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Biomedical subjects

J N Sharma

Publications and source records attributed to J N Sharma.

At least 91 records · Page 5Linked to original sources
PubMed1979

Kinin system in clinical and experimental rheumatoid inflammation: a short review.

The kallikrein, kininogen, kinin and kininase system along with other inflammatory chemical mediators are important components for the initiation and maintenance of clinical and experimental rheumatoid-like inflammatory conditions. Numerous studies carried out in the last few years, however, strongly suggest that the kinin-forming system intervenes in a far wider range of physio-pathological processes than has been considered previously. The authors summarize present knowledge concerning the system and review some of the latest experimental findings and opinions.

Animals↗
PubMed1979

Central hypotensive action of alpha-methyldopa: an iontophoretic study in the cat.

The central site and mechanism of alpha-methyldopa-induced hypotension were examined with the microiontophoretic technique which permits the topical application of drugs to single neurons of the bulbar vasomotor center in decerebrate cats. Cardiovascular neurons were identified by their response to an increase in arterial blood pressure following a small intravenous pressor dose of norepinephrine. Microiontophoretic application of alpha-methyldopa was found to have an inhibitory effect on the spontaneous firing rate of cardiovascular neurons. Furthermore, alpha-methyldopa was found to completely block the excitatory response of cardiovascular neurons to iontophoretically applied norepinephrine. Non-cardiovascular neurons, recorded from the same brain area, were unaffected by iontophoretic application of alpha-methyldopa at the same or greater doses that produced responses in cardiovascular neurons. While peripheral factors cannot be entirely ruled out, the present findings are contrary to the postulate that alpha-methyldopa lowers arterial blood pressure by stimulating central alpha-adrenoceptors, causing a reduction of sympathetic outflow to the periphery. Rather, the data indicate that alpha-methyldopa or its metabolites act directly on central alpha-adrenoceptors in a manner which results in reduced activity.

Action Potentials↗
PubMed1978

CNS site of clonidine induced hypotension: a microiontophoretic study of bulbar cardiovascular neurons.

To localize the central site and mechanism of clonidine induced hypotension, the drug was applied by the technique of microiontophoresis to neurons of the bulbar cardiovascular center in decerebrate cats. The excitatory and inhibitory cardiovascular neurons (CVN) were identified by their response to an increase in the arterial blood pressure induced by intravenous injections of small doses of norepinephrine (NE). Clonidine had an inhibitory effect on the spontaneous firing rate of excitatory CVN but had no effect on the firing rate of inhibitory CVN. At the same doses, it had no effect on the firing rate of NCVN recorded from the same area. Furthermore, clonidine had a blocking action on the excitatory response of CVN induced by microiontophoretic application of NE. It is concluded that clonidine produces its hypotensive response by acting on alpha-adrenergic receptors of bulbar CVN.

Action Potentials↗
PubMed1978

Gallium citrate Ga 67 imaging in noninfectious interstitial nephritis.

Gallium citrate Ga 67 has been reported to be of value in the diagnosis of both malignant and infectious intra-abdominal diseases. The drug may also be taken up by mononuclear phagocytes in noninfectious tubulo-interstitial disease of the kidney. Positive renal scans from patients with these diseases either become negative or show decreased uptake following treatment. With further support of these findings, gallium citrate Ga 67 may become a valuable tool in both diagnosis and follow-up of noninfectious interstitial nephritis.

Adult↗
PubMed1977

Comparison of the anti-inflammatory activity of Commiphora mukul (an indigenous drug) with those of phenylbutazone and ibuprofen in experimental arthritis induced by mycobacterial adjuvant.

In the present investigation a method of induction of experimental arthritis in animals was modified to provide a better model replica of human arthritis. Inflammatory syndrome, resembling rheumatoid arthritis in man, was induced in the right hock joint of albino rabbits by intra-articular injection of the killed mycobacterial adjuvant in liquid paraffin. Development of this arthritic syndrome was studied from a period of five months with and without drugs. Anti-inflammatory agents such as phenylbutazone, ibuprofen and fraction "A" of gum-guggual from Commiphora mukkul were administered orally at a daily dose of 100, 100 and 500 mg/kg, respectively, for a period of five months. All three drugs decreased the thickness of the joint swelling during the course of drug treatment. These results indicate the beneficial role of phenylbutazone, ibuprofen and fraction "A" of gum-guggul in experimental arthritis.

Animals↗
PubMed1977

Changes in biochemical parameters associated with experimental arthritis in rabbits.

Peripheral venous blood samples were drawn before and after induction of adjuvant arthritis in rabbits at intervals of 15 days. Using these samples, biochemical parameters were measured, including total protein, albumin, globulin, cholesterol, alkaline phosphatase, glutamic oxaloacetic transaminase and glutamic pyruvic transaminase. The various biochemical tests exhibited an abnormal pattern in adjuvant animals as compared to the normal rabbits. The significance of these findings has been discussed.

Alanine Transaminase↗
PubMed1976

Characteristicas and response differences to iontophoretically applied norepinephrine, D-amphetamine and acetylcholine on neurons in the medial and lateral vestibular nuclei of the cat.

Midcollicular decerebrate cats, with their cerebellum removes, were tested with controlled acceleratory motion in order to identify neurons in the medial vestibular nucleus (MVN) and lateral vestibular nucleus (LVN) which responded to a motion stimulus. Five-barredled micropipettes were used to record single neuron activity and to apply norepinephrine (NE), d-amphetamine and acetylcholine (ACh). These agents were studied on spontaneously firing cells which responded to a motion stimulus and others which were in the MVN were inhibited by NE and d-amphetamine but were unaffected by iontophoresis of the alpha-adrenergic blocking agent phentolamine or the beta-antagonists, MJ-1999 or propranolol. In the LVN a majority of the cells tested were excited by NE and d-amphetamine. NE excitation in the LVN was antagonized by phentolamine but not by MJ-1999 or propranolo. Cats pretreated with reserpine to deplete brain catechlamines showed typical responses to NE BUT IONTOPHORESIS OF D-AMPHETAMINE WAS WITHOUT EFFECT. Unlike the differential sensitivity observed for NE, ACh excited most cells in both the MVN and LVN. NE and ACh produced similar responsed on vestibular neurons modulated by motion and those not responsive to motion. These observations suggest that NE-containing terminals are in close proximity to the vestibular neurons which were tested and further implicate both NE and ACh as neurotransmitters in afferent pathways to the vestibular nuclei.

Acetylcholine↗