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Biomedical subjects

A Banerjee

Publications and source records attributed to A Banerjee.

At least 343 records · Page 19Linked to original sources
PubMed1993

Inhibition of sarcoplasmic reticulum calcium release reduces myocardial stunning.

Recent findings indicate that ischemia/reperfusion (IR) is associated with phospholipase C (PLC)-induced inositol 1,4,5-triphosphate production, as well as abnormal sarcoplasmic reticulum (SR) Ca2+ release. Therefore, we hypothesized that increased SR Ca2+ release may contribute to Ca2+ overload and myocardial stunning. Neomycin (NEO) was used to inhibit PLC, and sodium dantrolene (DAN) was used to inhibit myocardial SR Ca2+ release. The purposes of this study were (1) to determine if PLC inhibition would reduce IR-induced ventricular dysfunction, (2) to examine ventricular function during inhibition of SR Ca2+ release prior to ischemia, and (3) to examine the influence of SR Ca2+ release inhibition on post-IR ventricular function. Left ventricular developed pressure (DP) and +/- dP/dt of isolated crystalloid perfused rat heart (Langendorff apparatus) paced at 350 bpm were compared before and after global IR (38 degrees C, 20 min I, 40 min R) to assess functional recovery. PLC was inhibited with NEO (10 microM x 5 min prior to ischemia), and SR Ca2+ release was retarded with DAN (12.5 microM) in 0.05% DMSO (vehicle) infused for 3 min via the aortic cannula 13 min prior to ischemia. No effect on DP was observed during NEO or DAN infusion. NEO and DAN pretreatment each improved recovery of DP (% recovery +/- SEM) following IR: control, 46.5 +/- 5.1%; NEO + IR, 71.0 +/- 6.3%,* vehicle + IR, 44.4 +/- 2.9%; DAN + IR, 71.0 +/- 4.7%, *, # (*P < 0.05 vs control IR, #P < 0.05 vs vehicle + IR, ANOVA, Scheffe F test, n = 5 all groups). We conclude that SR Ca2+ release during IR contributes to myocardial stunning.

Adenosine Triphosphate↗
PubMed1993

Gut ischemia mediates lung injury by a xanthine oxidase-dependent neutrophil mechanism.

Neutrophils (PMNs) are believed to play a key role in the pathogenesis of postinjury adult respiratory distress syndrome. We have previously shown that gut ischemia/reperfusion (I/R) produces lung injury by a process that requires PMNs. More recently, we have shown that xanthine oxidase (XO) plays a role. The purpose of this study was to characterize the mechanistic sequencing of XO activity versus the PMN in this model of gut I/R-induced lung injury. Normal and XO-inactivated (tungsten enriched, molybdenum depleted diet) rats underwent 45 min of superior mesenteric artery occlusion. After 6 hr reperfusion, blood was sampled and gut and lungs harvested. Myeloperoxidase (MPO) was used to quantitate PMN presence in the gut and lungs, while circulating PMN priming was measured as the difference in superoxide production with and without the activating stimulus, fMLP. 125I-labeled albumin leak was used as a marker for lung endothelial permeability. We observed that the gut I/R increased gut MPO levels, primed circulating PMNs, increased lung MPO levels, and provoked distant lung leak. XO inactivation abolished gut MPO activity, attenuated circulating PMN priming, and blocked lung leak. In conclusion, XO plays a proximal role in the pathogenesis of remote organ injury following splanchnic hypoperfusion.

Animals↗
PubMed1993

Effects of PEG-electrolyte (Colyte) lavage on serum acetaminophen concentrations. A model for treatment of acetaminophen overdose.

The purpose of this study was to evaluate whole gut lavage with polyethylene glycol electrolyte solution (Colyte), as a potentially adjunctive measure in lowering serum acetaminophen levels. The effect of bowel lavage was evaluated on serial serum acetaminophen concentrations after 2-g and 4-g doses in 7 and 12 male patients, respectively. Mean peak level of serum acetaminophen after 2 g (60 min after intake) was not significantly lowered by bowel lavage. After 4 g, peak acetaminophen serum levels were significantly lower after bowel lavage (65.4% of controls, P < 0.001). Urinary concentrations of the mercapturic acid conjugate of the toxic metabolite were also significantly reduced by lavage (55% after 2 g and 45% after 4 g, P < 0.01). Activated charcoal given orally after administration of 4 g of acetaminophen had no significant effect on peak serum levels and had no additive effect on lavage. These studies suggest that rapid, complete bowel lavage with a polyethylene glycol electrolyte solution may be beneficial as an adjunct to the treatment of the acetaminophen intoxication.

Acetaminophen↗
PubMed1993

Cardiac preconditioning does not require myocardial stunning.

Efforts to minimize the deleterious effects of intraoperative myocardial ischemia-reperfusion (I/R) injury have been primarily directed at optimizing cardioplegic solutions and altering reperfusion conditions. Classically, myocardial I/R has been associated with cardiac mechanical dysfunction ("stunning"). Recently, we reported an alpha 1-adrenergic receptor-mediated mechanism of paradoxical myocardial protection against I/R insult induced by a prior episode of transient ischemia, a phenomenon known as "ischemic preconditioning." Myocardial stunning resulting from transient ischemia has previously been associated with ischemic preconditioning, prompting intuitively negative bias against the clinical application of this phenomenon. The purpose of this study was to determine whether transient ischemia of insufficient duration to cause prolonged mechanical dysfunction (stunning) can induce favorable cardiac preconditioning. Isolated-perfused rat hearts were allowed to equilibrate for 8 minutes and were then subjected to either 2 minutes of global, normothermic transient ischemia or 2 minutes of 50 mumol/L phenylephrine infusion. A stabilization period of perfusion lasting 10 minutes after the termination of transient ischemia or phenylephrine infusion was followed by a standard I/R challenge (20 minutes of global, normothermic ischemia; 40 minutes of reperfusion). Ventricular function (measured as developed pressure in millimeters of mercury) recovered rapidly after transient ischemia such that no impairment was present before the subsequent standard I/R challenge. Phenylephrine treatment was associated with no residual inotropy before I/R challenge. Control hearts were subjected only to the standard I/R challenge after an initial 20-minute equilibration period. After reperfusion control hearts exhibited 54.4% recovery of initial left ventricular developed pressure. Transient ischemia- and phenylephrine-preconditioned hearts recovered 84.4% (p < 0.01) and 82.4% (p < 0.01), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Higher white blood cell counts and band forms in newborns delivered vaginally compared with those delivered by cesarean section.

The authors retrospectively reviewed complete blood counts in the medical records of all babies admitted to a normal newborn nursery from January through December 1989. The subjects consisted of 326 babies who were delivered vaginally (VgD) and 138 who were delivered by Cesarean section (CS). All blood samples were drawn by warmed or unwarmed heel sticks or by venipuncture. The subject's age at the time of blood drawing was similar in both VgD and CS groups (13.4 vs. 13.9 hours, P = 0.51). The number of total leukocytes, neutrophils, band forms, and platelets was significantly higher in VgD newborns than in CS newborns. The mean and standard error of the mean for each of these blood counts (each per microliter) were 23.9 x 10(9) +/- 0.33 versus 21.1 x 10(9) +/- 0.6, 14.6 x 10(9) +/- 0.26 versus 12.8 x 10(9) +/- 0.39, 1.18 x 10(9) +/- 0.08 versus 0.82 x 10(9) +/- 0.08, and 304 x 10(9) +/- 4.1 versus 286 x 10(9) +/- 0.6, respectively (P values for the first three comparisons were all less than 0.005). However, there was no difference between the two groups with regard to hemoglobin, hematocrit, and absolute number of lymphocytes, eosinophils, basophils, and monocytes (P > 0.5). It was speculated that the higher leukocyte, neutrophil, and band counts in VgD babies are the consequences of physical stress and periodic hypoxia, which are more frequent and prolonged with VgD compared with CS delivery. The authors suggest that the mode of delivery should be considered when interpreting blood counts in neonates.

Cesarean Section↗
PubMed1993

Preconditioning against myocardial dysfunction after ischemia and reperfusion by an alpha 1-adrenergic mechanism.

Preconditioning may find ready applicability in humans facing scheduled global cardiac ischemia-reperfusion (IR) during bypass or transplantation, where such a maneuver is feasible before arrest. Our objective was to delineate and exploit the endogenous preconditioning mechanism triggered by transient ischemia (TI) and thereby attenuate myocardial postischemic mechanical dysfunction by clinically acceptable means. Preconditioning by 2 minutes of TI followed by 10 minutes of normal perfusion protected isolated rat left ventricle function assessed after 20 minutes of global, 37 degrees C ischemia and 40 minutes of reperfusion. Final recovery of developed pressure (DP) was improved (91.5 +/- 1.9% of equilibration DP versus unconditioned IR control, 57.4 +/- 2.4%, P < .01) and was accompanied by increased contractility (+/- dP/dt). Norepinephrine release increased after TI, and reserpine pretreatment abolished TI preconditioning. This suggests that endogenous norepinephrine mediates functional preconditioning in rat. Brief pretreatment (2 minutes) with exogenous norepinephrine reproduced the protection (89.1 +/- 1.4%) of postischemic function. Functional protection persisted after the hemodynamic effects had resolved. Norepinephrine-induced preconditioning was simulated by phenylephrine and blocked by alpha 1-adrenergic receptor antagonist. TI preconditioning was similarly lost after selective alpha 1-adrenergic receptor blockade. We conclude that transient ischemic preconditioning is mediated by the sympathetic neurotransmitter release and alpha 1-adrenergic receptor stimulation. Although the postreceptor mechanism remains unclear, functional protection after IR does not seem related to the magnitude of ATP depletion and elevation of resting pressure during ischemia. Rather, the endogenous mechanisms facilitate both recovery of mechanical function and ATP repletion during reperfusion.

Animals↗
PubMed1993

Effectiveness of glass-ionomer surface protection treatments: a scanning optical microscope study.

Due to their complex setting reaction, glass-ionomer cements require careful control of hydration during the initial 48-hour maturation period. This in vitro study was designed to evaluate the efficacy of three surface protection treatments (copal varnish, unfilled bonding resin and a dentine bonding agent) in preventing water penetration into 40 restorations placed in recently extracted third molars. The sealing ability was analysed using confocal light microscopy to visualise dye penetration into the samples. The results indicate that the dentine bonding agent, in vitro, provides a comprehensive barrier to water movement.

Acrylates↗
PubMed1993

Microbial reduction of 1-(4-fluorophenyl)-4-[4-(5-fluoro-2-pyrimidinyl)-1- piperazinyl]butan-1-one.

Among various micro-organisms screened for the stereoselective reduction of 4-chloro-1-(4-fluorophenyl)butan-1-one (1), Hansenula polymorpha [American Type Culture Collection (A.T.C.C.) 26012 and 86014], Nocardia salmonicolor [Squibb Culture (S.C.) 6370], Arthobacter simplex (A.T.C.C. 6949), Mycobacterium vaccae (A.T.C.C. 29678), Candida boidinii (A.T.C.C. 13821) and Saccharomyces cerevisiae (A.T.C.C. 13792) reduced compound 1 to the corresponding (R)-(+)-alcohol (2). In contrast, Lactobacillus kefir (A.T.C.C. 35411), Pullularia pullulans (A.T.C.C. 16623), Trigonopsis variabilis (A.T.C.C. 10679) and Cunninghamella echinulata (A.T.C.C. 26269) reduced compound 1 to the (S)-(-)-alcohol (2). When 1-(4-fluorophenyl)-4-(1-piperazinyl)butan-1-one (3) was used as substrate for the reduction, only Nocardia globerula (A.T.C.C. 12505) and Saccharomyces cerevisiae (A.T.C.C. 13792) converted compound 3 into the corresponding (R)-(+)-alcohol (4). Organisms which reduced compound 1 were inactive for the reduction of compound 3. 1-(4-Fluorophenyl)-4-[4-(5-fluoro-2- pyrimidinyl)butan-1-one (5) was reduced to the corresponding (R)-(+)-alcohol (6) by Mortierella ramanniana (A.T.C.C. 38191) and to the (S)-(-)-alcohol (6) by Pullularia pullulans (A.T.C.C. 16623). (R)-(+)-compound 2 and compound 4 are key chiral intermediates in the total chemical synthesis of (R)-(+)-compound 6, an effective antipsychotic agent under development at Bristol-Myers Squibb. A single-stage (fermentation/biotransformation) process and two-stage (fermentation and subsequent biotransformation by cell suspensions) process were developed for the stereoselective reduction of compound 5 to (R)-(+)-compound 6 by Mortierella ramanniana (A.T.C.C. 38191). In both processes, the reaction yield of 98% and the optical purity of 99.4% were obtained for (R)-(+)-compound 6. The enzyme which catalysed the reduction of compound 5 to (R)-(+)-compound 6 was purified to homogeneity. The purified protein consisted of a single polypeptide of 29 kDa.

Bacteria↗
PubMed1993

Cold ischemia and reperfusion each produce pulmonary vasomotor dysfunction in the transplanted lung.

Pulmonary vascular resistance is significantly increased in the transplanted lung. We hypothesized that the ischemic or reperfusion injuries incurred by the transplanted lung may produce pulmonary vasomotor dysfunction, which in turn may produce increased pulmonary vascular resistance. In a dog model of autologous lung transplantation, the purpose of this study was to examine the following mechanisms of pulmonary vasomotor control and to relate each of them to cold ischemia and to reperfusion: (1) endothelium-dependent cyclic guanosine monophosphate-mediated vasorelaxation (response to acetylcholine 10(-6) mol/L), (2) endothelium-independent cyclic guanosine monophosphate-mediated vasorelaxation (response to sodium nitroprusside 10(-6) mol/L), and beta-adrenergic cyclic adenosine monophosphate-mediated vasorelaxation (response to isoproterenol 10(-6) mol/L). Autologous right lung transplantation was performed in five dogs. At each of three times, two third-order pulmonary arteries were dissected from each transplanted lung and studied: control (immediately after harvest), cold ischemia (3 hours in 4 degrees C saline solution), and cold ischemia plus reperfusion (1 hour after lung reimplantation). The vasorelaxing effects of acetylcholine, sodium nitroprusside, and isoproterenol were studied in isolated pulmonary arterial rings, suspended on fine wire tensiometers in individual organ chambers. Statistical analysis was by analysis of variance. Results demonstrated significant dysfunction of beta-adrenergic cyclic adenosine monophosphate-mediated relaxation after cold ischemia alone, and this dysfunction was exacerbated by reperfusion. Endothelium-dependent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia alone but was significantly impaired by reperfusion. Endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia or reperfusion. We conclude that cold ischemia and reperfusion each produce different patterns of pulmonary vasomotor dysfunction. Cumulatively, such dysfunction may contribute to increased pulmonary vascular resistance in the transplanted lung.

Animals↗
PubMed1993

Use of a rule based graph-theoretical system in evaluating the activity of a class of nucleoside analogues against human immunodeficiency virus.

A rule based graph-theoretical system has been used to evaluate qualitatively the activity of a class of nucleoside analogues against human immunodeficiency virus (HIV). The system identifies biologically relevant vertices (atoms) in the molecular graphs of the compounds which have the biological activity of interest. The idea is to relate biological activity with the structural or substructural characteristics of the compounds from the point of view of molecular topology (connectivity). The system brings vertices of similar or close topological environment in the respective compounds together and this is reflected in the ranges of values formed by a distance based index of the vertices, the 'distance exponent index (Dx)', where x is any real number. It is found that the system makes correct prediction of the activity of all the compounds (active as well as inactives) of both training set and the test set against HIV. It is also apparent from this study that the index D-4, which has been used here, can make a useful classification of the vertices according to their molecular environment and the system can produce significant result in a small as well as diverse data base.

Antiviral Agents↗
PubMed1993

The relationship between ischemia-reperfusion injury, myocardial stunning and cardiac preconditioning.

The high incidence of coronary disease in the current population renders myocardial ischemia a leading cause of morbidity and death. Recent efforts have made rapid restoration of coronary flow a clinical reality. Despite progress in hypothermic arrest and cardioplegia, the widespread performance of open cardiac operation and increasing use of cardiac transplantation obligate myocardial I/R stress. Advances in understanding the pathophysiologic factors of reversible and irreversible I/R injury have been significant, but are incomplete. Myocardial infarction and myocardial "stunning" remain clinically important sequelae of coronary disease. In the long term, the solution to heart disease will likely come through preventative health measures. In the interim, however, measures to limit ischemic duration and prepare the heart for reperfusion are clinically desirable. The presence of intrinsic cellular protective mechanisms intimate the feasibility of the latter measure. Furthermore, recently delineated receptor-mediated mechanisms of ischemic preconditioning may render this phenomenon clinically exploitable. The multifactorial pathophysiologic nature of the I/R process suggests that optimal intervention will likely require a combination of pharmacologic adjuncts intended for the specific type and severity of I/R insult. Continued exploration of I/R pathophysiologic factors is needed to develop practical therapeutic interventions.

Humans↗
PubMed1993

Platelet-activating factor-induced polymorphonuclear neutrophil priming independent of CD11b adhesion.

BACKGROUND: Our previous studies have implicated phospholipase A2-dependent platelet-activating factor (PAF) production in the genesis of polymorphonuclear neutrophil (PMN)-mediated tissue injury after gut ischemia-reperfusion. Further, these studies have suggested a discordance of PMN sequestration and tissue injury. CD11B-dependent PMN-endothelial cell adhesion has been purported to play a dominant role in PMN-mediated tissue injury. We therefore undertook this study with the hypothesis that PAF-induced PMN superoxide production requires CD11B-mediated PMN-endothelial cell adherence. METHODS: Human PMNs, isolated by Percoll gradient centrifugation, were exposed to PAF (10 ng/ml). At fixed times of exposure during 120 minutes, (1) superoxide production, (2) CD11B receptor expression, and (3) PMN adhesion to unstimulated human umbilical vein endothelial cell cultures were assayed. RESULTS: PAF induced prompt changes in PMN priming (increased superoxide production after N-formyl-methyl-leucyl-phenylalanine activation), adhesion to unstimulated endothelial cells, and CD11B receptor expression. Priming was temporally concordant with the rise and fall of CD11B expression but appeared to precede adhesion. CD11B blockade (F(Ab') 2 anti-CD11B [60.1] antibodies), before or at maximal PAF priming, reduced PMN adhesion but had no effect on superoxide production. CONCLUSIONS: In summary, PAF-induced PMN priming occurs in temporal concordance with the expression of CD11B and subsequent endothelial cell adherence, but CD11B-mediated adherence is not essential for this process.

Cell Adhesion↗
PubMed1993

Intracellular mechanisms of pulmonary vasomotor dysfunction in acute lung injury caused by mesenteric ischemia-reperfusion.

BACKGROUND: A major hemodynamic feature of adult respiratory distress syndrome is pulmonary hypertension secondary to avid pulmonary vascular smooth muscle constriction. This study was undertaken to study the hypothesis that this pulmonary vasoconstriction may derive from pulmonary vasomotor dysfunction. METHODS: A rat model of acute lung injury was studied after 2 hours of superior mesenteric arterial occlusion followed by 4 hours reperfusion. Lung neutrophil accumulation was assessed by myeloperoxidase assay, and lung leak was assessed by iodine 125-labeled albumin lung/blood ratio. The following mechanisms of pulmonary vascular smooth muscle relaxation were studied in isolated pulmonary arterial rings: (1) endothelial-dependent cyclic guanosine monophosphate-mediated, (2) endothelial-independent cyclic guanosine monophosphate-mediated, (3) beta-adrenergic cyclic adenosine monophosphate-mediated. Control rats underwent sham laparotomy. Statistical analysis was done with unpaired Student t test. RESULTS: Lung myeloperoxidase increased from 6.2 +/- 2 to 42 +/- 5 units/gm (p < 0.05), and 125I-labeled albumin lung/blood ratio increased from 0.028 +/- 0.02 to 0.063 +/- 0.03 (p < 0.05) after mesenteric ischemia-reperfusion. beta-adrenergic cyclic adenosine monophosphate-mediated pulmonary vascular smooth muscle relaxation was dysfunctional in the lung-injured rats (62% +/- 5% relaxation versus 95% +/- 3% in controls) (p < 0.05). CONCLUSIONS: These data suggest a mechanistic imbalance of pulmonary vascular smooth muscle contraction and relaxation in acute lung injury. Such imbalance may contribute to the pulmonary hypertension found in adult respiratory distress syndrome.

Acute Disease↗