta, beta'-iminodipropionitrile-induced dyskinetic syndrome in rats.

The present investigation was undertaken to study the effect of proglumide, a cholecystokinin (CCK) receptor antagonist, on iminodipropionitrile (IDPN)-induced excitation, chorea, and circling (ECC) syndrome in rats. The animals were exposed to IDPN in the dose of 100 mg/kg/day IP for 9 days. Proglumide (PG) was administered IP daily 1 h before IDPN in the doses of 250, 500, and 750 mg/kg body weight in three different groups of rats. The animals were observed daily for neurobehavioral abnormalities including dyskinetic head movements, circling, tail hanging, air righting reflex, locomotor activity, and contact inhibition of the righting reflex. After behavioral studies, blood and brain samples were collected for the analysis of malondialdehyde (MDA), conjugated dienes, vitamin E, and glutathione peroxidase (GSH-Px). The temporal bones were also collected for inner ear histopathology. Our results showed that proglumide significantly and dose-dependently exacerbated the incidence and the severity of IDPN-induced ECC syndrome during the treatment period as well as up to 3 weeks of postdosing. Administration of IDPN produced a significant increase in MDA and conjugated dienes and a decrease in vitamin E and GSH-Px, suggesting the role of oxygen-derived free radicals (ODFR) in IDPN-induced neurotoxicity. Concomitant treatment with proglumide potentiated IDPN-induced oxidative stress. The histopathology of the inner ear showed significantly high degeneration of sensory hair cells in the crista ampullaris of the rats treated with IDPN plus proglumide compared to IDPN-alone-treated animals. Further studies are warranted to determine the role of CCK in nitrile toxicity and drug-induced dyskinesia.

Animals↗
PubMedDate not supplied

Attenuation of acrylamide-induced neurotoxicity in diabetic rats.

In recent years, an increasing number of cases of neuropathy have been reported as a result of accidental or occupational exposure to chemicals. Acrylamide (Acr), a widely used industrial chemical, is known to produce peripheral neuropathy that resembles diabetic neuropathy in many ways. However, the interaction between diabetes and Acr has not been studied. The present study was undertaken to examine the effect of streptozotocin (STZ)-induced diabetes on Acr-induced neurotoxicity in rats. Male Sprague-Dawley rats weighing 300 +/- 10 g were divided into four groups of 10 animals each. The rats in group 1 served as control, and received normal saline. The animals in group 2 were given Acr dissolved in physiological saline (50 mg/kg IP 3 days/week) for 2 weeks. The rats in group 3 and 4 were made diabetic by administering a single IP injection of STZ (50 mg/kg). The animals in group 3 served as diabetic control, whereas the rats in group 4 received Acr in the same dose regimen as in group 2, a week after induction of diabetes. Neurobehavioral responses including foot print length, hind limb function, landing foot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. The animals were then sacrificed, and sciatic nerves were collected for biochemical analysis. The results of this study clearly showed a significant deterioration of neurobehavioral and electrophysiological responses in Acr-treated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was significantly reduced in diabetic animals. However, the difference in electrophysiological response in Acr-treated diabetic and nondiabetic rats was not found to be statistically significant (p 0.05). The precise mechanism by which Acr induced neurobehavioral toxicity is reduced in diabetic animals warrants further investigations.

Acrylamide↗
PubMedDate not supplied

Exacerbation of iminodipropionitrile-induced behavioral toxicity, oxidative stress, and vestibular hair cell degeneration by gentamicin in rats.

This study describes the effect of gentamicin, an aminoglycoside antibiotic on iminodipropionitrile (IDPN)-induced abnormal neurobehavioral syndrome in female Sprague-Dawley rats. The animals were exposed to IDPN in the dose of 100 mg/kg/day intraperitoneally for 7 days. Gentamicin (GM) was administered intraperitoneally daily 1 h before IDPN in the doses of 10, 40, and 80 mg/kg body weight in three different groups of rats. One more group of animals received gentamicin alone (80 mg/kg) and served as the gentamicin-alone group. The intensity of IDPN induced characteristic excitation with choreiform, and the circling movement (ECC) syndrome was examined using an observational test battery including dyskinetic head movements, circling, tail hanging, air righting reflex, and contact inhibition of the righting reflex on days 6, 8, 10, 12, 19, 26, and 33. The animals for histopathological observation were sacrificed on day 10, whereas the remaining animals that were used for long-term behavioral studies were sacrificed on day 35 for biochemical observations. The blood and brain samples were collected for the analysis of blood urea nitrogen (BUN), serum creatinine, cerebral malondialdehyde (MDA), conjugated dienes, and lipid hydroperoxides, whereas temporal bones were collected for inner ear histopathology. Our results showed that gentamicin significantly and dose dependently exacerbated the incidence and the severity of the IDPN-induced behavioral syndrome. The histopathology of the inner ear demonstrated more severe loss of sensory hair cells in the crista ampullaris of the rats treated with IDPN plus gentamicin compared to the IDPN-alone treated animals. Concomitant treatment with gentamicin also potentiated IDPN-induced increase in free radical indices, suggesting a possible role of oxidative stress in gentamicin-induced aggravation of IDPN toxicity. Further studies are warranted to determine the role of aminoglycosides in nitrile toxicity and drug-induced movement disorders.

Animals↗
PubMedDate not supplied

Effect of nicotine and alcohol pretreatment on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats.

The effect of nicotine and alcohol pretreatment by feeding nicotine (2.5 mg/100 ml), alcohol (25%, v/v) and their combination (nicotine 2.5 mg/100 ml + alcohol 25%, v/v) in drinking water ad libitum for 21 days was studied on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats. When given alone, neither nicotine nor alcohol produced any visibly discernible gastric lesions. Their concurrent administration, however, produced minor injury to the gastric mucosa appearing as 5-7 circular ulcers of less than 1 mm in diameter. Pretreatment with nicotine, alcohol, and their combination resulted in the significant augmentation of gastric ulcers produced by aspirin, phenylbutazone, and reserpine. The augmentation of gastric lesions in the group pretreated with the combination of nicotine and alcohol was significantly greater than in the groups treated by either of them alone. The effect of nicotine on the mucus neck cell population of the gastric mucosa and pancreatic bicarbonate secretion, and the gastric mucosal damaging effect of chronic alcohol treatment may be responsible for the potentiation of ulcerogenic effects of aspirin, phenylbutazone, and reserpine.

Animals↗
PubMedDate not supplied

Emergency coronary stenting for complete thrombotic occlusion of an unprotected left main coronary artery in acute myocardial infarction complicated by cardiogenic shock in an octogenarian patient--a case report.

This report concerns an 82-year-old white man, who was admitted with cardiogenic shock secondary to an acute anterior myocardial infarction with right bundle branch block requiring an intra-aortic balloon pump for hemodynamic support and mechanical ventilatory support for respiratory distress. An immediate cardiac catheterization with coronary angiography revealed a complete thrombotic occlusion of the left main coronary artery. Prompt stent-supported percutaneous transluminal coronary angioplasty to the occluded left main coronary artery, a critical stenosis of the ostial left anterior descending artery, and the left circumflex coronary artery, allowed for recovery from this life-threatening condition and subsequent discharge from the hospital of this octogenarian patient. It is suggested that in a critical clinical condition with particularly challenging coronary anatomical findings, stent-supported coronary angioplasty can be lifesaving treatment in selected patients with octogenarian status with acute myocardial infarction.

Aged↗
PubMedDate not supplied

Effect of physical fitness on myocardial damage and circulation after myocardial necrosis.

The effect of physical training (conditioning) on myocardial circulation and myocardial damage has been evaluated in experimental myocardial necrosis in albino rats. Conditioning was done by making the animals swim in a tank of water, thermostatically controlled at 32 degrees +/- 1 degrees C, 60 minutes daily, six days a week, for eight weeks. Myocardial necrosis was produced by subcutaneous injection of isoproterenol, 85 mg/kg body weight, on two consecutive days. Investigations included ECG (lead II), SGOT, SGPT, SLDH, SCPK, histopathology of the heart, and myocardial Rubidium 84 uptake. It was observed that, in conditioned animals, elevation of serum enzymes was less, incidence of cardiac arrhythmia was lower, myocardial damage was less marked, and myocardial circulation was better after myocardial necrosis in comparison to unconditioned animals. Less myocardial damage and lower incidence of cardiac of cardiac arrhythmia are presumably associated with a better prognosis.

Animals↗
PubMedDate not supplied

A foreign body in the bronchus still presents problems.

Aspiration of a foreign body in young children is rare but can still cause considerable morbidity and mortality. The case of a 5 1/2-month-old infant with aspiration of a piece of apple is presented, together with a review of the literature.

Airway Obstruction↗
PubMedDate not supplied

Effect of (+-)-propranolol and clonidine on stress- and chemically induced gastric ulcers in rats.

The influence of (+-)-propranolol and clonidine on stress- and various chemically induced gastric ulcers in rats, together with their influence on various biochemical parameters which affect the development of the induced ulcers, was examined. Pretreatment of rats with (+-)-propranolol (10-100 mg/kg) and with clonidine (0.03-0.3 mg/kg) given orally, significantly reduced indomethacin- (30 mg/kg, orally) and reserpine- (5 mg/kg, i.p.) induced ulcers. In addition, propranolol pretreatment significantly reduced ethanol- and cold-stress-induced ulcers, whereas pretreatment with orally given clonidine significantly enhanced these ulcers. Pretreatment with propranolol significantly increased gastric mucus synthesis and the nonprotein sulfhydryl content and reduced gastric lipid peroxidation without affecting gastric acid secretion. Pretreatment of the animals with clonidine significantly increased gastric mucus secretion and decreased total gastric acidity. It did not affect the gastric nonprotein sulfhydryl content and lipid peroxidation. The drug-induced effects on the experimentally induced ulcers may be related to their induced biochemical alteration in the gastric parameters measured.

Animals↗