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Biomedical subjects

P K Ganguly

Publications and source records attributed to P K Ganguly.

At least 19 recordsLinked to original sources
PubMed2006

Effect of dietary hempseed intake on cardiac ischemia-reperfusion injury.

Polyunsaturated fatty acids (PUFAs) have significant, cardioprotective effects against ischemia. Hempseed contains a high proportion of the PUFAs linoleic acid (LA) and alpha-linolenic acid (ALA), which may have opposing effects on postischemic heart performance. There are no reported data concerning the cardiovascular effects of dietary hempseed intake. A group of 40 male Sprague-Dawley rats were distributed evenly into four groups that were fed for 12 wk a normal rat chow supplemented with hempseed (5% and 10%), palm oil (1%), or a 10% partially delipidated hempseed that served as a control. Plasma ALA and gamma-linolenic acid levels were significantly elevated in the rats that were fed a 5% or 10% hempseed-supplemented diet, but in heart tissue only ALA levels were significantly elevated in the rats fed these diets compared with control. After the dietary interventions were completed, postischemic heart performance was evaluated by measuring developed tension, resting tension, the rates of tension development and relaxation, and the number of extrasystoles. Hearts from rats fed a hempseed-supplemented diet exhibited significantly better postischemic recovery of maximal contractile function and enhanced rates of tension development and relaxation during reperfusion than hearts from the other groups. These hearts, however, were not protected from the occurrence of extrasystoles, nor were the increases in resting tension altered during ischemia or reperfusion as a function of any dietary intervention. Our data demonstrate that dietary hempseed can provide significant cardioprotective effects during postischemic reperfusion. This appears to be due to its highly enriched PUFA content.

Animals↗
PubMed2002

Prophylaxis of radiation-associated mucositis in conventionally treated patients with head and neck cancer: a double-blind, phase III, randomized, controlled trial evaluating the clinical efficacy of an antimicrobial lozenge using a validated mucositis scoring system.

PURPOSE: Mucositis occurs in almost all patients treated with radiotherapy for head and neck cancer. The aim of this multicenter, double-blind, prospective, randomized trial was to evaluate the clinical efficacy of an economically viable antimicrobial lozenge (bacitracin, clotrimazole, and gentamicin [BcoG]) in the alleviation of radiation-induced mucositis in patients with head and neck cancer. PATIENTS AND METHODS: One hundred thirty-seven eligible patients were randomized to treatment with either antimicrobial lozenge (69 patients) or placebo lozenge (68 patients). The primary end point of the study was the time to development of severe mucositis from the start of radiotherapy. Secondary end points included severity and duration of mucositis, pain measurement, radiation therapy interruption, and quality of life. Mucositis was scored using a validated mucositis scoring system. RESULTS: Toxicity profiles were similar between the two arms of the study. The median time to development of severe mucositis from the start of radiotherapy was 3.61 weeks on BCoG and 3.96 weeks on placebo (P =.61). There were no statistically significant differences between the arms in the extent of severe mucositis as measured by physician, in oral toxicities as recorded by patients, or in radiotherapy delays. CONCLUSION: This study was conducted on the basis of a pilot study that demonstrated the BCoG lozenge to be tolerable and microbiologically efficacious. A validated mucositis scoring system was used. However, in this group of patients treated with conventional radiotherapy, the lozenge did not impact significantly on the severity of mucositis. Whether such a lozenge would be beneficial in treatment situations where rate of severe mucositis is higher (ie, in patients treated with unconventional fractionation or with concomitant chemotherapy) is unknown.

Administration, Oral↗
PubMed2000

Dexamethasone for the prophylaxis of radiation-induced emesis: a National Cancer Institute of Canada Clinical Trials Group phase III study.

PURPOSE: To investigate the efficacy of dexamethasone as a prophylactic antiemetic for patients receiving fractionated radiotherapy to the upper abdomen in a randomized controlled trial. PATIENTS AND METHODS: One hundred fifty-four patients planned to receive fractionated radiotherapy to fields involving the upper abdomen (minimum total dose, 20 Gy; minimum number of fractions, five) were randomized to receive prophylactic dexamethasone (2 mg orally three times a day [tid], starting in the morning of first treatment and continuing until after their fifth treatment) or placebo. The primary end point of the study was the proportion of patients free from emesis during the study period. Secondary end points included a quality-of-life assessment using the core questionnaire of the European Organization for Research and Treatment of Cancer and side effects of dexamethasone therapy in this population of patients. RESULTS: Fifty-four (70%) out of 75 patients receiving dexamethasone had complete protection versus 37 (49%) out of 75 patients on placebo (P = .025). Most emetic episodes occurred during the initial phase of treatment. Although there was no difference in global quality of life between the two sets of patients, patients receiving dexamethasone had less nausea and vomiting and less loss of appetite but more insomnia. CONCLUSION: Dexamethasone 2 mg tid seems to be an effective prophylactic antiemetic in this situation. Side effects were acceptable, but there seemed to be no overall effect on global quality of life.

Abdomen↗
PubMed1999

Extracorporeal liver perfusion system for successful hepatic support pending liver regeneration or liver transplantation: a pre-clinical controlled trial.

BACKGROUND: There is a well recognized need for a system capable of providing effective support for patients with hepatic failure pending liver regeneration or liver transplantation. Recent attempts of using bioartificial liver containing encapsulated porcine hepatocytes, the deployment of emergency whole liver, or hepatocyte transplantation are complex and not consistently successful. The technique of ex vivo hepatic perfusion developed and used clinically by Abouna in the 1970s, has now been redesigned in a perfusion circuitry that mimics the physiological conditions of a normal liver. Before clinical application of this system, a preclinical trial was carried out in dogs with induced hepatic failure. METHODS: Acute hepatic failure was induced in dogs by an end-to-side porto caval shunt, followed 24 hr later, by a 2-hr occlusion of the hepatic artery. All animals (n=18) were medically supported and were divided into three groups. In the control group (n=6) only medical support was used. In the experimental group (n=12) the animals were connected to the ex vivo liver support apparatus during acute hepatic failure via an AV shunt using a dog liver (n=6) or calf liver (n=6) (after a temporary extracorporeal bovine kidney transplant to remove preformed xeno antibody). Hepatic perfusion was carried out at 37 degrees C through the hepatic artery and portal vein at physiological pressures, and blood flow rate for 6-8 hr. RESULTS: All control animals died of progressive hepatic failure at 14-19 hr after clamping the hepatic artery. The animals treated with ex vivo liver showed remarkable clinical and biochemical improvement. Five animals survived for 36-60 hr. Another seven animals recovered completely and became long-term survivors with biochemical and histological evidence of regeneration of their own liver. Biopsy of the allogeneic ex vivo liver at the end of perfusion showed some interstitial edema. Similar biopsy of the xenogeneic calf liver showed only mild and delayed xenograft rejection, which was most likely due to removal of preformed xeno antibody by temporary transplantation of the calf kidney before liver perfusion. CONCLUSIONS: The observations and results obtained in this trial strongly confirm that extracorporeal perfusion through a whole liver, using the system described, is very successful and cost effective for the treatment of acute, but reversible hepatic failure, as well as serving as a bridge to liver transplantation. The time has come for this form of liver support technology to be reintroduced and widely used.

Animals↗
PubMed1999

Captopril treatment improves the sarcoplasmic reticular Ca(2+) transport in heart failure due to myocardial infarction.

Although captopril, an angiotensin-converting enzyme (ACE) inhibitor, has been shown to exert a beneficial effect on cardiac function in heart failure, its effect on the status of sarcoplasmic reticulum (SR) Ca(2+) transport in the failing heart has not been examined previously. In order to determine whether captopril has a protective action on cardiac function, as well as cardiac SR Ca(2+)-pump activity and gene expression, a rat model of heart failure due to myocardial infarction was employed in this study. Sham operated and infarcted rats were given captopril (2 g/l) in drinking water; this treatment was started at either 3 or 21 days and was carried out until 8 weeks after the surgery. The untreated animals with myocardial infarction showed increased heart weight and elevated left ventricular end diastolic pressure, reduced rates of pressure development and pressure fall, as well as depressed SR Ca(2+) uptake and Ca(2+)-stimulated ATPase activities in comparison with the sham control group. These hemodynamic and biochemical changes in the failing hearts were prevented by treatment of the infarcted animals with captopril. Likewise, the observed reductions in the SR Ca(2+) pump and phospholamban protein contents, as well as in the mRNA levels for SR Ca(2+) pump ATPase and phospholamban, in the failing heart were attenuated by captopril treatment. These results suggest that heart failure is associated with a defect in the SR Ca(2+) handling and a depression in the gene expression of SR proteins; the beneficial effect of captopril in heart failure may be due to its ability to prevent remodeling of the cardiac SR membrane.

Animals↗
PubMed1999

Beneficial effects of propionyl L-carnitine on sarcolemmal changes in congestive heart failure due to myocardial infarction.

OBJECTIVE: Earlier studies have revealed sarcolemmal (SL) defects in congestive heart failure due to myocardial infarction; however, the mechanisms of SL changes in the failing heart are poorly understood. Since congestive heart failure is associated with various metabolic abnormalities including a deficiency of carnitine, we examined the effects of propionyl L-carnitine, a carnitine derivative, in animals with congestive heart failure. METHODS: For this purpose, heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated with 100 mg/kg (i.p. daily) propionyl L-carnitine for 4 weeks. The sham control group received saline injections. The animals were assessed for their left ventricular function. SL membranes were examined for Na(+)-K+ ATPase, Na(+)-Ca2+ exchange and adenylate cyclase activities. RESULTS: A marked improvement in the attenuated left ventricular function of the experimental animals was seen upon treatment with propionyl L-carnitine. The SL adenylyl cyclase activities in control, untreated failing hearts and treated failing hearts were 590 +/- 36, 190 +/- 22 and 320 +/- 21 pmol cAMP/mg/10 min, whereas the SL Na(+)-K+ ATPase activities were 35.7 +/- 2.8, 22.5 +/- 2.4 and 30.1 +/- 2.8 mumol Pi/mg/h, respectively. Furthermore, the SL Na(+)-dependent Ca(2+)-uptake activity, which decreased in the failing hearts (4.6 +/- 0.4 vs. 9.3 +/- 0.7 nmol Ca2+/mg/2 s for control), was improved (6.8 +/- 0.5 nmol Ca2+/mg/2 s) significantly following treatment with propionyl L-carnitine. CONCLUSION: These results indicate that metabolic therapy with propionyl L-carnitine may attenuate defects in the SL membrane and thus may improve heart function in congestive heart failure due to myocardial infarction.

Adenylyl Cyclases↗
PubMed1999

Profile of non-compressive myelopathy in eastern India: a 2-year study.

Eighty-two patients with non-compressive myelopathy have been studied from July 1994 to June 1996 in Bangur Institute of Neurology and S.S.K.M. Hospital, Calcutta, of which 48 patients were men and 34 patients were women. Presentation was acute in 40 patients (48.78%), subacute in 7 (8.53%), chronic in 27 (32.92%) and history of relapse and remission in 8 (9.75%) patients. Preceding as well as simultaneous fever was observed in 16 cases (19.5%); vaccination (anti-rabies) in 1 case (1.21%); drug abuse in 1 case (1.21%); arthralgia-myalgia and rash in 2 cases (2.42%) and history of electrocution in 2 cases (2.42%). Only pyramidal tract involvement was present in 24 cases (29.26%) and remaining 58 cases (70.73%) had pyramidal tract affection with other sites of involvement. CSF study carried out in 60 cases, revealed rise of protein in 31 (37.8%); oligoclonal band had been detected in 6 (7.31%), pleocytosis in 18 cases (21.95%) and increased IgG index greater than 6.66 in 2 cases (2.42%). CT myelogram done in 23 cases revealed no abnormality. MRI study carried out in 59 cases showed myelomalacia in 1 (1.21%); demyelination plaque in 14 cases (17.07%); atrophy of cord in 3 (3.65%); infarction of cord in 1 (1.21%) and in 40 cases (48.78%) no abnormality could be detected. Etiological diagnosis could be established in 59 (71.95%) cases such as transverse myelitis or myelopathy (post infectious) in 24 (29.26%); demyelination in 16 (19.51%); vascular and vasculitis in 3 (3.65%); toxic in 1 (1.21%); physical (electrocution) in 2 cases (2.42%). In the remaining 23 cases (28.04%) no aetiological factors could be found.

Adult↗
PubMed1998

Clinical profile of myasthenia gravis.

Seventy three patients with myasthenia gravis were studied over 9 years period (1987-1995) in departments of neuromedicine, respiratory care unit, cardiothoracic unit of Institute of Postgraduate Medical Education and Research and Bangur Institute of Neurology, Calcutta, with reference to their clinical presentations, laboratory findings and various modes of treatment. Commonest age of presentation was 5th decade in men and 3rd decade in women. Fifty five percent of patients belong to type 2A myasthenia gravis (Osserman classification). Presentation was insidious (67.2%) and course was slowly progressive (65.7%) in majority of cases. Fatigability and ptosis were commonest clinical presentation and diurnal variation was noticed in 60% of cases. Edrophonium test was positive in 90.4% of cases and repetitive nerve stimulation showed 93.5% positivity in 30 cases. 27 patients (36.9%) underwent thymectomy and out of these, 89% of patients showed hyperplastic change and thymoma in 11% of cases. Mortality rate including both operated and nonoperated patients was recorded to be 9.6%. We observed earlier onset of myasthenia in male, higher incidence of oculo-bulbar involvement and lower incidence of respiratory problem and thymoma.

Adolescent↗
PubMed1998

Hypertension, calcium channel and pyridoxine (vitamin B6).

The moderately pyridoxine (vitamin B6)-deficient male rat was introduced by us as an animal model (B6DHT) for the study of hypertension. Hypertension in this rat is associated with increased sympathetic stimulation. Arterial segments from B6DHT rats maintained a higher resting tone. The influx of 45calcium into intracellular compartment of the vascular smooth muscle of the caudate artery of B6DHT rats was also enhanced. Administration of pyridoxine attenuated the hypertension in B6DHT rats as well as in genetic or dietary-induced moderately hypertensive conditions such as in the Zucker obese rat and sucrose or low calcium-fed rats. However, pyridoxine did not have any effect on the spontaneously hypertensive rat. All classes of calcium channel blockers were effective in lowering the systolic blood pressure of B6DHT rats. The increased in vitro influx of 45calcium into intracellular compartment of artery segments of B6DHT rats as well as the BAY K 8644-induced influx of 45calcium into artery segments from normal rats were blocked by pyridoxal phosphate as well as by dihydropyridine-sensitive calcium channel blockers (DHP). Pyridoxal phosphate (PLP) in vitro enhances the binding of calcium channel antagonists to membrane preparations from vascular tissue. PLP corrects the membrane abnormality in responsive hypertensive conditions and thus, could be an endogenous modulator of DHP-sensitive calcium channels.

Animals↗
PubMed1997

Differential changes in sympathetic activity in left and right ventricles in congestive heart failure after myocardial infarction.

Although congestive heart failure subsequent to myocardial infarction is known to be associated with increased sympathetic activity, very little information regarding changes in the sympathetic nerves in the left and right ventricles at various stages after infarction is available. Male Sprague-Dawley rats were subjected to coronary artery ligation and studied 4 and 8 weeks later; these animals had mild and moderate stages of congestive heart failure. A sham group, without coronary ligation, was used as control. Four weeks after myocardial infarction, plasma and ventricular (left and right) epinephrine (EPI), unlike norepinephrine (NE), were markedly increased. Whereas plasma catecholamine (EPI and NE) levels were increased 8 weeks after infarction, NE concentration in the left ventricle was unchanged but EPI concentration was increased in comparison with sham control. The right ventricle showed an increased level of both NE and EPI 8 weeks after infarction. Measurement of the rate of change in the specific activity of NE (NE turnover) in the left and right ventricles 8 weeks after infarction revealed an increase in NE turnover in the left ventricle, without any changes in the right ventricle. The concentration of EPI, unlike NE, was increased in the kidney, spleen, and brain 8 weeks after coronary occlusion. These results are interpreted to mean that congestive heart failure caused by myocardial infarction is associated with differential changes in the status of sympathetic nerves in the left and right ventricles; sympathetic activity is increased only in the left ventricle, whereas the right ventricle may play an adaptive role by increasing catecholamine stores during the development of heart failure.

Animals↗
PubMed1997

Arsenate resistance as a possible marker in the differentiation of environmental and clinical isolates of Vibrio parahaemolyticus.

Strains of Vibrio parahaemolyticus were isolated from clinical, marine and freshwater fish of Calcutta, West Bengal, India. Drug and metal resistance characteristics were compared for differentiation of clinical and environmental strains. Eighteen out of the twenty environmental isolates were resistant to arsenate, unlike the clinical isolates which were all susceptible. All the thirty-five isolates of V. parahaemolyticus were resistant to ampicillin and streptomycin.

Animals↗
PubMed1996

Neuropeptide Y modulation of sympathetic activity in myocardial infarction.

OBJECTIVES: We examined the possible effect of neuropeptide Y in modulating central sympathetic activity after myocardial infarction in rats. BACKGROUND: Previous studies have shown the coexistence of neuropeptide Y and norepinephrine in the brain and a possible functional interaction between the two. Neuropeptide Y inhibits the release of norepinephrine at the presynaptic level and can be considered to act as a neuromodulator. METHODS: Two groups of rats were examined in this study-an experimental group, defined as those rats undergoing left coronary artery ligation, and a sham group without coronary artery ligation, serving as the control group. The animal in both groups underwent microdialysis in the paraventricular nucleus at 2, 4 and 8 weeks after operation. Microdialysis samples were collected with and without injecting neuropeptide Y in the paraventricular nucleus. The concentration of norepinephrine was determined by injecting purified microdialysate samples during high performance liquid chromatography. To explore the receptor's possible role, autoradiographic localization of neuropeptide Y receptors in the paraventricular nucleus was also carried out in the experimental and sham groups. RESULTS: The concentration of norepinephrine measured in the samples was decreased by 50% with neuropeptide Y in 2- and 4-week old rats after infarction, but by only 20% (p < 0.05) in 8-week old rats after infraction. The diminished inhibitory effects of neuropeptide Y on norepinephrine release was associated with increased sympathetic activity, as reflected by plasma norepinephrine; 8-week old rats after infarction had almost a 100% (p < 0.05) increase in their plasma norepinephrine level compared with the sham group. Autoradiography revealed a significant decrease in density of neuropeptide Y receptors in the paraventricular nucleus in 8-week old rats after infarction (p < 0.05). CONCLUSIONS: The data presented in this report suggest that the reduction of the inhibitory activation of neuropeptide Y on sympathetic release may contribute to elevated norepinephrine levels after myocardial infarction.

Animals↗
PubMed1996

Neurally mediated cardiac effects of forskolin in conscious dogs.

Because major cardiovascular disease states are characterized by defects in adenylyl cyclase regulation, it becomes important to understand the mechanisms by which adenylyl cyclase activators affect inotropy and chronotropy in intact conscious animals. Accordingly, we examined the inotropic and chronotropic responses to forskolin in 11 normal conscious, chronically instrumented dogs and 3 dogs with ventricular denervation (VD). Left ventricular first derivative of pressure (LV dP/dt) increased by 96 +/- 7%, P < 0.05, in response to forskolin (50 nmol.kg-1.min-1) in normal dogs and by significantly less, 52 +/- 14%, in VD dogs. Circulating norepinephrine (NE) levels increased similarly in both groups (from 226 +/- 18 to 389 +/- 33 pg/ml in normal dogs, from 177 +/- 23 to 329 +/- 71 pg/ml in VD dogs). In the presence of ganglionic blockade, the increase in LV dP/dt in response to forskolin was reduced (+62 +/- 4%) in normal dogs but was unchanged in VD dogs (+52 +/- 12%). Ganglionic blockade abolished the increase in circulating NE levels in both groups. Increases in heart rate in the presence of ganglionic blockade (+54 +/- 6 beats/min) were less than in the presence of atropine alone (+92 +/- 10 beats/min). Notably, the LV dP/dt and heart rate responses to forskolin were further attenuated by beta-adrenergic receptor blockade in the presence and absence of ganglionic blockade. Morphine also attenuated the increases in both LV dP/dt and plasma NE in response to forskolin. Increases in LV dP/dt in response to NKH-477 (30 micrograms/kg), a water-soluble forskolin derivative, were similar before and after ganglionic blockade (+63 +/- 8 and +51 +/- 10%, respectively). However, in vitro experiments in LV sarcolemmal membrane preparations demonstrated that stimulation of adenylyl cyclase by forskolin and NKH-477 was not affected by beta-adrenergic receptor blockade. These results indicate that in conscious dogs, inotropic and chronotropic effects of forskolin are not only due to direct activation of adenylyl cyclase, but the effects also are mediated by neural mechanisms and potentiated by the prevailing level of sympathetic tone.

Adenylyl Cyclases↗
PubMed1995

Cholecystokinin-induced release of dopamine in the nucleus accumbens of the spontaneously hypertensive rat.

Changes in dopamine neurotransmission in the nucleus accumbens of the spontaneously hypertensive rat (SHR) may be involved in the pathogenesis of hypertension. This investigation tested the hypothesis that the sulfated octapeptide cholecystokinin (CCK8S) induced release of dopamine is greater in the SHR than in its normotensive control, the Wistar-Kyoto rat (WKY). Dopamine and its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were sampled using microdialysis in the caudal half of the nucleus accumbens of 10-week-old anesthetized SHRs and WKYs. Samples were collected in the following order: 3 baseline, 3 CCK8S (10 mumol/l), and 3 postdrug samples. The samples were then analyzed using high pressure liquid chromatography with electrochemical detection. CCK8S increased dopamine and DOPAC levels in both the SHR and WKY with a larger increase in basal dopamine in the SHR (greater than 200%). Perfusion of the nucleus accumbens with 1 mumol/l of CCK8S or the nonsulfated form of CCK8 (CCK8US, 10 mumol/l) produced no significant increase in the release of dopamine in the SHR. These results indicate that CCK8S-induced release of dopamine in the nucleus accumbens is greater in the SHR. Changes in CCK8S neurotransmission/receptor function may be responsible for the alterations in dopaminergic function of the SHR and the pathogenesis of hypertension.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Up-regulation of cholecystokinin receptors in the nucleus accumbens of the young prehypertensive spontaneously hypertensive rat.

We employed receptor autoradiography to test the hypothesis that changes in cholecystokinin neurotransmission in the striatum of the young spontaneously hypertensive rat (SHR) is involved in the development of hypertension. The binding density of 125I-Bolton Hunter labelled cholecystokinin octapeptide (125I-BH-CCK8) in the striatum of 5-week-old prehypertensive SHRs and its normotensive control the Wistar-Kyoto rat (WKY) was determined using computer-assisted densitometry. We found a significant increase in 125I-BH-CCK8 binding density in the nucleus accumbens of the SHR. No difference between the binding density of 125I-BH-CCK8 was found in the caudate-putamen and the prefrontal cortex of SHRs and WKYs. These results suggest that changes in CCK8S neurotransmission or receptor function are not secondary to an increase in arterial blood pressure and, therefore, may be involved in the development of hypertension.

Animals↗
PubMed1995

Renal dopamine receptors are involved in the development of cardiac hypertrophy.

The present study examined the effect of fenoldopam, a known dopamine-1 receptor (DA1) agonist in order to understand its involvement in the cardiac hypertrophic process. Male Sprague-Dawley rats underwent abdominal aortic constriction (AB) with placement of a suprarenal ligature while sham operated animals served as controls. The AB groups showed an increase in their heart wt, left ventricular (LV) wt, heart wt/body wt and LV wt/body ratio. Furthermore, the length of these hearts, as measured from the auriculoventricular border to the apex, LV wall and interventricular (IV) septal thickness were increased from control levels. Treatment with SCH 23390, a DA1 antagonist, on the other hand, was able to partially regress the cardiac hypertrophic changes. All these parameters were also increased in control animals treated with fenoldopam (F). Such changes were more striking in the F+AB group which showed a significant acceleration of the cardiac hypertrophic process on superimposing the two treatments. Plasma dopamine and renin activity were increased in all the groups as compared to control. These results indicate that dopamine receptors are implicated in the development of cardiac hypertrophy.

Animals↗