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Biomedical subjects

M U Naidu

Publications and source records attributed to M U Naidu.

At least 19 recordsLinked to original sources
PubMed2000

Carvedilol: a beta blocker with antioxidant property protects against gentamicin-induced nephrotoxicity in rats.

Gentamicin is an antibiotic effective against gram negative infections, whose clinical use is limited by its nephrotoxicity. Since the pathogenesis of gentamicin-induced nephrotoxicity involves oxygen free radicals, the antioxidant carvedilol may protect against gentamicin-induced renal toxicity. We therefore tested this hypothesis using a rat model of gentamicin nephrotoxicity. Carvedilol (2 mg/kg) was administered intraperitoneally 3 days before and 8 days concurrently with gentamicin (80 mg/kg BW). Estimations of urine creatinine, glucose, blood urea, serum creatinine, plasma and kidney tissue malondialdehyde (MDA) were carried out, after the last dose of gentamicin. Kidneys were also examined for morphological changes. Gentamicin caused marked nephrotoxicity as evidenced by increase in blood urea, serum creatinine and decreased in creatinine clearance. Blood urea and serum creatinine was increased by 883% and 480% respectively with gentamicin compared to control. Carvedilol protected the rats from gentamicin induced nephrotoxicity. Rise in blood urea, serum creatinine and decrease in creatinine clearance was significantly prevented by carvedilol. There was 190% and 377% rise in plasma and kidney tissue MDA with gentamicin. Carvedilol prevented the gentamicin induced rise in both plasma and kidney tissue MDA. Kidney from gentamicin treated rats, histologically showed necrosis and desquamation of tubular epithelial cells in renal cortex, whereas it was very much comparable to control with carvedilol. In conclusion, carvedilol with its antioxidant property protected the rats from gentamicin-induced nephrotoxicity.

Adrenergic beta-Antagonists↗
PubMed2000

Oxidant stress and essential fatty acids in patients with risk and established ARDS.

Oxygen free radicals are important mediators of both physiological and pathological events. In acute lung injury, the activated lymphocytes stimulate tumor necrosis factor (TNF) and other cytokines. These lymphokines augment free radical generation by polymorphonuclear leukocytes (PMNLs), macrophages and other cells which may ultimately produce acute respiratory distress syndrome (ARDS). This is supported by our results presented here in that there is a significant increase in lipid peroxidation products in patients with established ARDS. The amount of lipid peroxidation was significantly higher in the established ARDS group compared to patients who are at risk for ARDS. Nitric oxide concentrations were significantly decreased in established ARDS compared to the control and those who are at risk for ARDS. Fatty acid analysis of the plasma phospholipid fraction revealed a significant decreased in linoleic acid, gamma-linolenic acid, dihomo-gamma-linolenic acid and arachidonic acid levels of n-6 series and alpha-linolenic acid, eicosapentaenoic acid, docosa-hexanenoic acid of n-3 series. Patients who are at risk for ARDS have decreased levels of gamma-linolenic acid of the n-6 series, alpha-linolenic acid and eicosapentaenoic acid of the n-3 series. These results suggest that lipid peroxides and alteration in essential fatty acid metabolism may have a role in the pathogenesis of ARDS.

Arachidonic Acid↗
PubMed2000

Ginkgo biloba extract ameliorates gentamicin-induced nephrotoxicity in rats.

The effect of Ginkgo biloba (EGb), a plant extract with an antioxidant effect, has been studied on gentamicin-induced nephrotoxicity in male wistar rats. Ginkgo biloba extract (300 mg/kg BW) was administered orally 2 days before and 8 days concurrently with gentamicin (80 mg/kg BW). Saline treated animals served as control. Estimations of urine creatinine, glucose, blood urea, serum creatinine, plasma and kidney tissue MDA were carried out after 8 days of gentamicin treatment. Kidneys were examined using histological techniques. Blood urea and serum creatinine were increased by 896% and 461% respectively, with gentamicin, compared to saline treated group. Creatinine clearance was significantly decreased with gentamicin. Ginkgo biloba extract protected rats from gentamicin-induced nephrotoxicity. Changes in blood urea, serum creatinine and creatinine clearance induced by gentamicin were significantly prevented by Ginkgo biloba extract. There was a 177% and 374% rise in plasma and kidney tissue MDA with gentamicin, which were significantly reduced to normal with Ginkgo biloba extract. Histomorphology showed necrosis and desquamation of tubular epithelial cells in renal cortex with gentamicin, while it was normal and comparable to control with Ginkgo biloba extract. These data suggest that supplementation of Ginkgo biloba extract may be helpful to reduce gentamicin nephrotoxicity.

Administration, Oral↗
PubMed2000

Evaluation of amlodipine, lisinopril, and a combination in the treatment of essential hypertension.

Angiotensin converting enzyme (ACE) inhibitors and dihydropyridine calcium antagonists are well established and widely used as monotherapy in patients with mild to moderate essential hypertension. Earlier studies combining short acting drugs from these classes require multiple dosing and were associated with poor compliance. Availability of longer acting compounds allows once daily administration to avoid the inconvenience of a multiple daily dose. It was decided to perform a randomised double blind, crossover study with the long acting calcium channel blocker amlodipine and the long acting ACE inhibitor lisinopril, given either alone or in combination in essential hypertension. Twenty four patients with diastolic blood pressure (DBP) between 95 and 104 mm Hg received amlodipine 2.5 mg and 5 mg, lisinopril 5 mg and 10 mg, and their combination as per a prior randomisation schedule. Supine and standing blood pressure and heart rate were recorded at weekly intervals. Higher doses of both the drugs individually or in combination were used if the target supine DBP below 90 mm Hg was not achieved. There was a significant additional blood pressure lowering effect with the combination when compared either with amlodipine or lisinopril alone. Five mg amlodipine and 10 mg lisinopril monotherapy achieved the target blood pressure in 71% and 72% patients respectively. The combination of 2.5 mg amlodipine with 5 mg lisinopril produced a much more significant lowering of blood pressure in a higher percentage of patients than that with an individual low dose.

Adult↗
PubMed2000

Melatonin, a pineal hormone with antioxidant property, protects against gentamicin-induced nephrotoxicity in rats.

The present study investigated the effects of melatonin, an antioxidant, on gentamicin-induced nephrotoxicity in rats. Melatonin (5 mg/kg p.o.) was used 3 days before and 8 days simultaneously with gentamicin (80 mg/kg i.p.) Saline-treated animals served as controls. Determinations of urinary creatinine, N-acetyl-beta-D-glucosaminidase, glucose, protein, blood urea, serum creatinine, plasma and kidney tissue malondialdehyde (MDA), and antioxidant enzyme levels in kidney tissue were done after 8 days of gentamicin treatment. The kidneys were also examined for morphological changes using histological techniques. Gentamicin caused nephrotoxicity as evidenced by marked elevation in blood urea and serum creatinine. Mean blood urea and serum creatinine levels were 289+/-50, and 2.5+/-0.5 mg/dl, respectively, in rats treated with gentamicin. Melatonin significantly protected the rats from gentamicin-induced nephrotoxicity; blood urea and serum creatinine levels were 23+/-2.7 and 0.88+/-0.19 mg/dl, respectively. The creatinine clearance was decreased with gentamicin treatment (0.048+/- 0.007 ml/min) as compared with controls (0.41+/-0.08 ml/h/kg). In rats treated with melatonin plus gentamicin, the creatinine clearance was similar to controls (0.41+/-0.08 ml/h/kg). The product of lipid peroxidation (MDA) was markedly increased in plasma (2.10+/-0.15 nmol) and kidney tissue (8.87+/-3.2 nmol/mg protein) with gentamicin treatment. Melatonin prevented the gentamicin-induced rise in plasma MDA (1.03+/-0.27 nmol) and kidney tissue MDA (2.57+/-0.87 nmol/mg protein). An increased excretion of urinary N-acetyl-beta-D-glucosaminidase, glucose, and protein by gentamicin was also prevented by melatonin. Kidneys from gentamicin-treated rats showed tubular epithelial loss with intense granular degeneration involving more than 50% of renal cortex, while there were findings comparable to controls in melatonin plus gentamicin treated rats. The present study indicates that melatonin significantly protects against gentamicin-induced renal toxicity in Wistar rats.

Animals↗
PubMed2000

Effect of pentoxifylline on cyclosporine-induced nephrotoxicity in rats.

Effect of unique hemorrheologic agent pentoxifylline (PTX) was investigated on cyclosporine (CsA) induced nephrotoxicity in rats. Compared to saline control, CsA produced significant increase in blood urea and serum creatinine. Pentoxifylline treatment prevented the CsA-induced rise in blood urea and serum creatinine. Creatinine clearance (Ccr) and lithium clearance (Licr) was decreased with CsA. PTX treatment prevented the CsA-induced decrease in Ccr and Licr. Malondialdehyde (MDA) was increased with CsA compared to saline treated animals. PTX prevented the CsA-induced MDA rise. Kidney form CsA treated rat showed marked vacuolar degeneration of tubular epithelium with excess of microcalcification. Severity of the lesions was markedly reduced in rats treated with PTX plus CsA. The results indicate that PTX reduces CsA-induced renal toxicity in rats.

Animals↗
PubMed1999

Melatonin: an antioxidant protects against cyclosporine-induced nephrotoxicity.

BACKGROUND: Cyclosporine (CsA) causes a dose-related decrease in renal function in experimental animals. Different mediators for CsA nephrotoxicity have been suggested; oxygen free radicals are one of them. In experimental model of Wistar rats, the role of antioxidant melatonin (Mel), the main product of pineal secretion, was investigated in CsA nephrotoxicity. METHODS: Male Wistar rats were divided into four groups: saline control, 50 mg/kg CsA, 500 microg/kg Mel, and CsA + Mel. At the end of 14th day of treatment, blood urea, creatinine, malondialdehyde, and creatinine and lithium clearance were estimated. Histopathological examination of kidney from all the groups was performed. RESULTS: CsA caused marked elevation in blood urea, serum creatinine, and plasma malondialdehyde and a decrease in creatinine and lithium clearance. Mel significantly antagonized CsA-induced renal impairment. Microcalcification in corticomedullary junction seen with CsA was prevented by Mel. CONCLUSION: These results indicate that Mel, through its antioxidant properties, provides protection against CsA-induced nephrotoxicity.

Animals↗
PubMed1999

Lacidipine protects against cyclosporine-induced nephrotoxicity in rats.

The effect of lacidipine (LA), a new calcium channel blocker with an antioxidant effect, has been studied on cyclosporine (CsA)-induced nephrotoxicity in male Wistar rats. Lacidipine (1 mg/kg BW) was administered orally 3 days before and 14 days concurrently with CsA (50 mg/kg BW orally). Urine volume, Na+, K+, Li+ and creatinine in urine, and blood urea, serum creatinine, lithium, plasma malondialdehyde (MDA) and CsA levels were estimated in blood after 14 days CsA treatment. Kidneys were examined using histological techniques. Blood urea and serum creatinine were increased by 305 and 211%, respectively, with CsA when compared to the saline-treated animals. Creatinine clearance (Ccr) and lithium clearance (Licr) were decreased and proximal tubule fractional reabsorption 1-(Licr/Ccr) was significantly increased with CsA. Lacidipine protected rats from CsA-induced nephrotoxicity. Changes in blood urea, serum creatinine, Ccr, Licr and proximal tubule fractional reabsorption induced by CsA were significantly prevented by LA. There was a 160% rise in MDA levels with CsA, which was significantly reduced equal to control with LA. Histomorphology showed microcalcification with CsA, while it was normal with LA. In rats treated with LA, CsA did not show any microcalcification. Our data suggest that supplementation of LA may be helpful to reduce CsA nephrotoxicity.

Animals↗
PubMed1999

Cardioprotective effect of magnesium chloride in experimental acute myocardial infarction.

Cardioprotective role of intravenous administration of magnesium chloride was evaluated in rabbits by biochemical and histopathological parameters. Myocardial damage was induced by injecting (i.v.) isoprenaline 1, 2.5, 5 and 7.5 mg/kg body weight of animal. There was a dose dependent increase in the activity of cardiac enzyme creatinine kinase CK (C Max). Maximal elevation of CK (C Max) was observed with 2.5 mg isoprenaline. The mean T-max (mean of the time duration in hr at which maximum creatinine kinase activity of individual rabbit was observed in a group) shifted early, significantly with 2.5, 5 and 7.5 mg isoprenaline compared to control group. Histopathologically, myocardial damage was quite significant in 2.5 mg isoprenaline subgroup of animals. A mortality of 29% was observed in animals injected with 5 and 7.5 mg isoprenaline, whereas all animals subjected with 1 and 2.5 mg isoprenaline were alive for 72 hr. Considering the data on serial determination of cardiac enzyme CK and histopathological changes, 2.5 mg isoprenaline was chosen as standard dose to study efficacy of cardioprotection by gold standard verapamil and magnesium chloride. Verapamil (5 microM) injected prior to 2.5 mg isoprenaline administration revealed significant reduction of CK (C Max) activity (P < 0.05) compared to animals infused with isoprenaline alone. T-max value did not show any alteration in both the groups. Histopathological findings showed no areas of necrosis and cellular infiltrates in animals primed with 2.5 mg isoprenaline following verapamil. Highly significant reduction in CK (C-max) activity was observed in animals administered with 40 mg magnesium chloride prior to isoprenaline compared to animals treated with isoprenaline alone (P < 0.001). In addition to this, significant delay in T-max of CK activity was observed in group treated with 40 mg magnesium chloride and isoprenaline compared to group treated with only isoprenaline (P < 0.01). The study clearly highlighted and confirmed the valuable role of magnesium chloride as cardioprotective agent.

Animals↗
PubMed1998

Determination of terazosin in human plasma, using high-performance liquid chromatography with fluorescence detection.

A selective, sensitive, rapid and reproducible high-performance liquid chromatographic method for the determination of terazosin in plasma is described. The structurally related compound prazosin was used as an internal standard. The method comprises extraction with methylene chloride followed by chromatography on a C18 reversed-phase column. The compounds were detected using spectrofluorimetry. The absolute recoveries were more than 90% with a minimal detection of 1 ng/ml and calibration curve was linear between 1 and 80 ng/ml.

Adrenergic alpha-Antagonists↗
PubMed1997

Rapid and selective analysis of secnidazole in human plasma using high-performance liquid chromatography with ultraviolet detection.

A rapid, reproducible high-performance liquid chromatographic method for the determination of secnidazole, 5-nitroimidazole class of antiprotozoals from blood is described. Metronidazole was used as an internal standard. A simple extraction step with dichloromethane was done before chromatography on a C18 column with the wavelength fixed at 276 nm on the UV detector. Blood levels up to 500 ng/ml have been measured with good precision in the healthy volunteers after 1 g of secnidazole was administered. The present described method can readily be utilized for routine pharmacokinetic studies.

Antiprotozoal Agents↗
PubMed1996

An evaluation of antidepressants in rheumatic pain conditions.

In a randomized, double-blind, parallel study, fluoxetine and amitriptyline were compared with placebo in the treatment of chronic rheumatic pain. A total of 59 patients were evaluated during 4 wk of treatment and received 20 mg fluoxetine, 25 mg amitriptyline, or placebo daily. Pain intensity, pain relief, vital variables, and global evaluation were used to assess efficacy. To evaluate safety variables, the incidence of side effects was noted. Both amitriptyline and fluoxetine significantly reduced pain intensity compared with placebo. Similarly, pain relief was greater with both amitriptyline and fluoxetine than with placebo. At the end of the fourth week, fluoxetine was superior in efficacy to amitriptyline. The incidence of adverse effects was significantly greater with amitriptyline; dryness of the mouth was the most predominant side effect. We conclude that fluoxetine is an effective analgesic with fewer side effects.

Adult↗
PubMed1995

Comparison of phenytoin with auranofin and chloroquine in rheumatoid arthritis--a double blind study.

OBJECTIVE: To evaluate efficacy of phenytoin in modifying the course of rheumatoid arthritis (RA) by comparing it to gold (auranofin) and chloroquine. METHODS: A double blind, randomized study of 6 months' duration was conducted at the Nizam Institute of Medical Sciences, Hyderabad, India. One hundred and thirty-two patients with active RA (defined by the 1987 ARA criteria) were entered into the study and randomized into 3 groups: phenytoin, chloroquine, or auranofin. RESULTS: Full data were evaluable in 100 patients who satisfactorily completed the protocol (phenytoin, 35; auranofin, 30; and chloroquine, 35). Twenty-four patients were noncompliant and did not take medication or return for evaluation; 8 patients had the drug withdrawn because of side effects before study completion. For each of the 3 drugs all clinical and laboratory variables improved when pre and posttreatment values (p < 0.05 to 0.001) were compared. There was a greater reduction in posttreatment mean morning stiffness in the chloroquine group than in the phenytoin and auranofin groups (p < 0.05). Posttreatment grip strength was also greatest in the chloroquine group. On the other hand, there were statistically significant decreases in IgM levels in both the phenytoin and auranofin groups (p < 0.001), but not with chloroquine. Among the 53 patients with a disease history of 3-6 months, global outcome was best with phenytoin (16/17), compared to chloroquine (12/18) and auranofin (12/18) (p < 0.03). However, there was no such difference in the 47 patients in all 3 groups with a disease history longer than 6 months. Eight patients had side effects (phenytoin, auranofin, 2; chloroquine, 1) requiring withdrawal of the drug. However, the incidence of side effects was not significantly different for the 3 drugs. CONCLUSION: Our data indicate that phenytoin is comparable to auranofin and chloroquine in its efficacy in RA and may be considered an alternative disease modifying agent for RA.

Adult↗
PubMed1992

Comparative study of omeprazole and famotidine in the treatment of duodenal ulcer.

In a double blind, multicenter, parallel group clinical trial in patients with symptomatic duodenal ulcers, 129 patients were randomized to receive either omeprazole 20 mg once daily (n = 65) or famotidine 40 mg once daily (n = 64) for 2 weeks, and if the ulcers were not healed, for a total of 4 weeks. Seventy four percent of these receiving omeprazole had healed ulcers after 2 weeks compared with 34.3% of those receiving famotidine (p < 0.001). At 4 weeks, the respective figures were 97.3% and 77.6% (p < 0.001). After 2 weeks of treatment, only 11.1% and 29.8% of omeprazole and famotidine treated patients respectively had day time pain (p < 0.02). Diary cards (successfully completed by 2/3rd of patients) showed that omeprazole treated patients required smaller amounts of antacids (p = ns). Over the first two weeks, ulcer healing rate was similar in smokers and non- smokers. No significant side effects were reported in either group. Omeprazole 20 mg/day provides more rapid relief of symptoms and heals a greater proportion of duodenal ulcers at 2 and 4 weeks than famotidine 40 mg/day.

Adolescent↗
PubMed1991

Evaluation of phenytoin in rheumatoid arthritis--an open study.

In an open study, thirty-five patients with active rheumatoid arthritis were treated with phenytoin. Various clinical and laboratory parameters showed good improvement after phenytoin. Early morning stiffness was significantly reduced after 8 weeks (p less than 0.05); pain index (p less than 0.001), articular index (p less than 0.01) and grip strength (p less than 0.01) showed significant improvement after 24 weeks. There was significant reduction in erythrocyte sedimentation rate (p less than 0.01). Except for three patients (skin rash in one and gastric irritation in two), all others tolerated phenytoin well. The results of the present study support the usefulness of phenytoin as a disease-modifying drug for rheumatoid arthritis.

Adult↗
PubMed1991

A rapid method for evaluation of analgesic and anti-inflammatory activity in rats.

Carrageenin (2%) was used to produce edema and hyperalgesia; indomethacin, phenylbutazone, aspirin, ibuprofen, analgin, paracetamol and phenacetin were tested at different doses for anti-inflammatory and analgesic activity in the same rats as the peak for the edema reached at the end of 3rd hr and for the hyperalgesia at the end of 4th hr. Indomethacin, phenylbutazone and ibuprofen reduced edema and increased the pain threshold. Analgin and aspirin increased the pain threshold relatively at a low dose. Paracetamol and phenacetin were inactive in the doses tested. Carrageenin (2%) was observed to possess both phlogistic and allogenic properties.

Analgesics↗
PubMed1990

Early beneficial effects of low dose oral methotrexate in rheumatoid arthritis.

The effect of low dose methotrexate pulse therapy was studied in 21 patients with active rheumatoid arthritis. Three doses of oral methotrexate 2.5 mg at 12 hourly intervals weekly was administered to all the patients. Patients were followed up for clinical, radiological and serological evaluation. Significant reduction in the number of painful and swollen joints, decrease in the duration of morning stiffness, fall in the erythrocyte sedimentation rate, and improvement in global assessment were seen in 15 patients (71.4%) by the end of 16 weeks. Five patients (23.8%) complained of minor gastric discomfort. None of the patients discontinued the treatment because of any side effect.

Administration, Oral↗