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Biomedical subjects

Y Chandrashekhar

Publications and source records attributed to Y Chandrashekhar.

At least 19 recordsLinked to original sources
PubMed1999

Preliminary study of non-psychotic disorders in people from the Indian subcontinent living in the UK and India.

OBJECTIVE: The prevalence of anxiety and depressive disorders in people of South Asian origin in the UK is not accurately known. METHOD: A population-based study of UK residents from the Indian subcontinent was screened for anxiety and depressive disorders with the Self-Rating Questionnaire (SRQ) and for life events using the brief list of threatening life events. Similar measures were administered to siblings in India. RESULTS: The UK sample included 223 Sikhs, 100 Hindus and 49 Muslims. Elevated SRQ scores were recorded in 5%, 13% and 23%, respectively, of men from these groups and in 16%, 27% and 57%, respectively, of females. Subjects reporting one or more threatening life events (most commonly unemployment and financial problems) also had raised SRQ scores. A total of 117 siblings in India reported similar SRQ scores to their index subjects in the UK, but reported more threatening life events, notably deaths and illness in the family and financial problems. CONCLUSION: This preliminary study indicates that psychiatric disorder in ethnic groups varies across religious groups. The prevalence may be high in some religious groups in association with social difficulties. The patterns of stress in India and the UK are different.

Adult↗
PubMed1997

Isolated myocyte contractile function is normal in postinfarct remodeled rat heart with systolic dysfunction.

BACKGROUND: Postinfarction ventricular remodeling is associated with lengthening and contractile dysfunction of the remote noninfarcted myocardium. Mechanisms underlying this phenomenon remain unclear. METHODS AND RESULTS: We studied serial changes in global left ventricular (LV) structure and function in infarcted (1, 2, 4, and 6 weeks after myocardial infarction) and sham-operated rat hearts and correlated them with structural and functional changes in myocytes isolated from the remote LV myocardium in the same hearts. Rats with myocardial infarction developed significant remodeling. The heart weight-to-body weight ratios were increased. LV volumes at filling pressure of 10 mm Hg were higher (305+/-28 versus 215+/-12 microL, P<.01). This was accompanied by global LV dysfunction (in vivo LV end-diastolic pressure, 4+/-1 versus 23+/-1.6 mm Hg; Langendorff LV developed pressure, 105+/-4 versus 62+/-9 mm Hg, P<.001 for both). Myocytes isolated from these hearts showed significant structural remodeling (LV myocytes, 24% longer and 15% wider; right ventricular myocytes, 38% longer and 31% wider, all P<.05). LV myocyte length correlated with changes in LV volume (r=.79) and function (LV developed pressure, r=-.81). However, LV myocytes from the same hearts showed normal contractile function and intracellular Ca2+ transients at baseline and during inotropic stimulation with increasing extracellular Ca2+ (1 to 6 mmol/L). The shortening-frequency relationship was also similar in myocytes from sham and myocardial infarction rats. CONCLUSIONS: Postinfarct LV remodeling occurs predominantly by myocyte lengthening rather than by myocyte slippage. However, contractile function of the unloaded myocytes from the remote noninfarcted LV myocardium of the remodeled heart is normal. Therefore, myocyte contractile abnormalities may not contribute to global dysfunction of the remodeled heart. Reduced myocyte mass and nonmyocyte factors like increased wall stress, altered LV geometry, and changes in the myocardial interstitium may be more important in the genesis of postinfarct LV dysfunction in this model.

Animals↗
PubMed1995

Coronary risk factors in people from the Indian subcontinent living in west London and their siblings in India.

Several reports have shown that migrants from southeast Asia tend to have an increased risk of coronary heart disease when settled in their new country. We compared coronary risk factors in a randomly selected group of 247 migrants from the Indian subcontinent of Punjabi origin living in West London and 117 of their siblings living in the Punjab in India. The West London cohort had a greater body mass index (p < 0.001), systolic blood pressure (p = 0.0087), serum cholesterol (p < 0.001), apolipoprotein B (p < 0.001), lower high-density lipoprotein cholesterol (p < 0.05) and higher fasting blood glucose (p < 0.05) than their siblings in the Punjab. Insulin sensitivity, derived from the homoeostatic assessment mathematical model, was lower in men in West London than in their counterparts in India (p < 0.05). Indians in West London had lower beta cell function than those in the Punjab (p < 0.001). Serum lipoprotein (a) concentrations were similar in both the West London and Punjab population, but were significantly higher (p = 0.01) than those of white European populations in the UK. Increases in serum cholesterol after migration from India lead to increased coronary risk conferred by high serum lipoprotein (a) concentrations and greater insulin resistance. Such between-country comparisons are an important means of establishing the importance of coronary risk factors.

Adult↗
PubMed1995

Endothelium-derived relaxing factor is important in mediating the high output state in chronic severe anemia.

OBJECTIVES: We evaluated the endothelial and vascular smooth muscle function in patients with chronic severe anemia to determine whether increased basal nitric oxide levels contribute to the systemic vasodilation and high cardiac output seen in these patients. BACKGROUND: Patients with chronic severe anemia have a high output state due to a low systemic vascular resistance. However, the cause of the low vascular resistance is unclear. Because hemoglobin is a potent inhibitor of endothelium-derived relaxing factor, we postulated that in chronic severe anemia, low circulating hemoglobin results in reduced inhibition of endothelium-derived relaxing factor. The basal endothelium-derived relaxing factor activity therefore increases, and this contributes significantly to the low systemic vascular resistance and the hyperdynamic state seen in this condition. METHODS: Hemodynamic variables and forearm blood flow (using plethysmography) were measured in eight patients with chronic severe anemia before (hematocrit 16 +/- 2% [mean +/- SD]) and within 24 h of red blood cell transfusion (n = 6, hematocrit 30 +/- 1%) and in six control subjects. The effect on baseline blood flow of blocking endothelium-derived relaxing factor activity with NG-monomethyl-L-arginine was investigated. In addition, the effects of both endothelium-dependent and endothelium-independent vasodilators on forearm blood flow were tested. RESULTS: Baseline forearm blood flow was markedly increased in untreated patients (6.5 +/- 1.2 ml/min per 100 ml) compared with that in control subjects (2.8 +/- 0.7 ml/min per 100 ml, p < 0.0001, 95% confidence interval [CI] for difference -5 to -2.5). Red blood cell transfusion significantly reduced blood flow in the anemic patients to 3.5 +/- 1.1 ml/min per 100 ml (p < 0.001, 95% CI for difference -4.9 to -1.9), which was not significantly different from that in control subjects; increased systemic vascular resistance (796 +/- 141 to 1,230 +/- 151 dynes.s.cm-5, p < 0.001); and decreased cardiac output (4.9 +/- 0.6 to 3.5 +/- 0.5 liters/min per m2, p < 0.001). NG-monomethyl-L-arginine (16 mumol/min), a specific inhibitor of endothelium-derived relaxing factor, reduced forearm blood flow by an equal amount (p = 0.9, 95% CI for difference -0.7 to 0.8) in control subjects (0.98 +/- 0.39 ml/min) and treated patients (1.03 +/- 0.8 ml/min) but caused a threefold greater decrease in flow (2.9 +/- 0.9 ml/min) in untreated patients (p = 0.0003, 95% CI for difference between untreated patients and control subjects 1.1 to 2.7). These findings suggest increased basal endothelium-derived relaxing factor activity in patients with anemia. Stimulated forearm blood flows (both endothelium dependent and endothelium independent) were similar in all groups, confirming normal endothelial and smooth-muscle function. CONCLUSIONS: These findings support the hypothesis that enhanced basal endothelium-derived relaxing factor activity makes an important contribution to the low systemic vascular resistance in chronic severe anemia.

Adult↗
PubMed1993

Rate-dependent hemodynamic responses during incremental atrial pacing in chronic constrictive pericarditis before and after surgery.

Chronic constrictive pericarditis is a frequent cause of diastolic dysfunction, and results in impaired ventricular filling. Unlike in normal subjects, ventricular filling in constrictive pericarditis occurs almost entirely in the initial one third of diastole, and cardiac output is dependent predominantly on heart rate. Tachycardia impairs ventricular filling in normal subjects, but its effects in patients with constrictive pericarditis have not been studied. The effect of increasing heart rate alone with atrial pacing on the central and peripheral hemodynamics of patients with untreated chronic constrictive pericarditis before and after pericardiectomy was evaluated. Increased heart rate with atrial pacing increased cardiac output, whereas stroke volume remained unchanged up to heart rates of 140 beats/min. Further increases in heart rate resulted in reductions of cardiac output and stroke volume. There were no significant changes in ventricular filling pressures. Infusion of 300 ml of saline solution at peak pacing rates did not improve cardiac output. After successful surgical pericardiectomy, the hemodynamic effects of atrial pacing returned to normal. It is concluded that moderate tachycardia improves the hemodynamic profile of patients with constrictive pericarditis.

Adult↗
PubMed1993

Pathogenesis of oedema in chronic severe anaemia: studies of body water and sodium, renal function, haemodynamic variables, and plasma hormones.

BACKGROUND: Patients with chronic severe anaemia often retain salt and water. Fluid retention in these patients is not caused by heart failure and the exact mechanisms remain unclear. This study was designed to examine some of the possible mechanisms. METHODS AND RESULTS: Haemodynamic variables, body fluid compartments, renal function, and plasma hormones were measured in four patients with oedema caused by chronic severe anaemia (mean (SE) haematocrit 13 (1.7)) who had never received any treatment. Cardiac output was increased (6.1 (0.6) l/min/m2) and right atrial (7.8 (1) mm Hg), mean pulmonary arterial (20.5 (2.0) mm Hg), and mean pulmonary arterial wedge (13 (2.7) mm Hg) pressures were slightly increased. The mean systemic arterial pressure (81 (1.3) mm Hg) and systemic vascular resistance (12.3 (1.1) mm Hg x min x m2/l were low. There were significant increases in total body water (+14%), extracellular volume (+32%), plasma volume (+70%), and total body exchangeable sodium (+30%). Renal blood flow was moderately decreased (-46%) and the glomerular filtration rate was slightly reduced (-24%). There were significant increases in plasma noradrenaline (2.1-fold), renin activity (15-fold), aldosterone (3.2-fold), growth hormone (6.3-fold), and atrial natriuretic peptide (12-fold). CONCLUSION: In patients with oedema caused by chronic severe anaemia there is retention of salt and water, reduction of renal blood flow and glomerular filtration rate, and neurohormonal activation similar to that seen in patients with oedema caused by myocardial disease. However, unlike patients with myocardial disease, patients with anaemia have a high cardiac output and a low systemic vascular resistance and blood pressure. It is suggested that the low concentration of haemoglobin in patients with anaemia causes a reduced inhibition of basal endothelium-derived relaxing factor activity and leads to generalised vasodilatation. The consequent low blood pressure may be the stimulus for neurohormonal activation and salt and water retention.

Adolescent↗
PubMed1993

Body fluid compartments, renal blood flow, and hormones at 6,000 m in normal subjects.

We previously described a syndrome of congestive heart failure occurring in healthy young men at extreme altitude (Anand et al. Lancet 335: 561-565, 1990). The pathogenesis of this condition is unclear. We therefore measured body fluid compartments, renal blood flow, and a variety of plasma hormones in 10 asymptomatic young men staying above 6,000 m for > 10 wk and compared the results with controls at sea level. Body compartments were measured with isotope dilution techniques and renal blood flow with o-[125I]iodohippurate sodium. There was a marked expansion of all the fluid spaces: total body sodium was 14% above normal (P < 0.05), total body water was 18% above normal (P < 0.05), plasma volume was 33% above normal (P < 0.05), and blood volume was 84.5% above normal (P < 0.001). The effective renal plasma flow was lower than normal by 55% (P < 0.001), but the reduction in the effective renal blood flow was 37% below normal (P < 0.001) because the hematocrit was high (41.6% above normal). Plasma norepinephrine was nearly 3 times normal (P < 0.01), cortisol 3 times normal (P < 0.001), and growth hormone 18 times normal (P < 0.01). Aldosterone was twice normal (P < 0.03). Plasma epinephrine, atrial natriuretic peptide, and plasma renin activity were unchanged. The degree of fluid retention in these normal subjects was similar to that in patients with severe untreated congestive heart failure (Anand et al. Circulation 80: 299-305, 1989), whereas sodium retention and reduction in effective renal blood flow were less.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1993

Giant congenital left ventricular aneurysm in an adult--a case report.

Congenital cardiac aneurysms are extremely rare. The echocardiographic features of this condition have never been described. The authors report a case of giant congenital left ventricular aneurysm wherein the diagnosis was made by echocardiography and confirmed at cardiac catheterization. The aneurysm was surgically removed. The histologic examination showed that the aneurysmal wall was only 1.5 to 2 mm thick but contained all the layers of the heart.

Adult↗
PubMed1993

Study of acute mountain sickness during "rapid ascent" trekking to extreme altitude.

Acute mountain sickness (AMS) is an important cause of morbidity and mortality following acute exposure to high altitude. Several clinical variables were evaluated during the 1990 Trans-Kalindi Exploration to extreme altitude (5949 m) in 10 healthy adult lowlanders (age 31.7 +/- 6.4 yrs) who undertook a relatively rapid ascent from sea level to 5949 m with short periods of acclimatisation at 4393 m, 4898 m and 5700 m. 40% of the subjects had definite AMS. Only one subject had features of early cerebral oedema at 4393 m and had to be brought down temporarily to 3878 m. All subjects completed the trek without needing medication. Proper acclimatisation was characterised by absence of significant symptoms of AMS above 4500 m, absence of sustained tachycardia, fall in daily positive fluid balance from 1.7 +/- 0.9 (sea level) liters to 0.7 +/- 0.3 litres (at 5700 m) (p < 0.05), increase in 24 hours urinary sodium excretion from 174 +/- 78 mmol to 344 +/- 145 mmol (p < 0.01) and an increase in the ratio of urinary excretion of sodium and potassium from 3.1 (sea level) to 3.6 (5700 m). We conclude that the incidence of AMS at extreme altitude is similar to that at lower altitude. Reasonable acclimatisation is possible during the climb to extreme altitude.

Acclimatization↗
PubMed1992

Quantitation of immunoglobulin-containing cells in the jejunal lamina propria in tropical sprue.

Ten patients with tropical sprue (TS) and 10 with irritable bowel syndrome (IBS) as controls were studied to characterize the immunocytes in the jejunal mucosa. IgA cells numbered 516,155 +/- 48,715 cells/mm3 in TS and 729,308 +/- 146,011/mm3 in the IBS patients. IgG cell counts were 28,885 +/- 8,081/mm3 in TS and 10,615 +/- 4,100/mm3 in IBS; IgM counts were 170,729 +/- 25,015/mm3 in TS and 169,253 +/- 45,353/mm3 in IBS. A positive correlation was present between IgM-bearing plasma cells and corresponding serum immunoglobulins (r = +0.71; p less than 0.05). No correlation was evident between the different immunocytes (IgA, IgG, and IgM) and the duration of illness, serum albumin, and tests for absorption of fat, B-12, and D-xylose (p greater than 0.05). The gut immunocytes expressed in absolute numbers were higher in our controls and TS patients than reported in Western populations.

Adult↗
PubMed1992

Pathogenesis of congestive state in chronic obstructive pulmonary disease. Studies of body water and sodium, renal function, hemodynamics, and plasma hormones during edema and after recovery.

BACKGROUND: The pathogenesis of salt and water accumulation in patients with chronic obstructive pulmonary disease is unclear and may differ from that in patients with congestive heart failure due to myocardial disease. This study was undertaken to investigate some of the mechanisms involved. METHODS AND RESULTS: Hemodynamics, water and electrolyte spaces, renal function, and plasma hormone concentrations were measured in nine patients with edema due to chronic obstructive pulmonary disease and in six patients after recovery. Mean cardiac output (3.8 +/- 0.26 l/min.m2) was normal, but right atrial (11 +/- 1 mm Hg) and mean pulmonary arterial (41 +/- 3 mm Hg) pressures were increased. Mean pulmonary arterial wedge pressure (11 +/- 1 mm Hg) was normal. Pulmonary vascular resistance (8.6 +/- 1.3 mm Hg.min.m2/l) was increased, but systemic vascular resistance (19.3 +/- 1.3 mm Hg.min.m2/l) and mean arterial pressure (83 +/- 4 mm Hg) were low. All patients were hypoxemic (PaO2, 40 +/- 2 mm Hg) and hypercapnic (PaCO2, 60 +/- 2 mm Hg). There was a significant increase in total body water (+21%), extracellular volume (+45%), plasma volume (+45%), blood volume (+88%), and exchangeable sodium (+38.2%). Renal plasma flow was severely reduced (-63.2%), but glomerular filtration rate was only mildly decreased (-32%). Significant increases were seen in plasma norepinephrine (3.5-fold normal), renin activity (7.6-fold normal), vasopressin (twice normal), atrial natriuretic peptide (9.4-fold normal), growth hormone (10.7-fold normal), and cortisol (1.9-fold normal). After recovery, the PaO2 increased (50 +/- 3 mm Hg) and PaCO2 fell (45 +/- 4 mm Hg), and the patients became free from edema. All the body compartments returned toward normal, although they did not entirely reach normal values. Renal plasma flow increased significantly, and glomerular filtration became normal. Right atrial and pulmonary arterial pressures and pulmonary vascular resistance decreased (p less than 0.01). Cardiac output decreased but not significantly. Blood pressure increased but not significantly. However, systemic vascular resistance increased significantly to a normal value. CONCLUSIONS: We conclude that patients with edema due to chronic obstructive pulmonary disease have severe retention of salt and water, reduction in renal blood flow and glomerular filtration, and neurohormonal activation similar to that seen in patients with edema due to myocardial disease. However, unlike the latter, in chronic obstructive pulmonary disease cardiac output is normal, and systemic vascular resistance and arterial blood pressure are low. This probably is due to the vasodilator properties of hypercapnia. The consequent low arterial blood pressure may be the stimulus for the neurohormonal activation and retention of salt and water.

Adult↗
PubMed1991

Exercise as a coronary protective factor.

Exercise has multiple beneficial actions, both in normal subjects and in patients with coronary artery disease, which can be cardioprotective. Apart from reducing known risk factors and protecting against their deleterious effects, exercise also reduces the risk of coronary artery disease by increasing cardiovascular fitness. The exact contribution of each of these mechanisms in reducing coronary artery disease morbidity and mortality is unclear. Although fitness may be desirable, much of the cardioprotection can be achieved through increased leisure time and recreational physical activity. The risk-benefit ratio is very much in favor of moderate intensity exercise. Even in the absence of a controlled trial, the available evidence suggests that efforts to encourage physical activity are justified.

Cardiovascular Physiological Phenomena↗
PubMed1991

Left anterior fascicular block: an ischaemic response during treadmill testing.

A patient in whom exercise induced reversible ischaemic left anterior fascicular block is reported. Glyceryl trinitrate relieved the fascicular block. Coronary angiography showed a 90% obstruction of the left anterior descending artery. The left anterior fascicular block induced by exercise disappeared after a successful coronary angioplasty.

Angina Pectoris↗