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Biomedical subjects

B Rajagopalan

Publications and source records attributed to B Rajagopalan.

At least 109 records · Page 6Linked to original sources
PubMed1987

Measurement of phosphocreatine to ATP ratio in normal and diseased human heart by 31P magnetic resonance spectroscopy using the rotating frame-depth selection technique.

31P magnetic resonance spectroscopy, using surface coils placed on perfused or surgically exposed animal hearts, shows that unequivocal changes in phosphocreatine (PCr) and adenosine triphosphate (ATP) occur during interventions, such as ischemia. Similar measurements seem warranted in man. We have used a modification of the rotating-frame imaging technique to measure PCr-to-ATP ratio non-invasively in human heart. The subject lay prone on a double-surface coil probe with the apex and the anterior surface of the heart covered by the coil in a 1.9 T magnet. 31P spectra were obtained from slices of tissue approximately 6 cm in diameter and 2 cm in thickness. Though skeletal and cardiac muscle contain similar phosphorus metabolites, animal studies show that the ratio in the two are different. We argued that the ratio should start high (skeletal muscle) and plateau at a low value representing cardiac muscle. Using this criterion, which makes no assumption on what the ratio is in heart muscle, the PCr:ATP in six normal subjects was 1.55 +/- 0.2. This protocol has been used in a preliminary study in patients with cardiomyopathies.

Adenosine Triphosphate↗
PubMed1987

Skeletal muscle metabolism in patients with congestive heart failure: relation to clinical severity and blood flow.

We and others have previously demonstrated excessive phosphocreatine (PCr) depletion and acidosis in skeletal muscle during exercise in patients with congestive heart failure (CHF). In the present study, we performed serial measurements of PCr and pH during gradually incremental flexor digitorum superficialis exercise in 22 patients with CHF and 11 age-matched controls to determine: (1) whether abnormalities were present at the same relative workloads (a comparison that would at least partially compensate for differences in muscle mass), (2) the temporable course of the metabolic changes, (3) the relationship of the metabolic findings to clinical variables, and (4) the relationship of the metabolic abnormalities to forearm blood flow. The patients with CHF had significantly lower [PCr] and pH at all submaximal levels of exercise, and these abnormalities were apparent from the onset of low-level exercise. There was considerable heterogeneity among the patients with CHF with respect to the metabolic findings, with 14 of 22 exhibiting either PCr or pH values more than 2 SDs below normal. Patients whose capacity was more limited during the protocol had lower [PCr], and especially pH, at low loads than did other patients with CHF or the control subjects. The more symptomatic patients and those with more limited bicycle exercise tolerance also had lower pH values. In contrast, there were no significant differences in forearm blood flow between the patients and controls and no relationship between forearm blood and either clinical variables or the metabolic findings. These results indicate that skeletal muscle metabolic abnormalities are present in many patients with CHF and that they are not primarily due to either muscle atrophy or impaired blood flow. These changes may explain in part the marked heterogeneity of symptom status and exercise capacity of patients with similar degrees of cardiac dysfunction.

Blood Flow Velocity↗
PubMed1987

The study of human organs by phosphorus-31 topical magnetic resonance spectroscopy.

The potential clinical use of topical magnetic resonance spectroscopy (volume selection by static magnetic field gradients) was tested in 50 studies in volunteers. Topical magnetic resonance spectroscopy (MRS) was shown to be a straightforward method for localising 31P spectra of brain and liver. However, the spherical shape and fixed position of the selected volume posed serious limitations to the study of heart and transplanted kidney by topical MRS. Phosphorus-31 spectra of approximately 30 cm-3 of brain or liver could be obtained in 8 min. Ratios of metabolite concentrations could be determined with a coefficient of variation ranging from 10% to 30%. The ratios of phosphocreatine/ATP and inorganic phosphate/ATP in brain were 1.8 and 0.3, respectively. The ratio of inorganic phosphate/ATP in liver was 0.9. Intracellular pH was 7.03 in brain and 7.24 in liver. The T1 relaxation times of phosphocreatine, inorganic phosphate and gamma-ATP in brain were 4.8 s, 2.5 s and 1.0 s, respectively.

Brain↗
PubMed1986

A study of intracellular orthophosphate concentration in human muscle and erythrocytes by 31P nuclear magnetic resonance spectroscopy and selective chemical assay.

In order to study the relationship between extracellular and intracellular concentrations of orthophosphate (Pi), phosphorus nuclear magnetic resonance spectra were recorded, at rest, from the flexor digitorum superficialis muscle of hypophosphataemic patients with vitamin D-resistant rickets, and patients with Paget's disease of bone before and after they had been made hyperphosphataemic by treatment with the drug ethylidene-1-hydroxy-1,1-bisphosphonate. Changes in intramuscular P1 were estimated from the ratio of the areas of the Pi to adenosine 5'-triphosphate peaks. Even though the plasma Pi concentration in these patients spanned a fourfold range (0.5-2.0 mmol/l) the corresponding intramuscular Pi concentration increased by only 70%. A similar effect was observed in erythrocytes, from patients with these disorders, which were incubated in autologous plasma at 37 degrees C, under an atmosphere of O2 + CO2 (95:5, v/v). However, chloride ions, which are transported passively across the cell membrane, showed no change in distribution between cells and plasma, indicating that there was no general effect on passive anion distribution. When erythrocytes from normal subjects were incubated in autologous plasma (1.0 mmol of Pi/l) and in plasma supplemented with Pi (2.3 mmol of Pi/l), the Pi concentration in the cells, at steady state, increased only from 0.57 to 0.78 mmol/l cells, suggesting that the effect was not an artifact of disease or drug therapy. It is concluded that, in human skeletal myocytes and erythrocytes, the percentage change in the concentration of cytoplasmic Pi is lower than that in plasma. This implies that these cells can buffer or regulate cytoplasmic Pi when the extracellular concentration is disturbed.

Adult↗
PubMed1986

The survival of treated hypertensive patients and their causes of death: a report from the DHSS hypertensive care computing project (DHCCP).

A prospective study has been carried out to determine the causes of death and risk factors for survival in 4994 patients referred with a diagnosis of hypertension to hospital specialist clinics and 457 patients treated by their general practitioners for this condition. At the time of entering the prospective study, 69% of the patients were already being treated for hypertension. Four hundred and eleven patients have died, and their causes of death and death rates have been compared with the rates for the population of England and Wales. Ischaemic heart disease accounted for over one-third of the deaths and stroke for one-fifth. The death rates for these conditions were two to five times those expected for men and women aged 50-59 years and up to twice the rate expected for the age group 60-69 years. Survival in these selected patients was impaired by the following independent risk indicators: cigarette smoking, previous history of myocardial infarction or stroke, diagnosis of angina, impaired renal function and raised blood sugar. The following factors were not independent positive risk factors: smoking a pipe or cigars, obesity, a low plasma potassium and an elevated serum uric acid.

Adolescent↗
PubMed1984

Changes in cerebral blood flow in patients with severe congestive cardiac failure before and after captopril treatment.

The intravenous 133xenon injection method was used to estimate global cerebral blood flow before and after treatment with captopril in nine patients with severe heart failure. The pretreatment mean blood pressure was 94.9 mm Hg (S.D. 13.9) and fell to 85.1 mm Hg (S.D. 18.1) after treatment with captopril for between four and 15 days. The cerebral blood flow before captopril was 61.1 ml/100 g per minute (S.D. 6.9), which was less than the value of 75.8 ml/100 g per minute found in control subjects. After treatment with captopril the cerebral blood flow increased to 73.8 ml/100 g per minute (S.D. 11.8, p less than 0.01). The fraction of carbon dioxide in the expired air was not significantly different in the two studies (4.1 +/- 0.88 versus 3.97 +/- 0.65). It is concluded that cerebral blood flow is reduced in severe heart failure and can be restored by treatment with captopril, but the reasons for the reduced flow and its improvement after converting enzyme inhibition are not known.

Adult↗
PubMed1984

Technetium-fibrinogen lung scanning in canine lung contusion.

To detect experimentally induced acute lung contusion in anesthetized dogs, serial radionuclide images of the lung were recorded following intravenous infusion of 99mTc-labelled human fibrinogen (Tc-HF). The accumulation of Tc-HF in canine lungs was serially quantitated for up to 20 hours after lung contusion. A contusion (#1) was produced in one lung, Tc-HF was injected IV after 15 minutes, and 75 minutes later a contralateral lung contusion (#2) was produced in a series of 14 dogs. At autopsy the excised lungs were scanned, sectioned, and counted for radioactivity. Radiolabelled fibrinogen accumulated within 2-4 minutes of contusion #2 and remained stable over the next 20 hours in 14 dogs; contusion #1 was barely visible in four dogs. Lung Tc-HF activity in the central region of contusion #2 remained sixfold higher than in normal lung tissue. These data suggest that following lung contusion, fibrinogen deposition occurs rapidly and remains stable over a 20-hour interval of observation.

Animals↗
PubMed1982

The effects of peripheral impedance and inotropic state on the power output of the left ventricle in dogs.

The power output of the left ventricle as measured by the product of the Fourier components of aortic pressure and aortic flow is linked by definition to the arterial impedance facing the heart as measured by the quotient of these components. Consequently, the use of power measurements to assess ventricular performance can be ambiguous when accompanied by afterload changes. The heart is considered to function normally between two extremes, a constant flow pump, and a constant constant pressure pump, and two power limits are defined from these. The power limits describe the extent to which impedance changes can affect the power delivered by the left ventricle. Measured power changes that are found to lie outside the two limits can be unambiguously ascribed to changes in inotropic state. The results from preliminary dog experiments designed to test this method are reported. Cardiac sympathetic stimulation and isoprenaline infusion were used to provide a pure inotropic stimulus and a mixture of inotropic and afterload changes, respectively. The technique was able to detect inotropic changes in the heart even in the presence of simultaneous changes in afterload. Eight conventional indices of cardiac performance were monitored for comparison. The extent of their afterload dependence may not be as easily quantified.

Animals↗
PubMed1981

Separate contribution of ventricular pumping and load impedance on ventricular power output.

The heart is a rather special type of fluid pump in the sense that it is an organic pump. In this paper, however, it is postulated that the heart behaves like any other mechanical pump whose power output may assume, for a primary change in load, values bounded by two limits which are power output values obtained had the pump been a pressure generator and a flow generator respectively. A power output value outside the limits would imply a definite alteration in ventricular pump function concomitant with the load change. A nomogram to illustrate the proposal is included. The hypothesis may be developed into a powerful tool for assessing the pumping capability of the left ventricle, and this has significant clinical and physiological implications.

Animals↗
PubMed1981

Assessment of myocardial performance in ischaemic heart disease: from changes in left ventricular power output produced by graded-dose isoprenaline infusion.

Current clinical indices of myocardial contractility derive from concepts of muscle mechanics developed from isolated muscle experiments. Numerous simplifying assumptions are needed to apply these concepts to contractility studies in the whole heart. An alternative is to consider the heart as a pump which generates both pressure (P) and flow (Q) and to estimate its performance from the power output of its ventricles (P X Q). A method is described for measuring peak left ventricular power output in patients during routine cardiac catheterisation. The measurements have been made at rest and following inotropic challenge with gradient infusions of isoprenaline intravenously. Results from 13 patients with coronary artery disease and severe angina pectoris, who were clinically indistinguishable from one another, are reported. The patients could be grouped according to their left ventricular peak power responses to isoprenaline, although no difference could be demonstrated between them at rest. The patients who showed no increase in left ventricular power response to isoprenaline had a poor prognosis.

Adult↗
PubMed1981

Aortic input impedance in man: acute response to vasodilator drugs.

In 18 patients who underwent coronary arteriography, aortic velocity and pressure data were obtained during a control state and during either isoproterenol infusion at 1, 2 and 3 micrograms/min or graded nitroprusside infusion (average peak dose 60 micrograms/min). Impedance moduli and phase angles were derived to 10 Hz for controls states, isoproterenol at 2 micrograms/min, and at peak nitroprusside effect. Averaged control data included a mean resistance of 1460 dyn-sec-cm-5 and a characteristic impedance of 88 dyn-sec-cm-5 The characteristic impedance did not correlate with age (r = 0.21), coronary artery disease score (r = 0.17) or mean aortic pressure (r = -0.01). In 11 patients, isoproterenol induced a 38% reduction in mean resistance and a 10% reduction in mean aortic pressure. There was slight reduction in characteristic impedance and phase angles became less negative, to 2 Hz. In seven patients, nitroprusside induced a 38% reduction in mean resistance and a 22% reduction in mean aortic pressure. Impedance moduli decreased to 1.8 Hz and phase angles became less negative, to 3 Hz. Based on the different cardiovascular actions of these two drugs, the data suggest that vasodilators do not induce significant changes in the aortic impedance spectrum when not associated with a decrease in mean aortic pressure.

Adult↗
PubMed1980

Captopril and frusemide in severe drug-resistant hypertension.

10 patients with severe refractory hypertension were treated with captopril and frusemide. All patients had uncontrolled blood pressure (mean arterial pressure > 140 mm Hg), and 7 had developed accelerated hypertension despite maximum conventional treatment. Captopril and frusemide controlled blood pressure in all 10 patients, without side effects in 9. There was a significant rise in plasma-potassium in 9 patients (1 mmol/l), and hyperkalaemia (plasma-potassium > 6 mmol/l) developed in 3 patients despite coincident treatment with frusemide.

Adolescent↗
PubMed1980

Total body potassium falls with age.

1. Plasma volume, 24 h urine sodium and total body potassium were similar among 89 previously untreated patients with mild hypertension and 89 control subjects matched for age and sex. 2. Total body potassium correlated with renin activity in both hypertensive patients and controls. 3. Renin activity and total body potassium fell significantly with age in both groups. 4. The relationship between renin and total body potassium was no longer present when the effects of age were allowed for in a partial correlation.

Aging↗
PubMed1979

Blood flow in pulmonary veins: I. Studies in dog and man.

The pattern of blood flow in the large extra parenchymal pulmonary veins is pulsatile in both dog and man. This pulsatility is dominated by the changes in left atrial pressure taking place throughout the cardiac cycle. No pulsatile component of low in the large pulmonary veins could be attributed to forward transmission of a flow pulse conducted from the lung capillaries. The findings suggest that there must be a region of considerable compliance in the pulmonary venous system which can absorb pulsations from the lung capillaries and eliminate their transmission to the left atrium.

Animals↗
PubMed1979

Blood flow in pulmonary veins: II. The influence of events transmitted from the right and left sides of the heart.

The wave form of blood flow in the large extra parenchymal pulmonary veins has an inverse relationship to the pressure wave form in the left atrium during each cardiac cycle. However, when vein flow from the lungs is separated from the left atrium by diverting it into a constant pressure reservoir, its wave form then resembles a lung capillary flow pulse, though delayed from it in time and reduced in ampliture. The pulsatility of flow in pulmonary veins separated from the left atrium is further reduced when transcapillary pressure is elevated by lung inflation. However, in the intact state, the relation between the pattern of pulmonary vein flow and left atrial pressure remains unaffected by lung inflation. It is postulated that the thin walled extraperenchymal pulmonary veins together behave as a collapsible reservoir which enables outflow from them to be determined by changes in left atrial pressure, in spite of variations of pulsatile flow into them from the lungs.

Animals↗