Search PubMed⌕ Search

Biomedical subjects

R Kapoor

Publications and source records attributed to R Kapoor.

At least 127 records · Page 7Linked to original sources
PubMed1994

Appraisal of surgical and endoscopic management of choledocholithiasis.

One hundred and ten patients with common bile duct (CBD) stones were treated in the Department of Surgical Gastroenterology at SGPGIMS, Lucknow, India between January 1989 and December 1992. The primary modality of treatment was surgery in 62 patients (group I) and endoscopic sphincterotomy (ES) in 48 (group II). The two groups were well matched with respect to clinical features and presence of medical risk factors. Surgical clearance of CBD stones was achieved in 58 patients (93.5%; group Ia). Four patients (7%) had retained stones following surgery (group Ib). In group II, the CBD was cleared by endoscopic means in 20 out of 48 patients (42%) and was categorized into group IIa. In the remaining patients ES was followed by CBD exploration (group IIb). Significantly higher morbidity was seen in patients needing CBD surgery following attempted endoscopic clearance, because of ES-related complications, such as bleeding, cholangitis, septicaemia and numerous others. Use of ES to treat CBD stones on a routine basis was therefore not found to be any better than one-time surgical exploration.

Adult↗
PubMed1994

Palliative surgical treatment of malignant obstructive jaundice.

One-hundred-and-forty-five cases of malignant obstructive jaundice were seen from January 1989-December 1992. Carcinoma gallbladder (74/145) and carcinoma pancreas (67/145) were the two common causes. Fifty patients underwent a palliative surgical biliary bypass procedure. Jaundice was present in all the patients. Pruritus (40/50), cholangitis (17/50) and gastric outlet obstruction (11/50) were the other predominant symptoms which required palliation. Surgical palliation was achieved with a morbidity and mortality of 38% and 8%, respectively. Jaundice, pruritus and cholangitis were relieved in 92%, 88% and 88%, respectively. All patients with gastric outlet obstruction had complete relief. The mean hospital stay was 18.5 days. The mean survival was 6.5 months and 8.6 months for carcinoma gallbladder and carcinoma pancreas, respectively.

Adult↗
PubMed1994

Role of oxyradicals in cardiovascular depression and cellular injury in hemorrhagic shock and reinfusion: effect of SOD and catalase.

We investigated the effects of hemorrhagic shock and reinfusion on the cardiac function and contractility, plasma CK and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL), cardiac chemiluminescence (LV-CL), antioxidant enzymatic activity [superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px)], and malondialdehyde (MDA) concentration in anesthetized dogs, to determine the role of oxyradicals in cardiac depression and cellular injury in hemorrhagic shock and reinfusion. The dogs were assigned to four groups: group I (sham), 4 hrs duration; group II, 4 hr of shock; group III, 2 hr of shock, followed by reinfusion for 2 hr; and group IV, as in group III, but pretreated with SOD and catalase. Hemorrhagic shock was produced by withdrawing blood to maintain the mean arterial pressure at 50 +/- 5 mm Hg. Cardiac function and contractility were depressed during hemorrhagic shock. Plasma CK; CK-MB and lactate; and cardiac MDA, Mn-SOD, and CuZn-SOD increased, while catalase activity decreased during shock. Following reinfusion after 2 hr of shock, hemodynamic parameters and plasma lactate tended to return toward control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total SOD, Mn- and CuZn-SOD increased further, while LV-CL and GSH-Px decreased. In spite of the increased antioxidant reserve, oxidative damage was noted. Pretreatment with SOD and catalase attenuated the deleterious effects of shock and reinfusion on the cardiovascular function, plasma CK, CK-MB, and lactate, PMNL-CL, cardiac MDA and SOD, and LV-CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals (O2-, H2O2) may be partly involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.

Animals↗
PubMed1994

Neonatal behavior in full-term small for date.

Fifty newborns, 25 full term SFDs (small for date) and 25 full term AGAs (appropriate for gestational age) were taken up for comparative study of their behavior using BNBAS (Brazelton's neonatal behavior assessment scale). The study revealed that full term SFDs performed significantly poorly on all items under cluster interactive processes compared to their counterparts full term AGAs on day 1. They also showed similar poor performance in clusters of motor processes and organizational processes (State control). Follow up assessment on day 30 revealed significantly better performance in these clusters. However, the performance of SFD babies in all items of cluster of organizational processes (physiological response) was comparable to that of AGA babies in the initial as well as follow up assessments.

Birth Weight↗
PubMed1993

Internodal potassium currents can generate ectopic impulses in mammalian myelinated axons.

Positive clinical symptoms can arise from ectopic action potentials in several disorders of myelinated axons. Here we report that an elevated K+ concentration in the periaxonal, internodal space can cause internodal K+ currents to become excitatory, resulting in slow potential oscillations and associated bursts of ectopic spikes. Ectopic firing may therefore be favoured by conditions in which periaxonal K+ buffering is compromised.

Action Potentials↗
PubMed1993

Utilization of beta-carotene from Spirulina platensis by rats.

The availability of beta-carotene from Spirulina as compared to standard all trans beta-carotene was studied by the liver and kidney vitamin A storage method. After 21 days of vitamin A depletion, the rats were repleted with beta-carotene from Spirulina and a standard source at two dietary levels (60 and 120 micrograms/day) for a 10 day period. At lower levels, the liver storage levels of vitamin A and the percent of beta-carotene absorption were comparable to those of the standard. At higher levels both these parameters of the Spirulina fed group were significantly (P < 0.01) inferior to the standard source fed group. However, the Spirulina fed group showed better (P < 0.05) growth than the standard fed group did at both low and high levels of feeding.

Animals↗
PubMed1993

Effect of supplementation of blue green alga (Spirulina) on outcome of pregnancy in rats.

To study the supplementary effect of Spirulina, pregnant rats were fed 5 different kinds of diets (casein, Spirulina, wheat gluten, Spirulina + wheat gluten, Spirulina-without additional vitamins and minerals), each providing 22% protein during the period of pregnancy. The outcome of pregnancy was assessed from litter and dams' weight and litter size. Maternal weight gain was found to be maximum with Spirulina + wheat gluten and least with the wheat gluten diet. Rats receiving Spirulina containing diets produced significantly (p < 0.05) higher litter size than those receiving casein and wheat gluten. In spite of having higher litter size, Spirulina containing diet groups produced pups with birth weights comparable to those of casein. Spirulina appears to be a good dietary supplement during pregnancy.

Animals↗
PubMed1993

Iron status and growth of rats fed different dietary iron sources.

The present study was carried out to investigate the availability of iron from spirulina, whole wheat, whole egg and standard ferrous sulphate in terms of haemoglobin formation, serum and tissue iron levels. Male albino Wistar rats were first depleted of iron by giving low-iron diet (9 ppm) and bleeding 1-2 ml blood at weekly intervals for a period of 21 days. The anaemic rats were repleted with iron sources at a level of 35 ppm for 21 days. Rats receiving whole egg gained significantly (p < 0.01) higher weight than the rest of the three groups. The increase in haemoglobin was significantly higher with ferrous sulphate than with whole wheat (p < 0.05), spirulina and whole egg (p < 0.01). Feeding of ferrous sulphate, whole egg and spirulina produced significantly higher tissue iron levels than feeding of whole wheat. Thus, availability of iron from spirulina and whole egg were found to be comparable to that of the standard.

Animals↗
PubMed1993

Endogenous catecholamines modulate growth hormone release in the conscious rat during hypoglycaemia but not in the basal state.

To investigate the role of endogenous catecholamines and 5-hydroxytryptamine in the control of growth hormone (GH) secretion, secretory profiles of GH and prolactin were measured in conscious, male rats following intravenous administration of either 1) alpha 2 antagonist idazoxan 2 mg/kg, a dose that blocked alpha 2 agonist induced GH rise, 2) alpha 1 antagonist prazosin 1 mg/kg, 3) non-specific beta-blocker propranolol 1.5 mg/kg, a dose that prevented beta 2 agonist (salbutamol) induced inhibition, 4) serotonin antagonist cyproheptadine 0.5 mg/kg, a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels and pulsatile GH release persisted. Unilateral injections of prazosin, propranolol and idazoxan were made into the medial basal hypothalamus and preoptic-anterior hypothalamic area and of cyproheptadine into the medial basal hypothalamus, all with no effect on short-term GH release. GH and prolactin secretory profiles were measured after giving rats 6 units/kg intravenous insulin. Blood glucose levels fell to less than 50% basal. Hypoglycaemia caused a non-significant 30% fall in mean 2 h GH. Intravenous idazoxan, prazosin, propranolol and cyproheptadine (doses as in first study) did not modify the blood glucose fall, but idazoxan produced a significant reduction of mean GH compared to insulin alone (4 +/- 1.1 ng/ml SEM, idazoxan/insulin versus 16 +/- 5.6 ng/ml, saline/insulin). The lack of an effect of alpha- and beta-blockers on normal, pulsatile GH release is against a role for endogenous catecholamines in controlling this release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1993

Alpha 2 and beta adrenoceptors in the mediobasal hypothalamus and alpha 2 adrenoceptors in the preoptic-anterior hypothalamus stimulate prolactin secretion in the conscious male rat.

Plasma prolactin concentrations were measured in unanaesthetized male rats before and after stereotaxic microinjection of adrenergic agents into the mediobasal and preoptic-anterior hypothalamus. In the mediobasal hypothalamus injection of the alpha 2 agonist clonidine produced a dose-dependent increase in prolactin secretion over the dose range 0.1 to 10 nmoles, the stimulation due to 1 nmole being blocked by idazoxan (alpha 2 antagonist). Stimulation of prolactin release was also caused by isoprenaline (beta agonist) and was significantly reduced by the beta antagonist propranolol. The beta 2 agonist salbutamol was also effective in stimulating prolactin secretion. However, the adrenergic agonists, noradrenaline (mixed alpha and beta), phenylephrine (alpha 1) and tyramine (sympathomimetic) failed to affect prolactin secretion. In the preoptic-anterior hypothalamus clonidine caused a dose-dependent increase in prolactin secretion over the dose range 0.001 to 10 nmoles, the stimulation due to 0.1 nmole being abolished by idazoxan. While prolactin levels were significantly elevated by noradrenaline and tyramine, phenylephrine was ineffective. We conclude that the activation of alpha 2 and beta 2 adrenoceptors in the mediobasal hypothalamus and of alpha 2 adrenoceptors in the preoptic-anterior hypothalamus, on or near prolactin-regulating neurons, results in increased prolactin secretion. An alpha 1 inhibitory action in the mediobasal hypothalamus has however not been ruled out. Adrenergic inputs in the preoptic-anterior hypothalamus appear to exert a predominant facilitatory effect on prolactin secretion.

Adrenergic alpha-Agonists↗
PubMed1993

Local hypothalamic adrenoceptor activation in rat: alpha 1 inhibits and alpha 2 stimulates growth hormone secretion.

We made stereotaxic microinjections of adrenoceptor agonists and the catecholamine-releasing agent, tyramine, into the preoptic anterior hypothalamic area (PO/AHA) or the medial basal hypothalamus (MBH) of unstressed rats. Growth hormone (GH) plasma concentrations were measured serially before and after intrahypothalamic injections. Noradrenaline and phenylephrine inhibited GH secretion wherever injected but were effective at lower doses in the PO/AHA. Clonidine stimulated GH secretion at both sites, at several doses in the MBH and only at one dose in the PO/AHA. Tyramine inhibited GH when injected in the PO/AHA, but not in the MBH. We conclude: (a) alpha 1 inhibition is predominant over alpha 2 stimulation of GH on or near somatostatin neurons; (b) alpha 2 stimulation predominates over alpha 1 inhibition of GH on or near GRF neurons, and (c) endogenous catecholamines in the PO/AHA have a predominantly inhibitory effect on GH secretion.

Animals↗
PubMed1993

Interactions between the effects of opioid, serotonin and alpha-2-adrenergic receptor agonists on growth hormone release in the male rat. Intrahypothalamic administration.

In a previous study, we identified a number of negative interactions between the growth hormone (GH)-releasing effects of opioid, alpha 2 and serotonin agonists when given intravenously together to male rats. To further characterise these interactions, conscious male rats were given unilateral intrahypothalamic injections of clonidine, the serotonin agonist quipazine and a mu opioid agonist (DAGO), and plasma GH levels were measured. Injection of all three drugs separately into the mediobasal hypothalamus (MBH) increased GH release. Combinations of DAGO-clonidine (p = 0.04), clonidine-quipazine (p = 0.04) and DAGO-clonidine-quipazine (p = 0.04) produced significantly less than additive GH release, whereas DAGO-quipazine produced additive release. MBH injection of the alpha 2 antagonist idazoxan 10 nmol prevented the GH rise due to clonidine, but did not inhibit release due to DAGO. Injection of DAGO and clonidine but not quipazine into the preoptic-anterior hypothalamic area (PO/AHA) increased GH release, and combination injections of DAGO and clonidine produced additive release. PO/AHA idazoxan 10 nmol prevented GH release caused by both clonidine and DAGO, suggesting that idazoxan prevents opioid-induced as well as clonidine-induced suppression of somatostatin release. The inability of MBH idazoxan to block DAGO-induced GH release suggests that opioid-adrenergic interactions here are not due to an opioid GH-releasing action exerted through catecholaminergic pathways. The negative interaction previously identified between intravenous opioids and quipazine probably occurs outside the hypothalamus.

Adrenergic alpha-Agonists↗