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Biomedical subjects

A Banerjee

Publications and source records attributed to A Banerjee.

At least 253 records · Page 14Linked to original sources
PubMed1996

The obligate role of protein kinase C in mediating clinically accessible cardiac preconditioning.

BACKGROUND: Cardiac preconditioning is an adaptation of cardiomyocytes that promotes tolerance to a subsequent ischemic insult. Adenosine receptor signaling is proposed as a mediator of preconditioning, but its mechanism of protection remains unknown. We hypothesized that protection against hypoxia-reoxygenation (H/R) injury could be conferred in a rat ventricle by adenosine-mediated protein kinase C (PKC) activation and that adenosine-mediated cardioprotection could be extended to human ventricular muscle. METHODS: Isolated rat and human ventricular muscle (VM) strips were subjected to 30 minutes of hypoxia and 60 minutes of reoxygenation (H/R control). The VM was pretreated with 125 mumol/L adenosine, an adenosine antagonist ((p-Sulfophenyl) theophylline [SPT] 50 mumol/L) and adenosine (adenosine + SPT), or with a PKC inhibitor (chelerythrine, 10 mumol/L) and adenosine (adenosine + chelerythrine) before H/R Developed force (DF) and tissue creatine kinase (CK) activity were assessed at end reoxygenation. Human trabeculae were obtained from diseased explanted hearts at cardiac transplantation and were also subjected to H/R injury. Human VM was pretreated with adenosine (125 mumol/L) before H/R injury. Results are expressed as mean +/- standard error of mean. RESULTS: In the rat, adenosine pretreatment conferred protection of DF against H/R injury (adenosine, 62% +/- 6%; H/R control, 27% +/- 2%, p < 0.05). Adenosine + SPT or adenosine + chelerythrine eliminated the functional recovery conferred by adenosine. This recovery of contractile function was associated with greater tissue CK activity (adenosine, 415 +/- 40 units/gm; H/R control, 78 +/- 13 units/gm, p < 0.05). The protective effects of adenosine against H/R were present in the human ventricle and with recovery of DF in adenosine (66% +/- 5%) and H/R control (24% +/- 4%), p < 0.05. CONCLUSIONS: Adenosine, a clinically accessible agonist, induces protection against H/R injury through a PKC-mediated mechanism in the rat ventricle. Further, the protection conferred by adenosine against H/R extends to the human ventricle.

Animals↗
PubMed1996

Balloon mitral commissurotomy: an intraoperative assessment.

OBJECTIVE: Advances in balloon catheter technology have revolutionized the management of obstructive cardiovascular diseases. For lesions like mitral stenosis, balloon commissurotomy has emerged as an alternative to surgical relief showing definite functional benefits in a few clinical trials, albeit with variable results. Such variability necessitated objective evaluation of the efficacy of balloon mitral commissurotomy. METHODS: The balloon mitral commissurotomy was carried out in 11 patients suffering from isolated mitral stenosis, under vision in a surgical setting. All patients were in NYHA class III/IV. Initially single balloon was used for mitral commissurotomy followed by double balloon, before completing the mitral valvotomy with surgical instruments whenever required. The commissural split was measured by firmly stretching the two commissures using nerve hooks and measuring the distance between the two hooks with the help of a caliper. Assessment of balloon dilation was made by calculating exact percentage of residual commissural split following balloon dilation as compared with completed mitral valvotomy. The exact percentage of commissural split was thus obtained by subtracting residual commissural split following balloon dilation from commissural split obtained after surgical open mitral valvotomy. RESULTS: Complete commissurotomy using the balloon technique was possible in two (18.2%) patients. In the remaining nine (81.8%) patients, balloon expansion provided only 50% to 80% of commissural split and required instrumental completion with good results. CONCLUSIONS: Balloon mitral commissurotomy, by virtue of its circumferential force, helps to develop a good cleavage and attains good hemodynamic improvement which may be life saving in critical mitral stenosis in selected group of patients with pliable mitral leaflets and minimal subvalvular pathology.

Adolescent↗
PubMed1996

Constructive priming of myocardium against ischemia-reperfusion injury.

Ischemia and ischemic stress hormones induce endogenous cardiac protection against ischemia-reperfusion (I/R) injury. Although ischemia and ischemic stress hormones are accompanied by increased [Ca2+], it is unknown whether either opening of the sarcoplasmic reticular ryanodine Ca2+ channel (SR RyR) or inhibition of Ca2+ uptake by the sarcoendoplasmic reticular Ca(2+)-ATPase (SERCA) prior to I/R can similarly induce post-I/R functional protection. To study this, isolated, crystalloid perfused Sprague-Dawley rat hearts were used to assess the effects of inducing a pre-ischemic [Ca2+]i load by either priming the SR RyR with ryanodine (Ry, 5 nM/2 min) or by transient blockade of the SERCA 10 min prior to global I/R (20 min). A pre-ischemic Ca2+ load by either SR RyR activation or SERCA blockade improved post-ischemic myocardial functional recovery (developed pressure, end diastolic pressure, coronary flow, heart rate, and left ventricular creatine kinase activity). We conclude that 1) Ca(2+)-induced myocardial functional protection involves the SR Ca2+ source, 2) a pre-ischemic Ca2+ load induced with either Ry or thapsigargin constructively primes against myocardial I/R injury, and 3) Ca(2+)-induced cardioadaptation to I/R injury may have important therapeutic implications prior to planned ischemic events such as cardiac allograft preservation and cardiac bypass surgery.

Animals↗
PubMed1996

Coital emergencies.

The act of heterosexual coitus is associated with morbidity due to a variety of conditions as well as with a small risk of sudden death. Awareness of the presentation of coital emergencies is essential to allow appropriate medical management and sexual counselling.

Cerebrovascular Disorders↗
PubMed1996

Improving the early diagnosis of acute myocardial infarction.

The diagnosis of early myocardial infarction, especially in association with atypical clinical presentations, can be difficult to establish. Continued observation of high-risk patients, with multiple serial electrocardiographs and the use of other diagnostic modalities as available, is essential to prevent the inadvertent premature discharge of patients with evolving myocardial infarcts from the accident and emergency department.

Biomarkers↗
PubMed1996

Endotoxin induces cardiac HSP70 and resistance to endotoxemic myocardial depression in rats.

Endotoxin (bacterial lipopolysaccharide, LPS) depresses myocardial function. However, heat shock and sublethal LPS can confer cardiac resistance to postischemic dysfunction. We hypothesized that a prior exposure to LPS stress induces the expression of cardiac heat shock protein 70 (HSP70) and resistance to endotoxemic myocardial depression. Moreover, induction of HSP70 by hyperthermia should also increase cardiac resistance to LPS toxicity. LPS (500 micrograms/kg ip) depressed rat left ventricular developed pressure (LVDP) maximally at 6 h (58.4 +/- 3.72 vs. 101 +/- 1.46 mmHg in saline control, P < 0.01), and myocardial contractile function recovered at 24 h. In rats pretreated with LPS 24 h earlier, subsequent LPS exposure did not depress LVDP (97.0 +/- 3.53 mmHg at 6 h, P < 0.01 vs. single exposure). Both LPS and hyperthermia (42 degrees C, 15 min) induced HSP72 mainly in the cardiac interstitial cells, including macrophages at 24 h after treatment. When hyperthermia-pretreated animals were similarly challenged with LPS, myocardial depression at 6 h was partially abrogated (LVDP 80.1 +/- 5.67 vs. 62.2 +/- 4.91 mmHg in sham+LPS group, P < 0.01). We conclude that LPS induces HSP70 in rat heart and that an exposure to LPS or heat stress confers cardiac resistance to endotoxemic myocardial depression.

Animals↗
PubMed1996

Ischemic preconditioning in human and rat ventricle.

The signal transduction of ischemic preconditioning involves activation of endogenous receptor-based systems, including alpha 1-adrenoceptors and adenosine receptors. Whereas preconditioning protects against ischemia-reperfusion injury, it is unknown whether this protective strategy might be useful clinically. Furthermore, human atrium has been successfully preconditioned, but it is unknown whether human ventricle can be functionally protected against hypoxia-reoxygenation. To study these questions, isolated rat ventricle and human ventricular trabeculae were suspended in an organ bath and subjected to 30 min of hypoxia and 60 min of reoxygenation. In the rat ventricle, preconditioning was induced by 5 min of rapid pacing at 3 Hz in hypoxic buffer without glucose (simulated ischemia), alpha 1-adrenoceptor stimulation (phenylephrine), or adenosine receptor stimulation (adenosine). In the human trabeculae the effects of preceding simulated ischemia and alpha 1-adrenoceptor and adenosine receptor stimulation were examined against hypoxia-reoxygenation. In the rat, pretreatment with simulated ischemia and alpha 1-adrenoceptor and adenosine receptor stimulation improved recovery of developed tension (56 +/- 3, 56 +/- 4, and 58 +/- 2%, respectively) compared with control trabeculae (25 +/- 2%) after hypoxia-reoxygenation (P < 0.05). In human trabeculae, simulated ischemic preconditioning and alpha 1-adrenoceptor and adenosine receptor stimulation augmented recovery of developed tension (65 +/- 5, 59 +/- 6, and 60 +/- 3%, respectively) compared with control (29 +/- 2%) after hypoxia-reoxygenation (P < 0.05). We conclude that functional cardioadaptation (preconditioning) against hypoxia-reoxygenation injury in rat and human myocardium exists and that alpha 1-adrenergic and adenosine receptor signaling participate in conferring this protection.

Adenosine↗
PubMed1996

Inhaled nitric oxide prevents pulmonary endothelial dysfunction after mesenteric ischemia-reperfusion.

This study examined the effect of inhaled nitric oxide (NO) on lung neutrophil accumulation and endothelial-dependent and -independent guanosine 3',5'-cyclic monophosphate (cGMP)-mediated mechanisms of pulmonary vasorelaxation after mesenteric ischemia-reperfusion (I/R) in mechanically ventilated rats. Inhaled NO (20 ppm) was administered in two protocols: 1) throughout mesenteric I/R and 2) during mesenteric reperfusion alone. Concentration-response curves were generated (10(-9) to 10(-8) M) for acetylcho-line (ACh), A23187, and sodium nitroprusside (SNP) in isolated pulmonary arterial rings preconstricted with phenylephrine. Lung neutrophil accumulation [myeloperoxidase assay (MPO)] was significantly increased from 2.4 +/- 0.2 units/g lung wt in controls to 10.3 +/- 0.4 after 1 h of superior mesenteric artery occlusion and 2 h of reperfusion. Lung MPO activity was not different from controls in rats receiving inhaled NO either 1) during mesenteric I/R or during mesenteric reperfusion alone. The concentration-response curves demonstrated significant impairment of pulmonary vasorelaxation by endothelial-dependent mechanisms (response to ACh and A23187) but not endothelial-independent pulmonary vasorelaxation (response to SNP) after mesenteric I/R. This pulmonary vasomotor dysfunction was prevented by administration of inhaled NO during either mesenteric I/R or during mesenteric reperfusion alone. We conclude that inhaled NO prevents lung neutrophil accumulation and pulmonary vascular endothelial dysfunction after mesenteric I/R.

Administration, Inhalation↗
PubMed1996

Protein kinase C mediates Ca2(+)-induced cardioadaptation to ischemia-reperfusion injury.

Although protein kinase C (PKC)-mediated cardioadaptation to ischemia-reperfusion (IR) is accompanied by increased intracellular Ca2+ concentration, it is unknown whether a preischemia sarcoplasmic reticulum (SR) Ca2+ release affects PKC-mediated post-IR functional protection. To study this, crystalloid-perfused (Langendorff) Sprague-Dawley rat hearts were used to assess the effects of a ryanodine (Ry)-induced preischemia Ca2+ load (Ry, 5 nM/2 min, retrograde coronary) 10 min before global IR (20 min). Ry was administered with and without each of two different PKC inhibitors (20 microM chelerythrine and 150 nM bisindolylmaleimide I-HCl). Ry improved myocardial functional recovery (developed pressure, end-diastolic pressure, coronary flow, and creatine kinase activity), which was eliminated after PKC inhibition. Immunohistochemical staining for PKC isoforms demonstrated that Ry induces specific PKC translocation of alpha-, delta-, and zeta-isoforms. We conclude that 1) a preischemia Ca2+ load from the SR results in post-IR myocardial functional protection 2) Ca(2+)-induced functional protection is PKC regulated via the translocation of specific isoforms, and 3) Ca(2+)-induced cardioadaptation to IR injury may have important therapeutic implications prior to planned ischemic events such as cardiac allograft preservation and cardiac bypass surgery.

Adaptation, Physiological↗
PubMed1996

Dr Robert Greenhill Cochrane CMG MD FRCP DTM&H: leprologist par excellence.

Dr Robert Cochrane devoted his entire working life to the study and control of leprosy. Most of his working life was spent in India, with interludes in Britain and East Africa. He initiated epidemiological surveys of leprosy, was instrumental in the introduction of sulphones for the definitive therapy of the disease, and contributed significantly to the development of rehabilitation programmes for sufferers from the disease. He campaigned actively for altering social attitudes to leprosy and latterly was in favour of replacing the often pejorative term with that of Hansen's disease. A devout Christian, he believed strongly in setting an example for others as an important means of introducing them to Christianity. At the same time, he was not a taciturn individual and had a well developed sense of humour.

History, 20th Century↗
PubMed1996

Alprazolam-induced hypomania.

OBJECTIVE: There are reports of alprazolam-induced hypomania/mania. Here is a case report of a patient who developed hypomania during treatment with alprazolam, but not with diazepam, another benzodiazepine derivative. CLINICAL PICTURE: The illness was of 2 months' duration and the patient received a diagnosis of anxious depression. Following treatment with alprazolam, the patient developed hypomania characterised by euphoria, overactivity, overtalkactivity, racing thoughts, oversocialisation, enhanced self-confidence and disturbed sleep. TREATMENT: Hypomania subsided when alprazolam was withdrawn. There was no recurrence with fluoxetine or diazepam that ameliorated the primary condition. OUTCOME: The patient was symptom-free on follow-up. CONCLUSIONS: Alprazolam can induce hypomania/mania and, perhaps, it differs from other benzodiazepines in its mode of action. Clinicians have to be alert to the possibility of their patients developing hypomania/mania while on alprazolam.

Adult↗
PubMed1996

Antistress activity of P-GABA in experimental animals.

A new gamma-aminobutyric acid derivative N-phthloyl GABA (P-GABA) was found to possess anticonvulsant, antiepileptic, antiulcer and antinociceptive activities. Effect of cold restrain stress (CRS) and its modulation by P-GABA were evaluated on some biochemical and biophysical parameters in rats. CRS induced elevations in blood sugar level were unaffected by P-GABA treatment. CRS also caused an increase of Na+K+ ATPase activities, and decrease of lipid peroxidation in RBC membrane. CRS also induced (a) membrane protein clusterization, (b) increased membrane fluidity and (c) reduced thickness. CRS induced RBC membrane dynamics were reversed by P-GABA in a differential manner. However, these parameters in synaptosomal membrane were unaffected by P-GABA.

Animals↗
PubMed1995

Echocardiographic evaluation of congenital mitral valve anomalies in children.

Congenital mitral valve anomalies were diagnosed in 65 children, whose ages ranged from newborn to 18 years, using 2-dimensional, color, pulsed-, and continuous-wave Doppler ultrasound. Data were collected over 7.5 years from 13,400 new studies. Data in these patients were compared with those obtained by cardiac catheterization, cardiac surgery, and autopsy. We detected 4 different lesions: (1) congenital mitral stenosis with 2 papillary muscles (n = 24); (2) parachute mitral valve, with a single papillary muscle (n = 24); (3) isolated cleft in the mitral valve (n = 10); and (4) double-orifice mitral valve (n = 7). A supravalvar mitral ring was detected in 21 patients with mitral stenosis; however, it never occurred as an isolated lesion and was invariably associated with some other left ventricular inflow or outflow obstruction. The supravalvar ring was associated with a parachute deformity of the mitral valve in 17 patients; in only 4 was this abnormality associated with mitral stenosis with 2 papillary muscles. In patients with congenital mitral stenosis, the peak and mean transmitral Doppler velocities were increased significantly compared with those in controls (peak velocity 1.53 +/- 0.74 vs 0.86 +/- 0.25 m/s, respectively, p < 0.01; mean velocity 1.13 +/- 0.61 vs 0.58 +/- 0.11 m/s, respectively, p < 0.01). The correlation between mean transmitral pressure gradient obtained by Doppler and cardiac catheterization was fair (r = 0.75). However, the correlation between the mitral valve areas calculated by the Doppler pressure half-time method and by the Gorlin formula was poor (r = 0.57).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗