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Biomedical subjects

A K Bajaj

Publications and source records attributed to A K Bajaj.

18 recordsLinked to original sources
PubMed1990

Contact depigmentation from free para-tertiary-butylphenol in bindi adhesive.

100 consecutive cases of contact depigmentation due to bindi during a period of 11 months were studied. Bindi adhesive material was found to contain 80% para-tertiary-butylphenol (PTBP), by thin-layer chromatography, infrared spectrophotometry and high-pressure liquid chromatography. The possibility of hypersensitivity to PTBP was ruled out as none of the 15 patients tested with 2% PTBP and 1% para-tertiary-butylphenol-formaldehyde resin gave any positive reactions. Development of depigmentation could have been due either to individual susceptibility or to constant use for a prolonged period. The area of contact being very small, generalised vitiligo as a result of systemic absorption appeared to be a remote possibility.

Adhesives↗
PubMed1990

Prevention of neutrophil-mediated injury to endothelial cells by perfluorochemical.

Myocardial salvage after reperfusion may be limited by neutrophil-mediated microvascular damage. The effect of the perfluorochemical, Fluosol-DA, and its various components on neutrophil adherence, cytotoxicity, and proteolytic enzyme release was examined on sheep large and small vessel endothelial cells in vitro. Cells were studied under normoxic (N) and anoxic conditions (A). Various concentrations of Fluosol (10%, 25%, and 50%) significantly reduced neutrophil adherence under both experimental conditions [mean 22 +/- 3.25% versus 7 +/- 0.8% (N) and 20 +/- 3.2% versus 7.5 +/- 0.9% (A); P less than 0.01]. The perfluorocarbons, perfluorodecalin (PFD), and perfluoro-tripropylamine (PFTP) in a 50 volume/percent concentration exhibited profound effects on adherence, particularly on cells subjected to anoxia (51% and 69% reduction in adherence, respectively; P less than 0.01). No effect on adherence was observed with other components, including the detergent, pluronic F68. A 25% reduction (P less than 0.02) in endothelial cytotoxicity was noted when neutrophils were preincubated with Fluosol. However, pretreatment of endothelial cells with Fluosol did not inhibit neutrophil adherence. Neutrophils stimulated with cytochalasin B and FMLP showed a significant reduction in lysozyme release after incubation with Fluosol (28 +/- 5% versus 17 +/- 4%; P less than 0.01). This study demonstrates that Fluosol significantly attenuates neutrophil adherence, cytotoxicity, and enzyme release in an in vitro model of microvascular injury. It also suggests that prevention of neutrophil-mediated microvascular damage may be an important mechanism whereby Fluosol enhances myocardial salvage after ischemia and reperfusion.

Animals↗
PubMed1989

Limitation of myocardial reperfusion injury by intravenous perfluorochemicals. Role of neutrophil activation.

Neutrophil activation and infiltration into the ischemic myocardium after reperfusion may limit the amount of salvageable myocardium (reperfusion injury). The effects of intravenous perfluorochemicals (Fluosol-DA) on infarct size, ventricular contractility, and neutrophil function were assessed in an occlusion-reperfusion canine model. Closed-chest dogs were subjected to 90 minutes of left anterior descending artery occlusion followed by 24 hours of reperfusion. Animals were randomized to receive either Fluosol-DA (FDA, n = 8) or Ringer's lactate (CONT, n = 10) intravenously over 30 minutes just before left anterior descending artery reperfusion. Neutrophil demargination and infiltration into the myocardium were assessed in vivo with In111. Neutrophil chemotaxis, superoxide radical production, and lysozyme degranulation were evaluated ex vivo at baseline, 1 hour after occlusion, and 1 hour after reperfusion. Perfluorochemicals significantly reduced infarct size expressed as percent of area at risk (FDA, 7 +/- 4%; CONT, 24 +/- 6%; p less than 0.01). This was associated with positive wall motion in the jeopardized zone of Fluosol-DA animals compared with dyskinesis in control animals (FDA, +4.4 +/- 2.1%; CONT, -1.1 +/- 1.5%; p less than 0.05). Electron microscopy showed reduced neutrophil and erythrocyte plugging of capillaries with relative preservation of endothelial cells in the Fluosol-DA animals. Myocardial blood flow was greater in the ischemic endocardium of Fluosol-DA animals 1 hour after reperfusion (FDA, 1.23 +/- 0.21; CONT, 0.62 +/- 0.08 ml/g/min; p less than 0.01). Neutrophil demargination and infiltration into the ischemic myocardium was reduced in the animals treated with Fluosol-DA. (FDA, 2.5 +/- 0.7 x 10(3); CONT, 14.1 +/- 2.7 x 10(3) neutrophils/g; p less than 0.01). Neutrophil chemotaxis and lysozyme release were also markedly suppressed in the Fluosol-DA groups ex vivo. These results show that intravenous Fluosol-DA significantly reduces reperfusion injury with greater salvage of myocardium and improved left ventricular function. The chief mechanism of action of Fluosol-DA appears to be the suppression of neutrophil function.

Animals↗
PubMed1989

Acute electrophysiologic effects of sodium administration in dogs treated with O-desmethyl encainide.

Conduction slowing is the major in vivo effect of sodium channel blocking drugs. Although this action may promote arrhythmia suppression, apparently paradoxical arrhythmia aggravation does occur. The latter outcome is most frequently seen during treatment with the class IC agents such as encainide or flecainide, which are potent depressors of conduction even at usual plasma concentrations and heart rates. Anecdotal reports in patients with such drug toxicity have suggested a beneficial effect of sodium lactate or NaHCO3 administration. The purpose of this study, therefore, was to examine the changes induced by sodium loading on the electrophysiologic properties of the canine ventricle pretreated with a class IC drug. Thirty dogs received loading and maintenance infusions of O-desmethyl encainide (ODE), an encainide metabolite that as a sodium channel blocker is approximately 10 times more potent than the parent drug. Interventions were administered during the maintenance phase when stable plasma ODE concentrations of 448 +/- 68 (SEM) ng/ml were present, and QRS was prolonged from 62 +/- 1 to 89 +/- 2 msec, and HV was prolonged from 28 +/- 1 to 50 +/- 1 msec. NaHCO3 (5 meq/kg during 1 minute) shortened QRS from 92 +/- 6 to 76 +/- 3 msec and shortened HV from 44 +/- 3 to 37 +/- 3 msec within 10 minutes (both p less than 0.01). NaHCO3 also significantly prolonged endocardial monophasic action potential duration from 231 +/- 22 to 272 +/- 33 msec and decreased serum [K+] from 3.8 +/- 0.2 to 3.0 +/- 0.2 meq/l, but it did not alter plasma ODE concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis, Respiratory↗
PubMed1989

Clinical profile and electrodiagnostic study of peripheral neuropathy.

A clinical analysis and electrophysiological study was performed in 40 cases of peripheral neuropathy. Motor nerve conduction velocity (MNCV) and electromyography (EMG) were also recorded in 20 healthy volunteers. Twelve cases were of diabetic neuropathy (DN), nine of Guillain-Barre syndrome (GBS), eight of idiopathic, six of leprous, three of toxic neuropathy and one each of acute intermittent porphyria (AIP) and carcinomatous neuropathy. The onset was insidious in a majority of the cases (70%), the presenting symptom being paraesthesia (27.5%). A variable sensory loss was the commonest finding (77.5%). Two patients each had evidence of cranial nerve involvement and affection of urinary bladder and bowel. In both DN and GBS there was a significant reduction in the MNCV especially in the peroneal nerves. In DN 41.6% had evidence of decreased motor unit potentials and 16.6% showed spontaneous fibrillatory activity. For GBS these figures were 77.7% and 8.3% respectively. The peripheral nerve involvement was variable in leprosy and the EMG was normal in all, but one case.

Adult↗
PubMed1987

Frequency- and orientation-dependent effects of mexiletine and quinidine on conduction in the intact dog heart.

Myocardial conduction depends on the magnitude of the fast inward sodium current as well as on cardiac fiber orientation, with more rapid propagation along myocardial fibers than across them. Although antiarrhythmic drugs depress the sodium current in a frequency-dependent fashion in vitro, their effects on conduction in the intact ventricle have been less well studied. We therefore evaluated the frequency- and orientation-dependent actions of mexiletine, quinidine, and their combination on epicardial conduction in 24 pentobarbital-anesthetized dogs. These interventions were chosen because the time constant of recovery from sodium-channel blockade by mexiletine in vitro is shorter than that from blockade by quinidine, and because we have previously shown that the combination of these drugs is often clinically effective when single-agent therapy fails. An electrode array that permitted measurement of conduction times in multiple orientations over short segments of epicardium without contamination by rapid Purkinje fiber propagation or by latency or virtual cathode effects at the stimulus site was developed for these studies. In all animals, the atrioventricular node was destroyed by injection of formalin to permit measurements over a wide range of cycle lengths (250 to 1500 msec). In the absence of drugs, conduction in any direction was frequency independent. In the presence of mexiletine, however, frequency-dependent increases in conduction times were found at cycle lengths of 600 msec or less; these changes were significantly greater in orientations for which baseline conduction was rapid. Quinidine, on the other hand, increased conduction times at all tested cycle lengths without significant orientation-dependent effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Monilethrix.

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Child↗
PubMedDate not supplied

Serum proteins and immunoglobulins in leprosy.

Serum proteins and immunoglobulins were studied in patients suffering from various types of leprosy. A significant increase in total protein and decrease in albumin was found in all types of leprosy except borderline-tuberculoid. Gamma globulin was found to be increased in all types. An increase of alpha-2-globulin in lepromatous, a decrease of beta globulin in borderline-lepromatous, and a decrease of alpha-2 and increase of beta globulin in borderline-tuberculoid were observed. These changes do not seem to be of diagnostic importance. A statistically significant increase of IgG in borderline-lepromatous and lepromatous, IgM in all types of leprosy and IgA only in lepromatous was found. The increase of different immunoglobulins in leprosy, especially the lepromatous type, suggests a humoral response which was found to be directly proportional to the severity of the lesion.

Blood Proteins↗