Prevalence of gastrointestinal parasites in dogs of Palampur, Himachal Pradesh.

A total of 246 faecal/scat samples of the dogs were screened by direct and floatation concentration technique to study the gastrointestinal (GI) tract parasitism in dogs of Palampur, Himachal Pradesh, India. Detailed coprological examination targeting different seasons, age groups and living styles of the dogs revealed an overall 28.04 % of GI parasitism with highest prevalence in summer season (37.87 %). Stray dogs harbored 47.29 % GI parasites in comparison to 19.19 % of pet dogs. Highest prevalence of GI parasitism was observed in the pups, below 3 months of age (39.13 %), followed by the dogs with the age ranging from 3 months to 1 year (26.38 %) and lowest in dogs of the age ranging from 1 to 3 years (6.77 %). Amongst all the parasites, Toxocara canis (44.93 %) infection was highest, followed by Dipylidium caninum (17.39 %) and hookworms (15.94 %).

Detection of flea-borne Rickettsia species in the Western Himalayan region of India.

Human infections by various rickettsial species are frequently reported globally. We investigated a flea-borne rickettsial outbreak infecting 300 people in Western Himalayan region of India. Arthropod vectors (ticks and fleas) and animal and human blood samples from affected households were analysed by gltA and ompB genes based polymerase chain reaction (PCR). Rat flea (Ceratophyllus fasciatus) samples were found harbouring a Rickettsia sp. Phylogenetic analysis based on gltA gene using PHYLIP revealed that the detected Rickettsia sp. has 100% identity with SE313 and RF2125 strains of Rickettsia sp. of flea origin from Egypt and Thai-Myanmar border, respectively and cf1 and 5 strains from fleas and lice from the USA. But, the nucleotide sequence of genetically variable gene ompB of R14 strain was found closely related to cf9 strain, reported from Ctenocephalides felis fleas. These results highlight the public health importance of such newly discovered or less recognised Rickettsia species/strains, harboured by arthropod vectors like fleas.

Increase in weight induced by muraglitazar, a dual PPARalpha/gamma agonist, in db/db mice: adipogenesis/or oedema?

BACKGROUND AND PURPOSE: Muraglitazar, a dual PPARalpha/gamma agonist, caused a robust increase in body weight in db/db mice. The purpose of the study was to see if this increase in weight was due to oedema and/or adipogenesis. EXPERIMENTAL APPROACH: The affinity of muraglitazar at PPARalpha/gamma receptors was characterized using transactivation assays. Pre-adipocyte differentiation, expression of genes for adipogenesis (aP2), fatty acid oxidation (ACO) and sodium reabsorption (ENaCgamma and Na+, K+-ATPase); haemodilution parameters and serum electrolytes were measured to delineate the role of muraglitazar in causing weight gain vis a vis rosiglitazone. KEY RESULTS: Treatment with muraglitazar (10 mg kg(-1)) for 14 days significantly reduced plasma glucose and triglycerides. Reduction in plasma glucose was significantly greater than after similar treatment with rosiglitazone (10 mg kg(-1)). A marked increase in weight was also observed with muraglitazar that was significantly greater than with rosiglitazone. Muraglitazar increased aP2 mRNA and caused adipocyte differentiation in 3T3-L1 cells similar to rosiglitazone. It also caused a marked increase in ACO mRNA in the liver of the treated mice. Expression of mRNA for ENaCgamma and Na+, K+-ATPase in kidneys was up-regulated after either treatment. Increased serum electrolytes and decreased RBC count, haemoglobin and haematocrit were observed with both muraglitazar and rosiglitazone. CONCLUSIONS AND IMPLICATIONS: Although muraglitazar has a better glucose lowering profile, it also has a greater potential for weight gain than rosiglitazone. In conclusion, muraglitazar causes both robust adipogenesis and oedema in a 14-day treatment of db/db mice as observed in humans.

Cholinesterase inhibition by aluminium phosphide poisoning in rats and effects of atropine and pralidoxime chloride.

AIM: To investigate the cholinesterase inhibition and effect of atropine and pralidoxime (PAM) treatment on the survival time in the rat model of aluminium phosphide (AlP) poisoning. METHODS: The rats were treated with AlP (10 mg/kg; 5.55 x LD50; ig) and the survival time was noted. The effect of atropine (1 mg/kg, ip) and PAM (5 mg/kg, ip) was noted on the above. Atropine and PAM were administered 5 min after AlP. Plasma cholinesterase levels were measured spectrophotometrically in the control and AlP treated rats 30 min after administration. RESULTS: Treatment with atropine and PAM increased the survival time by 2.5 fold (1.4 h+/-0.3 h vs 3.4 h+/-2.5 h, P < 0.01) in 9 out of 15 animals and resulted in total survival of the 6 remaining animals. Plasma cholinesterase levels were inhibited by 47 %, (438+/-74) U/L in AlP treated rats as compared to control (840+/-90) U/L (P < 0.01). CONCLUSION: This preliminary study concludes that AlP poisoning causes cholinesterase inhibition and responds to treatment with atropine and PAM.

Effect of change in oxygen tension on release pattern and nature of endothelium-derived substances in isolated rabbit aorta.

AIM: To observe the effect of change in oxygen tension on the release pattern and nature of endothelium-derived substances in isolated rabbit aorta. METHODS: Isometric contractions and relaxations in isolated rabbit strip were observed in response to changes in oxygen tension and effect of various drugs was noted on them. RESULTS: Change in oxygen tension from high [pO2 =(618.9 +/- 0.4) mmHg; 1 mmHg = 133.3 Pa] to low [pO2 = (117.6+/-0.6) mmHg] was observed to convert the relaxant effect of acetylcholine (ACh), in rabbit aorta precontracted with phenylephrine, to a marked contractile response. As the aerating gas was changed from 100 % to 20 % oxygen, the relaxant effect to ACh, recorded every hour, gradually decreased till it gave way to a significant contraction over a period of 3.5 h. On reoxygenation the relaxant effect to ACh was irreversibly inhibited, however, the relaxant effect to SOD (40 kU/L) was not. The per se constrictor effect to ACh was abolished by endothelium removal and by combination of SOD (40 kU/L), catalase (1000 kU/L) and indomethacin (1 x 10(-5 ) mol/L). SQ-030741(1 x 10(-5) mol/L) or GR-32191B (1 x 10(-5) mol/L), both TXA2-PGH2 receptor antagonists but not OKY-046, a TXA2-synthetase inhibitor, also attenuated the ACh-mediated contractions in combination with SOD and catalase. CONCLUSION: The above results implicate that some functional change occurs in the endothelium exposed to low p(O2) such that the stimulated release of endothelium-derived relaxing factor (EDRF) in response to ACh is completely and irreversibly inhibited, whereas, the basally released EDRF in response to SOD is not and marked increase in prostaglandin synthesis is stimulated.

Effect of N-acetylcysteine and L-NAME on aluminium phosphide induced cardiovascular toxicity in rats.

AIM: To investigate the protective effects of N-acetylcysteine (NAC) and Nomega-Nitro-L-arginine methyl ester (L-NAME) on aluminium phosphide (AlP) poisoning induced hemodynamic changes, myocardial oxygen free radical injury and on survival time in rats. METHODS: AlP (12.5 mg/kg) was administered intragastrically under urethane anaesthesia. The effect of pre- and post-treatment with NAC and L-NAME alone and in combination was studied on haemodynamic parameters [blood pressure (BP), heart rate (HR), and electrocardiogram (ECG)] and biochemical parameters (malonyldialdehyde, catalase, and glutathione peroxidase). RESULTS: AlP caused significant hypotension, tachycardia, ECG abnormalities, and finally marked bradycardia. The mean survival time was (90 +/- 10) min. There was significant increase in myocardial malonyldialdehyde (MDA), and decrease in catalase and glutathione peroxidase (GSH Px) levels. NAC infusion (6.25 mg . kg-1 . min-1, iv for 30 min) caused insignificant hemodynamic and biochemical changes. Pre- and post-treatment of NAC with AlP significantly increased the survival time, stabilized BP, HR, and ECG, decreased MDA and increased GSH Px levels compared to AlP group. L-NAME infusion (1 mg . kg-1 . min-1, iv for 60 min) as such caused significant rise in BP but precipitated ECG abnormalities. Pre- and post-treatment of L-NAME with AlP neither improved the survival time nor the biochemical parameters despite significant rise in BP. Co-administration of both the drugs with AlP worsened the hemodynamic and biochemical parameters with reduction in the survival time as compared to AlP. CONCLUSION: NAC increased the survival time by reducing myocardial oxidative injury whereas L-NAME showed no such protective effects in rats exposed to AlP.

5-Hydroxytryptamine-inhibiting property of Feverfew: role of parthenolide content.

AIM: To study the mechanism of antimigraine activity of Tanacetum parthenium (Feverfew), its extracts and parthenolide, a component of Feverfew, by observing their effect on 5-HT storage and release, and stimulation of 5-HT2B and 5-HT2A receptors. Also to standardize a dosage form of Feverfew with respect to its parthenolide content. METHODS: Isometric responses to 5-HT and an indirect acting serotonergic, d-fenfluramine, were obtained on rat fundus and ileum. In one set of experiments the effect of dichloromethane extract of Feverfew and parthenolide was observed on the above. The extract was then thermally degraded upto 10%, 23%, and 33% with respect to its parthenolide content by keeping at 60 degrees C and 75% relative humidity and the experiments were repeated. In another set of experiments rats were fed with 20 mg/kg Feverfew powder (equivalent to a human dose of 500 micrograms parthenolide per day) for 30 d or were i.p. injected with parthenolide (23.4 micrograms/day) for 7 d. In the same set of experiments one group of rats were fed with 15% and 77% degraded Feverfew powder in the same dose as mentioned above. After 30 days the effects of the above were observed on 5-HT and d-fenfluramine. Feverfew was specially formulated and tested for stability under accelerated conditions. RESULTS: Parthenolide (1 x 10(-5) mol/L) non-competitively antagonised the effects of d-fenfluramine but had no significant effect on 5-HT2B and 5-HT2A receptors in rat fundus and ileum at 30 min which turned significant on increasing the incubation time to 1.5 h, in rat fundus. Parthenolide (5 x 10(-5) mol/L) followed the same trend. However, Feverfew extract (1 x 10(-5) mol/L) potently and directly blocked 5-HT2B and 5-HT2A receptors and neuronally released 5-HT. At 5 x 10(-5) mol/L the extract potently and irreversibly blocked the above. Both parthenolide and Feverfew extract showed a time-dependency in their action. The extract when degraded thermally upto 10% could significantly block the 5-HT receptors and neuronal release of 5-HT, however, on further degradation it lost its inhibitory capacity markedly. Similar results were observed in rats fed orally with undergraded and degraded Feverfew powder and injected i.p. with parthenolide. Feverfew powder was more effective than any of its extracts or pure parthenolide. CONCLUSION: Feverfew powder is more potent than any of its extract or parthenolide alone in its antiserotonergic activity. Degraded Feverfew extracts show a marked decrease in their antiserotonergic activity. With thermally degraded Feverfew powder containing less contents of parthenolide no built-up antiserotonergic responses were observed after one month. This ascertains that Feverfew should be dispensed in a properly stabilized form wherein its parthenolide content is not degraded to less than 90% of the original content.

Possible mechanism of captopril induced endothelium-dependent relaxation in isolated rabbit aorta.

The mechanism of captopril, an angiotensin converting enzyme (ACE) inhibitor with sulfhydryl group (SH) in its structure, to produce an endothelium-dependent vasorelaxation was studied. In rabbit aorta with intact endothelium and precontracted with phenylephrine, captopril and superoxide dismutase (SOD) produced dose-dependent relaxation. Lisinopril, an ACE inhibitor without a -SH group in its structure, did not produce endothelium-dependent relaxation. It was observed that captopril, like SOD, produced the relaxation by protecting the EDRF from getting inactivated by superoxide anions as pyrogallol and methylene blue inhibited both the captopril and SOD-mediated relaxation. The free radical scavenging action of captopril is further substantiated by the observation that captopril, but not lisinopril, inhibited FeCl3/ascorbic acid-induced lipid peroxidation in whole tissue homogenates of rabbit aorta to a level comparable to that of SOD. These results suggest that endothelium-dependent vasodilation produced by captopril may be due to its ability to scavenge superoxide anion and this property may be ascribed to the -SH group present in its structure.

Fine needle aspiration cytology in the diagnosis of mediastinal seminomas.

Fine needle aspiration cytology (FNAC) was employed to diagnose 117 cases of mediastinal tumours from January, 1985 till December, 1994. Six cases were diagnosed as mediastinal seminomas which are rare mediastinal malignant neoplasms. All patients had complete resolution of the mediastinal masses after external beam radiotherapy. Diagnosis of mediastinal masses by FNAC can spare the patients from more invasive diagnostic procedures and help the thoracic surgeons to plan immediate treatment.

An experimental study on cardiotoxicity of aluminium phosphide.

Aluminium phosphide(AlP), a grain fumigant pesticide, was studied for its cardiotoxicity in anaesthetised rats. The hemodynamic and cardiac biochemical changes were investigated following intragastric administration of different doses of AlP (10, 20 and 40 mg). With 10 and 20 mg dose of AlP an immediate fall in BP was observed which recovered partially and stabilized for 10 minutes followed by a gradual fall till the animal died. However, with a higher dose (40 mg) there was no recovery in BP, instead the initial fall continued till the death of the animal. An increase in the heart rate was observed with 10 and 20 mg dose of AlP for 15 minutes which was followed by a marked fall till cardiac arrest ensued. On the other hand, 40 mg dose produced only a transient tachycardia followed by a prolonged bradycardia. ECG changes at all dose levels included initial tachycardia and ST segment elevation progressing to QRS broadening. However, marked conduction defects as evidenced by the ventricular ectopics were noticed only with 40 mg. The mean survival time dose dependently decreased with 10 mg(55 +/- 3 min), 20 mg(35 +/- 2 min) and 40 mg(18 +/- 2 min) of AlP. The cardiac glycogen, ATP and CP levels were significantly lowered in animals treated with 10, 20 and 40 mg of AlP. Higher levels of MDA in the cardiac tissue were observed with 10, 20 and 40 mg of AlP. Thus it is suggested that the deleterious effect of AlP on heart is mediated by both declined cellular metabolism of the myocardium as well as by necrosis of the cardiac tissue resulting in the release of reactive oxygen intermediates.

The surgical treatment of atrial myxomas. Clinical experience and results in eight patients.

Between 1983 and 1988, eight patients underwent excision of left atrial myxomas at the Institute of Postgraduate Medical Education & Research, Calcutta. There were five females and three males. The presenting symptoms and signs often simulated mitral stenosis or insufficiency, and the diagnosis was confirmed by echocardiography and angiocardiography. One patient presented with features of cerebral embolism. The myxomas were successfully removed under cardiopulmonary bypass in all patients, either by shaving them from the atrial septum, or by excising a portion of normal atrial septum with the tumour. Small tumours were removed through left atriotomy, while a biatrial approach was utilised for large tumours. There was one perioperative death, and another patient died one and half years later, probably due to tumour embolisation in brain. Late functional results have been excellent in all the other patients. Two dimensional echocardiography has proved to be extremely accurate in early diagnosis of myxomas and in the late follow up of patients. The pertinent literature is reviewed.

Experimental infection of pups with Ancylostoma caninum larvae from an abnormal host, the chicken.

The migration and distribution of Ancylostoma caninum larvae in the tissues of chickens, infected orally with 1,000 larvae, were studied. Larval yield at necropsy from different organs after digestion with artificial gastric juice revealed a 62.9% recovery four hours after inoculation, followed by a sharp decline to 5.4% at 72 hours. Larvae were found in the heart within four hours, the lungs within eight hours and the liver within 12 to 18 hours but no larvae were recovered from the spleen, kidney or brain. Migration in the muscles of head, neck, thorax and abdomen was detected at 12 hours and was maximal at 36 hours. The establishment of patent infection in the definitive host was studied by feeding infected chicks to hookworm-free pups (one chick/pup) 48 hours, 7 days and 14 days after infection. The mean worm burden at necropsy was highest (15) in the pups fed with chicks 48 hours after infection and was three and nil in the other groups respectively.

Experimental infection of pups with Ancylostoma caninum-infected mouse tissues.

Migration and distribution of Ancylostoma caninum larvae in the tissues of mice orally infected with 1000 larvae, and establishment of patent infection from the mice to the definitive host, were studied. Larval yield from different organs of mice, after digestion with artificial gastric juice, indicated that the highest recovery was at 4 h post-infection (62.8%), and thereafter a slight decline occurred up until 30 days post-infection (51.5%). Migration of larvae to the lungs occurred within 4 h, to the liver within 12 h and into the heart within 24 h. No larvae were recovered from spleen and kidney tissues. From the 9th day onwards larvae were also recovered from the brain. Migration in the muscles of head and neck occurred within 4 h, in the thoracic and abdominal muscles at 24 h and in lumbosacral and leg muscles at 48 h. The establishment of patent infections in the definitive host was studied by feeding the orally- and percutaneously-infected mice to hookworm-free pups at 10 and 30 days post-infection. The mean necropsy worm burden in the pups fed with the orally-infected mice was comparatively higher than in the pups fed cutaneously-infected mice.

Infectivity of Ancylostoma caninum in dogs by different routes of inoculation.

Infectivity of A. caninum in dogs inoculated with 500 larvae by different routes (percutaneous, subcutaneous, intravenous, per os, through a stomach tube and foot pad) was studied by ascertaining the worm burden at necropsy 21-27 days post-infection. Infection through foot-pads yielded the maximum number of worms. The percentage of worm establishment using foot-pad inoculation was 73.8%, followed by subcutaneous (49.0%), percutaneous (45.0%) and per os (35.0%) routes. These results show that active penetration of the larvae through skin and particularly foot-pad is the most favourable mode of infection of dogs.

The amylase-creatinine clearance ratio following cardiopulmonary bypass.

The incidence of unexplained pancreatitis in patients dying after cardiac operations has been recorded as 16%, with evidence to implicate ischemia in the pathogenesis of the pancreatitis. Increased amylase--to--creatinine clearance ratios (ACCR), suggesting pancreatic dysfunction, have been reported in patients following nonpulsatile cardiopulmonary bypass (CPB). Pulsatile CPB is increasingly recognized to be a more physiological form of perfusion, particularly with respect to capillary blood flow. In this study the ACCR has been determined before, during, and after cardiac operations performed with both nonpulsatile and pulsatile CPB. Twenty patients undergoing elective cardiac operations were studied. Ten patients had nonpulsatile CPB (nonpulsatile group) and 10 had pulsatile CPB (pulsatile group). The two groups were comparable as regards perioperative variables and perfusion parameters. In both groups the ACCR was estimated preoperatively, on three occasions during the operation, and daily on the first 5 postoperative days. A significant elevation in ACCR was observed in nine of 10 patients in the nonpulsatile group but in only one of 10 patients in the pulsatile group (p less than 0.001). The significant improvement of ACCR stability following pulsatile CPB may indicate that this form of perfusion will reduce the risk of pancreatitis following cardiac operations performed with CPB.

Transection denervation of the urinary bladder. An experimental study.

In an experimental study in the dog, deliberate partial denervation of the urinary bladder through partial horizontal transection achieved an alteration in detrusor activity similar to that noted in human beings following transection. It is postulated that neural escape is the mechanism responsible in the human.

Haemodynamic effects of angiotensin converting enzyme inhibition after cardiopulmonary bypass in dogs.

Recent studies have suggested a possible causative relationship between elevated plasma levels of Angiotensin II (AII) and the vasoconstriction associated with conventional cardiopulmonary bypass. The haemodynamic effects of SQ14225, a specific angiotensin converting enzyme inhibitor, have been studied in a group of five dogs submitted to a 60 min period of cardiopulmonary bypass (CPB). A 20 min infusion of SQ14225 in a dose of 2 microgram .kg-1 .h-1 was administered to each dog 2 h after the end of the period of CPB. Measurements of peripheral vascular resistance index (PVRI), cardiac index (CI) and plasma levels of Angiotensin II were obtained at the start and end of the infusion period. The results in the five blocked dogs were compared with a control series of ten unblocked dogs submitted to an identical cardiopulmonary bypass regine. In the blocked dogs, PVRI fell significantly during infusion of SQ14225 from 38.27 units to 21.70 units (P <0.01). There was a simultaneous significant increase in cardiac index from 3.00 to 3.98 litre.m2 .min-1 (P <0.01). Plasma Angiotensin 11 levels fell in the blocked dogs from 57 to 11.5 pg.cm-2 during the infusion period (normal levels <15 pg.cm-3). In the control unblocked dogs, there was no corresponding fall in PVRI, no rise in cardiac index, and no fall in elevated plasma AII levels. The difference between the groups were statistically highly significant (P <0.005). These results indicate that reduction in elevated plasma AII levels after CPB using converting enzyme inhibitor SQ14225 is associated with a significant fall in peripheral vascular resistance and a significant rise in cardiac index. In addition, the study confirms the causative relationship between elevated plasma levels of Angiotensin II and the increased vasoconstriction associated with non-pulsatile CPB.

Assessment of cerebral damage during open-heart surgery. A new experimental model.

A new experimental technique for the assessment of cerebral cellular damage during extracorporeal circulation is described. It is based upon the direct measurement of the enzyme creatine phosphokinase (CPK) and the brain-specific isoenzyme CPK-B in cerebrospinal fluid of dogs submitted to conventional techniques of cardiopulmonary bypass (CPB). Highly significant elevations occur during a 60 min period of CPB in CSF levels of total CPK and CPK-B isoenzyme. These elevated levels persist at 24 hours postoperation, despite full clinical recovery in the dogs. In a comparative study of the effects of introducing a 40 micrometer arterial line screen filter during the period of CPB, there was a highly significant reduction in total CPK and CPK-B levels in the filtered group (p < 0.005).