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Biomedical subjects

K R Reddy

Publications and source records attributed to K R Reddy.

At least 163 records · Page 9Linked to original sources
PubMed1983

Nonhealing duodenal ulceration due to candida.

An important role for candida in gastric and duodenal ulcer disease is being increasingly recognized. Causative factors implicated include the frequent use of cimetidine, and immunosuppressive or antibiotic therapy. Concerning cimetidine, there is no clear-cut evidence that the drug depresses cell mediated immunity; on the contrary, there is evidence that delayed hypersensitivity is enhanced. Acid reduction is the alternate and more likely explanation for any role of cimetidine in gastric and duodenal candidiasis. We report a patient with a duodenal ulcer, which repeatedly bled and failed to heal in hospital on standard antacid and cimetidine therapy. Candida was identified in the ulcer and treated, using mycostatin suspension, resulting in complete healing. We feel that candida involvement of duodenal ulcers may be more common than is generally recognized, and may be the cause for nonhealing in certain patients already on optimum therapy.

Aged↗
PubMed1983

Acute hepatitis associated with campylobacter colitis.

A patient with proven campylobacter fetus ss. jejuni acute colitis developed hepatocellular dysfunction, which paralleled the course of the colitis. Liver biopsy showed nonspecific reactive hepatitis. Other causes of acute hepatocellular damage were excluded. The patient made a complete recovery.

Acute Disease↗
PubMed1983

Hemosuccus pancreaticus: a cause for obscure gastrointestinal bleeding--diagnosis by endoscopy and successful management by total parenteral nutrition.

Hemorrhage through the pancreatic duct (hemosuccus pancreaticus) is discussed in a patient with alcoholic chronic pancreatitis and anemia. The pancreatic duct as the source of bleeding was determined by use of duodenoscopy; abdominal arteriograms were normal. It is postulated that the patient's bleed was intermittent and of venous origin, probably associated with pancreatic pseudocyst formation. Total parenteral nutrition could be considered in treatment of the condition if bleeding is not life threatening.

Adult↗
PubMed1982

Effect of acetaminophen and salicylate on aspirin-induced inhibition of human platelet cyclo-oxygenase.

Recent studies have shown that salicylic acid, a metabolite of aspirin, effectively competes for the same site on the platelet cyclo-oxygenase enzyme. In the present investigation we have evaluated the effect of salicylate and acetaminophen on aspirin induced inhibition of cyclo-oxygenase and platelet function. Results of our studies show that both drugs at equimolar concentrations had no inhibitory effect on aspirin induced blockage of cyclo-oxygenase or platelet function. Even at higher concentrations acetaminophen failed to protect cyclo-oxygenase or prevent inhibition of platelet function by aspirin. Salicylate at concentrations above 5 mM effectively blocked the inhibition of cyclo-oxygenase activity and platelet aggregation in response to arachidonate.

Acetaminophen↗
PubMed1982

Systemic vasopressin therapy for Mallory-Weiss bleeding.

Over a period of one year, five of 101 patients admitted to our center because of upper gastrointestinal bleeding were found to have a Mallory-Weiss tear. This condition usually responds to conservative management. Torrential bleeding necessitating surgery is uncommon. Three of the patients, reported here, bled torrentially and were considered surgical candidates. Two received systemic vasopressin while being prepared for operation, with rapid, dramatic cessation of bleeding. Although this is a limited experience, we are impressed enough to believe that intravenous vasopressin should be given a trial in all hospitalized patients who continue to bleed from a tear in the region of the esophagogastric junction.

Adult↗
PubMed1981

Modification of human platelet response to sodium arachidonate by membrane modulation.

Previous studies have shown that the majority of mongrel dogs have platelets that do not aggregate when stirred with sodium arachidonate, but respond normally to other aggregating agents. Here we have created a model in which human platelets mimic the unusual behavior of canine cells. Brief exposure of human platelets to low concentrations of prostacyclin will convert them to a physiologic state resembling that of canine platelets without causing elevation of intracellular levels of cAMP. Studies on the conversion of arachidonic acid showed that prostacyclin did not cause any inhibition of thromboxane B2 generation. Exposure of prostacyclin treated platelets to epinephrine restored their sensitivity to arachidonate without causing any detectable changes in levels of cAMP. The selective inhibition achieved by PGI2 could be mimicked by the endoperoxide analog. U44069, a thromboxane inhibitor, U-51605, and an endoperoxide/thromboxane receptor blocker, 13-APA. Inhibition induced by these compounds was also reversed by epinephrine. A calcium channel blocker, verapamil, and an alpha blocker, dihydroergocryptine, effectively blocked the corrective influence of epinephrine on prostacyclin-treated platelets. Results of these studies show that catecholamines and prostaglandin receptors share close sites on the membrane and exhibit a degree of cooperativity in calcium modulation. Dog platelets that do not respond to products of AA metabolism and the human platelets made to behave like canine platelets may have a defect in calcium mobilization and this defect is corrected by adrenaline through an alpha receptor modulation.

Adult↗
PubMed1980

Influence of pH on the prostacyclin (PGI2) mediated inhibition of platelet function.

Prostacyclin (PGI2) stimulates platelet adenylate cyclase, elevates intracellular levels of cyclic adenosine monophosphate and blocks the response to aggregating agents. It is rapidly hydrolyzed (T 1/2-5 min) to 6-keto prostaglandin F1 alpha at acid or neutral pH. As a result, platelets incubated with PGI2 will recover spontaneously and respond to aggregating agents within 15--60 min, depending on the initial PGI2 concentration. In the present study we have evaluated the influence of temperature and pH on the stability of PGI2 and its effects on platelet function. PGI1 in Tris buffer was stabilized at several pH levels and stored at 37 degrees C, 23 degrees C, and 4 degrees C. Inhibitory influence in platelet function was lost rapidly at pH 7.2--7.4, lasted several hours at pH 7.8 and was retained indefinitely at pH 7.8 and was retained indefinitely at pH 8 or above. PGI2 (2.8 nM) completely inhibited the response to arachidonic acid for 15 min. at pH 7.4, for at least 1 hour at pH 7.8 and showed no reversal of inhibition after 48 hours at pH 8. However, PGI2 inhibited samples at pH 8 completely recovered their sensitivity to arachidonic acid when the pH was reduced to 7.4. These findings indicate that the biological activity of PGI2, though labile at neutral pH, is stable at pH 8 and can inhibit, cAMP mediated platelet functions for at least 48 hours. Because of its pH dependence, PGI2 may be a useful agent for prolonging the sensitivity of stored platelets.

Adult↗
PubMed1980

The influence of epinephrine on prostacyclin (PGI2) induced dissociation of ADP aggregated plateletes.

Prostacyclin (PGI2) is a powerful inhibitor of platelet function and recent studies have indicated that it can dissociate aggregated platelets in vivo. The present investigation has evaluated the mechanism involved in the dissociation of ADP aggregated platelets by PGI2, the influence of epinephrine on the process of PGI2 mediated disaggregation, and effects of the catecholamine on the refractory state of PGI2 dispersed cells. Dissociation of ADP aggregates by PGI2 was concentration and time dependent, caused complete disappearance of sensitive platelet clumps and restored platelet discoid form. The dispersed platelets were refractory to further stimulation by ADP, thrombin, arachidonate or the calcium ionophore, A23187. Measurement of cAMP revealed no change in control levels after aggregation by ADP, but a sharp increase during and after dissociation by PGI2. Epinephrine added to ADP aggregates before or after PGI2 blocked disaggregation, or stopped dissociation if already in progress, and caused a rapid fall in the high levels of cAMP stimulated by PGI2. Agents to which PGI2 dissociated platelets were refractory, including ADP, arachidonate and A23187 caused no lowering of elevated cAMP levels. Reduction of high levels of cAMP in PGI2 dispersed platelets by epinephrine did not result in reaggregation. However, epinephrine addition to refractory platelets restored in large measure their sensitivity to aggregation by arachidonate, thrombin, ADP and A23187.

Adenosine Diphosphate↗
PubMed1980

Influence of trifluoperazine on platelet aggregation and disaggregation.

Calmodulin has been shown to activate platelet phospholipase A2 and initiate the metabolism of arachidonic acid. Trifluoperazine (stelazine), an agent which selectively binds calmodulin, inhibits phospholipase activity induced by calcium. We have evaluated the effect of this agent on the aggregation, disaggregation and reaggregation of human platelets. Results of our study have shown that stelazine is a selective inhibitor of the second wave response of platelets to the stimulation of agonists. The compound causes dissociation of aggregated platelet clumps and induces a refractory state in dispersed cells. Epinephrine reverses the refractory state and potentiates the response of dissociated cells to the action of thrombin, arachidonate and ionophore A23187. Stelazine elevates cAMP levels to some extent and inhibits release of labeled arachidonic acid from platelet membranes in response to thrombin induced stimulation. Epinephrine may correct stelazine induced inhibition by acting through alpha-adrenergic mechanism, by inducing changes in membrane permeability to calcium, by releasing membrane associated calcium or by directly promoting deacylation of phospholipids.

Arachidonic Acids↗
PubMed1980

Bacterial flora in acute small bowel obstruction.

The bacterial flora has been studied by direct sampling techniques at various levels in 25 cases of acute small bowel obstruction. The presence of coliform bacteria in the distal ileum below the level of obstruction and progressive increase of bacterial counts from the jejunum towards the distal ileum above the obstruction suggest that ingestion may not be the only factor of bacterial growth in the small bowel in acute intestinal obstruction. Moreover, indirect peritoneal contamination in 8 cases of long-standing acute small bowel obstruction indicates that possibly a combination of multiple factors like ingestion of food, retrograde spread from the large bowel, lymphatic and/or hematogenous spread are responsible for bacterial dissemination in and around the obstructed bowel.

Adolescent↗
PubMed1979

Tranylcypromine induced hypertension is not mediated by the inhibition of prostacyclin synthesis.

Tranylcypromine (TCP) is a monoamine oxidase inhibitor used extensively in the treatment of patients with reactive depression. Hypertensive crisis can complicate drug therapy, but the mechanism through which TCP causes high blood pressure is unknown. The present study was undertaken because recent investigations have shown that TCP can inhibit production of a potent vasodilator hormone, prostacyclin (PGI2), by blood vessels, possibly explaining the mechanism of pressor effects by the drug. Heart rate, left atrial, pulmonary artery and aortic pressures were monitored in dogs under control conditions and continuously following the IV infusion of TCP at the rate of 1 mg/kg over a period of one minute. Right femoral and the left internal mammary arteries were obtained during the control period and the left femoral and right internal mammary arteries resected between 6 and 30 minutes following drug infusion for PGI2 studies. Concentrations of the drug that caused significant elevation of the mean systemic pressure to 203 +/- 8 mmHg had no inhibitory effect on PGI2 production. Therefore, the influence of TCP on the hemodynamic parameters does not appear to be mediated through the inhibition of vascular PGI2 synthesis.

Animals↗
PubMed1978

Acute toxicity of 12,13-epoxytrichothecenes in one-day-old broiler chicks.

Acute toxic effects of several 12,13-epoxytrichothecenes were investigated in 1-day-old broiler chicks by single oral doses. The 7-day median lethal dose values of purified 8-acetylneosolaniol, diacetoxyscirpenol, T-2 toxin, HT-2 toxin, neosolaniol, deacetyl-HT-2 toxin, and T-2 tetraol were 3.22 +/- 0.26, 3.82 +/- 0.40, 4.97 +/- 0.44, 7.22 +/- 0.39, 24.87 +/- 2.64, 30.18 +/- 7.53 (incomplete value), and 33.79 +/- 5.39 mg/kg of body weight, respectively. Deaths occurred during the 8- to 60-h period after dosing with the tested trichothecenes. Within 4 to 10 h after dosing, inappetence, asthenia, diarrhea, and coma generally developed. Sublethal doses of each toxin decreased feed consumption and weight gain proportionally with the amounts of toxins administered. These results demonstrate that the toxic potency of 12,13-epoxytrichothecenes varies depending on the modification of side chains in the molecule.

Administration, Oral↗