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Biomedical subjects

P Kulkarni

Publications and source records attributed to P Kulkarni.

At least 37 records · Page 2Linked to original sources
PubMed1992

Torsade de pointes and long QT syndrome following major blood transfusion.

We report a rare complication following transfusion of a large volume of blood in an adult patient. An electrophysiological disturbance of the cardiac cycle with prolongation of the QT interval developed, which was followed by recurrent episodes of torsade de pointes, a unique form of ventricular tachycardia. The most likely cause of this acquired long QT syndrome was hypomagnesaemia secondary to massive blood transfusion. Treatment with a magnesium infusion restored the QT interval to normal and temporary ventricular pacing prevented further ventricular arrhythmias.

Adult↗
PubMed1992

Aerobic exercise in the psychological treatment of adolescents.

A small group of psychiatrically institutionalized adolescents (16 boys, 11 girls) were assigned to a three-day-per-week running/aerobic exercise program or a regular physical activity class. The complete program continued over 9 weeks, with 11 subjects remaining throughout the program. Dependent measures of body-mass index, timed performance on a one-mile run, resting, exercise, and recovery heart rates, and measures of depression, mood-states, and self-efficacy were assessed pre-, mid-, and post-9-wk. treatment and at a 4-wk. follow-up. Improvements in depression, anxiety, hostility, confused thinking, and fatigue were shown in treated girls, with increases in vigor and self-efficacy for all treated subjects.

Adolescent↗
PubMed1991

Regional cardiac adrenergic function using I-123 meta-iodobenzylguanidine tomographic imaging after acute myocardial infarction.

The effect of acute myocardial infarction (AMI) on regional cardiac adrenergic function was studied in 27 patients mean +/- standard deviation 10 +/- 4 days after AMI. Regional adrenergic function was evaluated noninvasively with I-123 meta-iodobenzylguanidine (MIBG) using a dedicated 3-detector tomograph. Four hours after its administration, there was reduced MIBG uptake in the region of infarction, 0.38 +/- 0.31 counts/pixel/mCi x 103 compared with 0.60 +/- 0.30 counts/pixel/mCi x 103 and 0.92 +/- 0.35 counts/pixel/mCi x 103 in the zones bordering and distant from the infarct area, respectively, p less than 0.001. In all patients, the area of reduced MIBG uptake after 4 hours was more extensive that the associated thallium-201 perfusion defect with defect scores of 52 +/- 22 and 23 +/- 18%, respectively, p less than 0.001. After anterior wall AMI, the 4-hour MIBG defect score was 70 +/- 13% and the degree of mismatch between myocardial perfusion and MIBG uptake was 30 +/- 9% compared with 39 +/- 17 and 21 +/- 17% after inferior AMI, p less than 0.001 and p = 0.016, respectively. The 4-hour MIBG defect score correlated inversely with the predischarge left ventricular ejection fraction, r = -0.73, p less than 0.001. Patients with ventricular arrhythmia of greater than or equal to 1 ventricular premature complexes per hour, paired ventricular premature complexes or ventricular tachycardia detected during the late hospital phase had higher 4-hour MIBG defect scores, 62.5 +/- 15.0%, than patients with no detectable complex ventricular ectopic activity and a ventricular premature complex frequency of less than 1 per hour, 44.6 +/- 23.4%, p = 0.036.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Iodobenzylguanidine↗
PubMed1991

Corticosteroids and immunosuppressive agents in rabbit heterolamellar corneal transplant model.

Bovine cornea (epithelium and stroma) was transplanted on to the rabbit cornea from which the epithelium and stroma had been removed. Conjuntival hyperemia and edema occurred from day 1-5 post-operation, followed by neovascularization and graft rejection within 7-10 days. Topical dexamethasone (0.1%) and prenisolone (1%) t.i.d. inhibited post-surgical hyperemia, edema, delayed hypersensitivity and neovascularization. These agents and the immunosuppressants (cyclosporin A and rapamycin) inhibited graft rejection observed up to 20 days. After cessation of treatment on the 20th day, grafts remained viable up to 35 days with dexamethasone, 10 days with prednisolone and rapamycin, and 5 days with cyclosporin A.

Adrenal Cortex Hormones↗
PubMed1991

Serum-free growth and karyotype analyses of cultured normal and tumorous (SqCC/Y1) human buccal epithelial cells.

Epithelial cell cultures were obtained following tryptic digestion of normal human buccal mucosa. Primary cultures exhibited markedly higher colony-forming efficiencies and growth rates using fibronectin/collagen-coated, as compared to non-coated culture dishes and a serum-free MCDB 153 medium developed for epidermal epithelial cells than a similar medium previously developed for buccal explant outgrowth cultures. At the preferred conditions, the cells could be transferred at least 5-fold, divided at about one population doubling per day, and commonly underwent 60 population doublings resulting in yields of 10(8) to 10(11) cells per cm2 mucosal specimen. Moreover, these conditions successfully cultivated a buccal carcinoma cell line (SqCC/Y1) for several months. The carcinoma cells were resistant to factors that inhibited growth or induced differentiation of normal cells, i.e., transforming growth factor type beta 1, Ca2+, or serum. Karyotype analyses of SqCC/Y1 cells showed 63 to 83 chromosomes per metaphase and consistent occurrences of monosomy 1, tetrasomy 19 and 20, as well as trisomy 22, and at least 7 marker chromosomes, whereas cells obtained from non-cancerous donors were diploid. It is concluded that the similarly defined culture conditions may now be applied to study characteristics of both normal and tumorous buccal epithelial cells.

Blood↗
PubMed1990

Effects of anti-inflammatory and immunosuppressive drugs on the heterolamellar corneal transplantation in rabbits.

We have studied the graft rejection of bovine lamellar cornea transplanted onto the rabbit cornea. In addition, the effect of inhibitors of arachidonic acid metabolism and immunosuppressive agents on this heterolamellar corneal transplant was investigated. The corneal lamellar transplant treated with saline were rejected at 9 +/- 1.4 day with 100% rejection rate. The postsurgical conjunctival hyperemia and edema occurred within 2-3 days. Corneal neovascularization took 5 to 9 days to reach the region of the graft. Intramuscular cyclosporin A (25mg/kg/day) and dexamethasone (0.1%) applied topically for 20 days (t.i.d.) inhibited the corneal opacity, edema, neovascularization and graft rejection. Topical Dexamethasone in the ipsilateral eye prolonged survival of grafts in the contralateral (untreated) eye. Cyclosporin A and dexamethasone probably inhibited the graft rejection process by their immunosuppressive action. Indomethacin and BW755C, respective cyclooxygenase and lipoxygenase inhibitors, applied topically did not inhibit graft rejection process while inhibiting postsurgical inflammatory response.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1990

[Experimental study on cyclosporin A (CsA) acting on rejection of heterolamellar corneal transplantation].

UNLABELLED: The experiment involved the transfer of lamellar corneas (0.3mm thick and 10mm diameter central epithelium with stroma) from fresh bovine eyes onto rabbits eyes. RESULTS: group 1, control, (4 rabbits), the donor corneas remained transparent for up to 7-10 days on the recipient rabbit eyes. After that time, all animals in this group rejected their grafts promptly. They showed markedly circumcorneal congestion, edema and vascularization of the cornea. Histopathology: There are apparently cellular infiltration of leukocytes in the grafts, and graft bed of the cornea, which are found also in the iris. Group 2: 3 rabbits were treated with 1% CsA in castor oil, 5 times per day. After 16 days, One of three rabbits showed mild rejection. Group 3: 4 rabbits were treated with CsA, I.M. 15 mg/kg/D. None has any immunological response to the grafts. The histopathology of group 2 and 3 shows no cellular infiltration, except one. CsA can 1. inhibit the rejection of the heterograft. 2. prolong the survive of the heterograft. 3. inhibit the vascularization. 4. has less side effects.

Administration, Topical↗
PubMed1989

Regression of left ventricular hypertrophy in hypertension. Effects of prazosin therapy.

Left ventricular hypertrophy is a common consequence of chronic hypertension. Although the hypertrophic response can be considered an adaptive mechanism in the initial stages, its progression is associated with increased cardiovascular morbidity and mortality rates. Therefore, reversal of left ventricular hypertrophy may provide considerable clinical benefits to hypertensive patients. Although treatment of hypertension per se is important, blood pressure alone may not explain the course of the hypertrophic process. Not all antihypertensive drugs cause a reversal of hypertrophy, though they may produce equal effects on blood pressure. Factors other than the severity of blood pressure may play a role in the genesis of left ventricular hypertrophy. Adrenergic inhibitors cause its regression, whereas direct vasodilators may promote progression. In this study, therapy with the alpha-adrenergic inhibitor prazosin resulted in significant regression of left ventricular hypertrophy in a group of patients with moderate-to-severe hypertension. This study utilized a new technique--[123I]phenylpentadecanoic acid myocardioscintigraphy--to measure the left ventricular mass. In this study, it was shown that monotherapy with prazosin produced significant relative reductions in systolic and diastolic blood pressure, along with significant reductions in left ventricular mass.

Blood Pressure↗
PubMed1988

Effect of thromboxane and serotonin receptor antagonists on intracoronary platelet deposition in dogs with experimentally stenosed coronary arteries.

We have reported previously that thromboxane A2 (TXA2) and serotonin (5-HT, 5-hydroxytryptamine) are important mediators of cyclic flow variations (CFVs) in a canine model of coronary artery stenosis and endothelial injury. The present study tested the hypothesis that a TXA2 receptor antagonist is more effective in reducing intracoronary platelet deposition at sites of endothelial injury and severe stenosis than a 5-HT2 receptor antagonist. CFVs developed after placing a plastic constrictor around the left anterior descending coronary artery (LAD) in 51 of 56 dogs. Autologous platelets labeled with 111In were injected in 48 animals. Ten control dogs (group 1A) were killed after CFVs were observed for 1 hour at the nadir of coronary blood flow. Five dogs (group 1B) did not develop CFVs after placement of the constrictor. CFVs were abolished with SQ 28668 (2.75 +/- 0.36 mg/kg, group 2) and SQ 29548 (0.45 +/- 0.1 mg/kg, group 3), two different TXA2 and PGH2 receptor antagonists, in eight of 10 and six of seven dogs, respectively. In eight of 10 dogs (group 4), CFVs were abolished with ketanserin (0.66 +/- 0.12 mg/kg), a 5-HT2 receptor antagonist. In group 2, 3, and 4 dogs, the respective drugs were given so that the minimal dose required to abolished CFVs was administered. In six of six dogs (group 5), a higher dose of ketanserin (i.e., 1.5 mg/kg) was used to abolish CFVs. At death, intracoronary platelet deposition was evaluated by calculating the LAD platelet accumulation ratio (111In activity in the LAD/111In activity in the circumflex coronary artery) in 43 dogs and, in 22 dogs, by microscopic examination of the LAD. A marked LAD platelet accumulation ratio was found in group 1A dogs at the stenotic site and in segments immediately distal to it. The LAD platelet accumulation ratio was significantly reduced by both the low and the high doses of ketanserin compared with group 1A dogs (p less than 0.001). However, the two TXA2 receptor antagonists further reduced the LAD platelet accumulation ratio compared with ketanserin-treated animals (p less than 0.01). Microscopic examination confirmed these findings. We conclude that SQ 28668 and SQ 29548, two different TXA2 receptor antagonists, reduce residual intracoronary platelet deposition associated with CFVs in this canine model more effectively than ketanserin, a 5-HT2 receptor antagonist.

Animals↗
PubMed1988

Abnormal I-123 metaiodobenzylguanidine myocardial washout and distribution may reflect myocardial adrenergic derangement in patients with congestive cardiomyopathy.

I-123 metaiodobenzylguanidine (MIBG) is a new radiopharmaceutical with properties that allow the characterization of the sympathetic innervation of several organ systems. In this study, we used MIBG with tomographic imaging to evaluate noninvasively the differences in myocardial sympathetic innervation in 14 healthy volunteers and 16 patients with severe dilated cardiomyopathy (CM). Initial (15-minute) images demonstrated no significant differences in MIBG concentration in the hearts of patients with CM and of healthy volunteers. However, the myocardial retention of MIBG was significantly reduced in the patients with CM. Expressed as the percent washout from 15 to 85 minutes, the patients with CM had a 28 +/- 12% washout rate compared with 6 +/- 8% in the controls (p less than 0.001). A small subset of patients from each group imaged at 4-hour intervals demonstrated even greater disparity in washout rates. In addition, the patients with CM had significantly greater heterogeneity in the MIBG activity distribution within the myocardial images. There was 47 +/- 15% intraimage variability in MIBG distribution in the patients with CM and 22 +/- 9% variation in the controls (p less than 0.001). We conclude from these data that the myocardial distribution and kinetics of MIBG in images obtained from patients with CM differ significantly from those of controls and that the MIBG patterns may be used as a relatively noninvasive means to evaluate the severity of altered adrenergic innervation in the hearts of these patients.

3-Iodobenzylguanidine↗
PubMed1986

Diclofenac and enolicam as ocular anti-inflammatory drugs in rabbit corneal wound model.

The anti-inflammatory effects of two nonsteroidal agents, enolicam and diclofenac, were assessed in rabbit corneal wound model. Topically applied diclofenac (50 microliter volume) at 0.01%, 0.1% and 0.5% concentrations inhibited the polymorphonuclear leukocyte (PMN) release into tear fluid following partial (6 mm central area) corneal deepithelialization in rabbits. Similarly, enolicam also inhibited this PMN response following corneal injury. Topical diclofenac was found to be more potent than topical enolicam in inhibiting the inflammatory PMN response following partial corneal injury. Both drugs did not affect the rate of reepithelialization following complete (limbal to limbal) corneal deepithelialization.

Administration, Topical↗
PubMed1984

The migration of bronchoalveolar macrophages into hilar lymph nodes.

The migration of bronchoalveolar macrophages ( BAMs ) into hilar lymph nodes ( HLNs ) was investigated in order to assess their potential importance in pulmonary immune responses. 51Chromium- or 111Indium-labeled broncholaveolar cells ( BACs ) or purified BAMs were inoculated into the tracheas of syngeneic guinea pigs, and the number of cells that reached HLN at 24-72 hours was estimated by 1) measuring the cell-associated radioactivity in HLN and 2) counting the radiolabeled cells in autoradiographic preparations. It was determined that 400-2900 BAM/10(7) inoculated BACs or BAMs reached the HLNs within a 3-day period. From this data, it was calculated that in a normal animal as many as 8700 BAMs might reach HLNs daily. These migratory phagocytes are potentially important in facilitating the systemic spread of macrophage-resistant intracellular organisms from the lung. Furthermore, following phagocytosis and killing of microorganisms in the alveolus, BAMs might migrate to HLNs and present antigen to stimulate a primary immune response.

Animals↗
PubMed1983

Iodine-123 phenylpentadecanoic acid: detection of acute myocardial infarction and injury in dogs using an iodinated fatty acid and single-photon emission tomography.

The ability of an iodinated fatty acid, iodine-123 phenylpentadecanoic acid (1-123 PPA), and single-photon emission computed tomography (SPECT) to detect myocardium injured by temporary or permanent coronary arterial occlusion was evaluated. In 5 control dogs, 11 dogs that underwent 90 to 120 minutes of fixed left anterior descending coronary artery (LAD) occlusion, and 8 dogs that underwent 90 minutes of temporary LAD occlusion and up to 90 minutes of reflow, 2 to 6 mCi of I-123 PPA were injected and the dogs were imaged with SPECT. Control dogs showed relatively uniform uptake and clearance of I-123 PPA in similar left ventricular (LV) regions. Dogs with permanent LAD occlusion were identified by computer algorithm as having regions of decreased I-123 PPA uptake in the infarct-related area and a reduced rate of I-123 PPA clearance (-9.4% in infarct sectors [washin], +3.7% in sectors adjacent to the area of infarction, and +15.4% in control LV sectors [p less than 0.01]). Dogs with temporary LAD occlusion and reperfusion had decreased clearance of I-123 PPA from the regions with infarction; I-123 PPA clearance was -5.2 +/- 16.4% in infarct sectors, 12.7 +/- 7.4% in periinfarct zones, and 30.4 +/- 12% in control LV regions. These data demonstrate that tomographic analysis of I-123 PPA uptake and clearance permits the relatively noninvasive detection of LV myocardium injured by permanent or temporary LAD occlusion and reperfusion.

Animals↗
PubMed1983

In vivo esterification of a synthetic 125I-labeled fatty acid into cardiac glycerolipids.

Recent studies have demonstrated that fatty acids can be successfully utilized as myocardial imaging agents. 125I-paraphenylpentadecanoic acid (IPPA), a synthetic fatty acid, accumulates within the myocardium and can be visualized by conventional gamma scintigraphy. To determine if IPPA was incorporated into cardiac lipids in a pattern similar to palmitate, IPPA was purified by liquid chromatography, bound to fat-free albumin, and administered by intravenous injection to male Sprague-Dawley rats. After 2.5, 5, 10, and 30 min, the hearts were excised and the lipids were extracted in chloroform-methanol. The uptake of IPPA into the myocardium reached a maximal value after 2.5 min, and 95% of the 125I was found in the cardiac lipid fraction after chromatographic separation. Over 65% of the IPPA was found in cardiac triglycerides, whereas approximately 10% was present in membrane phospholipids (predominantly phosphatidylcholine and phosphatidylethanolamine). This pattern of IPPA incorporation is similar to that reported for intravenously administered [3H]palmitate. The rate of turnover of IPPA present in the triglyceride fraction was threefold faster than the rate of the IPPA which was incorporated into membrane lipids. At all time periods examined, the methanol-water soluble end products of IPPA oxidation did not account for more than 5% of the total IPPA present within the myocardium. The present study indicates that IPPA is incorporated primarily into triglycerides and other cardiac lipids in a pattern similar to palmitate.

Animals↗