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Biomedical subjects

S V Reddy

Publications and source records attributed to S V Reddy.

At least 73 records · Page 4Linked to original sources
PubMed1981

Studies in the primate on the analgetic effects associated with intrathecal actions of opiates, alpha-adrenergic agonists and baclofen.

The effects of intrathecally administered opiates (morphine sulfate and meperidine), alpha-adrenergic agonists (clonidine and ST-91) and baclofen were examined on the shock titration threshold of macaque monkeys chronically prepared with intrathecal (I) or epidural (E) catheters. Spinal opiates produced a long-lasting analgesia which was antagonized by naloxone. The order of potency was I morphine greater than I meperidine greater than E meperidine greater than E morphine. Clonidine and ST-91, also produced a dose-dependent, long-lasting elevation in the shock titration threshold, antagonized by phentolamine, but not naloxone. L-baclofen, but not D-baclofen, resulted in a dose-dependent elevation of shock titration threshold, which was not antagonized by naloxone. Repeated administration at 24-h intervals over a 7-day period of morphine, clonidine or baclofen, resulted in a significant reduction in the analgetic effects of each drug. Cross tolerance between the three classes of agents was not observed. Intrathecal co-administration of inactive doses of ST-91 and morphine resulted in a near maximal increase in the shock titration threshold, which failed to show any significant tolerance over 21 days. Intrathecal ST-91 and morphine produced no change in either muscle strength, tendon reflexes, respiratory rate, urine formation, or the ability to locomote. Baclofen, in contrast, produced a dose-dependent decrease in muscle strength. That the intrathecal drugs did not produce anesthesia was demonstrated by their failure to block the avoidance response to ensuing ear shock cued by a light tactile stimulus applied to the hind paw. These results clearly indicate that a powerful analgesia can be produced by selectively activating adrenergic, opiate, and baclofenergic receptor systems in the spinal cord.

Adrenergic alpha-Agonists↗
PubMed1981

Giant traumatic false aneurysm of the internal carotid artery associated with a carotid-cavernous fistula. Case report.

A case of giant traumatic false aneurysm of the intracranial internal carotid artery (ICA) with a concomitant carotid-cavernous fistula is reported. The fistula and the aneurysm persisted after ipsilateral cervical ICA ligation was performed elsewhere. Successful obliteration of the aneurysm and the fistula, with preservation of cross filling of the ipsilateral middle cerebral artery system, was accomplished by ligation of the intracranial ICA proximal to the origin of the posterior communicating artery with a 7-0 prolene suture, followed by transaneurysmal packing of the fistula.

Adolescent↗
PubMed1980

Spinal noradrenergic terminal system mediates antinociception.

Intrathecal administration of norepinephrine (NE) into the lumbar subarachnoid space of rats and cats implanted with chronic spinal catheters produced a strong, dose-dependent, behaviorally defined analgesia. The effect appeared mediated by an alpha-receptor inasmuch as phenylephrine, but not isoproterenol produced the intrathecal effect. Moreover, the antinociceptive effect of NE was antagonized by the prior systemic or intrathecal administration of phentolamine (an alpha-blocker), but was unaffected by pretreatment with propranolol (a beta-blocker). The effect of intrathecal NE was significantly potentiated by prior administration of Lilly 51641 (a monoamine oxidase inhibitor) and protriptyline (a re-uptake inhibitor), and was not antagonized by the intrathecal administration of a non-specific vasodilator, papaverine. The antinociceptive effect of intrathecal NE showed tachyphylaxis following repeated injections. No cross-tolerance between intrathecal NE and morphine was observed, suggesting that the spinal action of morphine is not mediated by spinal noradrenergic terminals. Importantly, naloxone had no effect on the intrathecal NE effect. The present data provide further evidence for the modulatory role of a spinal noradrenergic system on the spinal processing of nociceptive transmission.

Animals↗
PubMed1980

Spinal cord pharmacology of adrenergic agonist-mediated antinociception.

Intrathecal administration of norepinephrine (NE) and alpha adrenergic agonists in rats with chronic spinal catheters produced a significant elevation of the nociceptive threshold as measured by hot plate and tail flick. The intrathecal NE effect was dose-dependent and antagonized in a competitive fashion by pretreatment with phentolamine (alpha antagonist) but not by propranolol (beta antagonist). Intrathecal administration of isoproterenol (beta agonist) did not alter the nociceptive threshold. Effective doses of intrathecal NE did not produce demonstrable motor effects. Doses 20 times greater than the maximum analgesic dose produced marked weakness of the hindlimbs and tails. The intrathecal NE effect was not antagonized by intrathecal papaverine of bradykinin (vasodilators) or mimicked by angiotensin-II (vasoconstrictor). The intrathecal NE effect was not altered by intrathecal administration of subconvulsant doses of either picrotoxin (gamma-aminobutyric acid antagonist) or strychnine (glycine antagonist) or by i.p. administration of either naloxone (opiate antagonist) or methysergide (serotinin antagonist). The nociceptive threshold was significantly decreased 1 week after intrathecal administration of 6-hydroxydopamine, which depleted spinal cord NE by 85%. Intrathecal administration of tyramine (indirectly acting sympathomimetic amine) produced an elevation of the nociceptive threshold in a control group of animals but was less effective in animals pretreated with intrathecal 6-hydroxydopamine. The tyramine effect was antagonized by intrathecal phentolamine. Intravenous administration of aminophylline (phosphodiesterase inhibitor) did not potentiate the intrathecal NE effect. The relative antinociceptive potencies of alpha adrenergic agonists after intrathecal administration were: l-norepinephrine = dl-epinephrine greater than dl-alpha-methyl norepinephrine greater than clonidine greater than or equal to l-phenylephrine greater than or equal to 3,4-dihydroxytolazoline greater than or equal to oxymetazoline. The relative potencies of intrathecally administered alpha antagonists in antagonizing the intrathecal NE effect were: phentolamine greater than phenoxybenzamine greater than tolazoline greater than or equal to yohimbine.

Animals↗
PubMed1977

A sibship with hypervalinemia.

During routine screening of amino-acid disorders, we detected hypervalinemia in two sibs (a girl of 4 and a boy of 3 years of age) of a consanguineous marriage. There was no excess accumulation or excretion of leucine or isoleucine, which presumably indicates the absence of valine transaminase.

Amino Acid Metabolism, Inborn Errors↗
PubMed1977

Familial incidence of L-xylulosuria.

During a survey for genetic disorders, L-Xylulosuria, an autosomal recessive condition, was found to affect three cousins in an inbred family. There were no clinical symptoms.

Carbohydrate Metabolism, Inborn Errors↗