Biomedical subjects
Publications and source records attributed to M Ramanathan.
This report deals with a father and his son who developed acute renal failure following multiple bee stings. The renal lesion in these patients appears to be due to rhabdomyolysis caused by the bee venom. The other mechanisms are also discussed. The need for clinicians to be aware of acute renal failure as a complication of bee stings is stressed.
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Three-dimensional kinematics of radiopaque markers in anterior, posterior, septal, and lateral regions of a major equatorial plane were evaluated in anesthetized dogs by biplane fluoroscopy. Stationary coordinate systems measured marker locations recorded during diastole and systole from a contractile origin at the center of contraction at end systole and from a geometric origin at the intersection with the equatorial plane of the ventricular long axis at end diastole. A time-indexed system measured marker locations at end diastole and at end systole, respectively, from the locations of the geometric origin at end diastole and end systole. Compared to the stationary system with the geometric origin, both the stationary system with the contractile origin and the time-indexed system reduced the variability of the radial components of the contractile displacements between ventricular regions. In contrast to the other two systems, the system with the contractile origin reduced circumferential components to values not significantly different from zero. These results indicate that 1) abnormally contracting regions of the ventricle may be located and their size measured by determining the region where the radial component differs from that in the rest of the equatorial plane and 2) rotation in a major equatorial plane of the ventricle is significant, but the influence of rotation can be minimized by referencing ventricular dimensions to a coordinate system with an origin at the center of contraction.
Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.
The presenting features of 236 thyrotoxic patients seen in the thyroid clinic were reviewed. 18.65% of these patterns had one or more dermatological complaints at presentation. There was no specific difference in this group of patients when compared with the general hyperthyroid population with regard to age, race, sex, duration of hyperthyroidism or biochemical indices of thyrotoxicosis. The two major complaints were itching and alopecia. The prevalence of pruritus at 6.4% in our series was identical to that of other workers, but we had a much lower occurrence of alopecia at 2.6%. The diagnosis of thyrotoxicosis was delayed in two patients in whom the only major complaint was pruritus. These symptoms cleared quickly when these patients became euthyroid. However there were other patients who noted hair loss with anti-thyroid medications. The incidence of vitiligo, eczema, onycholysis in our series was much lower those quoted in the Western literature The occurrence of pretibial myoxoedema in our series is similar to that of other workers from this region. The other miscellaneous manifestations include urticaria, xanthelasma and systemic lupus erythematosis. In conclusion we feel the cutaneous manifestations of hyperthyroidism are common in our patients.
Adult Still's disease is now a well recognised distinct clinical entity. Two cases of the disorder are presented to illustrate the protean nature of the syndrome. The literature is reviewed with regards to the diagnosis, management and complications of the condition. The need for the physician to be aware of this condition to avoid unnecessary investigations and delay in instituting effective therapy will be stressed.
This report deals with a middle aged man in whom the presenting symptom of the disorder was dysphagia. The clinical approach to the final diagnosis of thyrotoxic myopathy causing dysphagia is outlined and the pathophysiology of dysphagia then discussed. The need to include thyrotoxicosis in the differential diagnosis of an otherwise unexplained case of dysphagia is stressed.
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We have developed a method for measuring in vivo canine right ventricular (RV) volume at a frequency of 60 Hz. In six dogs (17-22 kg), under pentobarbital anesthesia, 18 radiopaque markers were surgically implanted in the RV myocardium to maximally represent the RV shell. The xyz-coordinates of the markers were obtained from biplane cineradiographic recordings. RV volume was calculated from the polyhedron created by the markers by decomposing the polyhedron into 24 tetrahedrons, each of whose volumes could be solved from the xyz-coordinates of markers. RV volume was obtained each 16.7 ms, permitting detailed representation if RV volume dynamics. RV end-diastolic volume, end-systolic volume, and ejection fraction averaged 41.3 +/- 10.9, 23.0 +/- 5.8, and 0.44 +/- 0.05 ml, respectively. By simultaneously measuring RV pressure, RV pressure-volume loops were constructed that demonstrated that RV ejection occurred without significant isovolumic contraction, although isovolumic relaxation occurred at end systole. RV systolic elastance was determined in two dogs by imposing four levels of RV afterload. Maximal systolic elastance averaged 4.14 mmHg/ml under control conditions and 9.20 mmHg/ml during dobutamine infusion.
Eigenvolumes calculated from a linear transformation model were found previously to be linearly related to balloon volumes in excised hearts. The present study analyzed endocardial marker kinematics in intact, contracting left ventricles by biplane cinefluorography. Ejection fractions of the linear transformation model were compared by linear regression analysis with those of an ellipsoidal model, whose ejection fractions had been documented previously in closed and open-chest dog preparations. Data from 10 dogs indicated a correlation coefficient of 0.98 and a regression equation with close similarity to the line of identity. Ejection fractions calculated from the linear transformation model are concluded to be proportional to actual ejection fractions in intact, beating left ventricles.
The purpose of these experiments was to quantify stagnant intrapulmonary blood caused by a pulmonary arterial occlusion (PAO). The hypothesis was that the diffusing capacity of the lung for CO (DLCO) would be altered little by PAO when measured with the usual inspired concentrations (0.3%) of CO, since stagnant blood distal to the occlusion takes up CO for 20 s or more before significant CO backpressure would develop. However, higher levels of CO (i.e., greater than or equal to 3%) would equilibrate faster with capillary blood (within 5-10 s), and DLCO measured 10-20 s subsequent to the high CO exposure would reflect only the DLCO in the unoccluded regions. Thus the fractional reduction in DLCO measured with 3% CO, with respect to that measured with 0.3% CO, should be related to the fractional occlusion of the pulmonary artery in a predictable way. We occluded the right pulmonary artery (RPAO), the left pulmonary artery (LPAO), or the left lower lobar artery (LLPAO) and found that DLCO measured during rebreathing a 0.3% CO mixture was 80, 87, and 94%, respectively, of the preocclusion value, whereas the DLCO measured during rebreathing a 3.3% CO mixture was 59, 73, and 87% of the preocclusion value. A computer model was developed to predict the reduction in DLCO at different levels of CO exposure that would be caused by varying fractions of PAO. Our data indicated that RPAO corresponded to a 42% vascular occlusion, LPAO a 35% occlusion, and LLPAO a 20% occlusion. Measurement of DLCO using low and high concentrations of CO might be useful in assessing the fraction of vascular bed occluded and in following noninvasively the course of vascular occlusion in a variety of pulmonary diseases.
In this study, noninvasive measurements of cardiac output and O2 consumption were performed to estimate the blood flow to and efficiency of the respiratory muscles that are used in elevated inspiratory work loads. Five subjects were studied for 4.5 min at a respiratory rate of 18 breaths/min and a duty cycle of 0.5. Studies were performed at rest without added respiratory loads and at elevated inspiratory work loads with the use of an inspiratory valve that permitted flow only when a threshold pressure was maintained. Cardiac output and O2 consumption were calculated using a rebreathing technique. Respiratory muscle blood flow and O2 consumption were estimated as the difference between resting and loaded breathing. Work of breathing was calculated by integrating the product of mouth pressure and volume. Increases in cardiac output and O2 consumption in response of 4.5 min loaded breathing averaged 1.84 l/min and 108 ml/min, respectively. No increases were seen in response to 20-s loaded breathing. In a separate series of experiments on four subjects, though, cardiac output increased for the first 2 min then leveled off. These results indicate that the increase in cardiac output was a metabolic effect of the increased work load and was not caused primarily by the influence of the highly negative intrathoracic pressure on venous return. Efficiency of the respiratory muscles during inspiratory threshold loading averaged 5.9%, which was similar to measurements of efficiency of respiratory muscles using whole-body O2 consumption that have been reported previously in humans and in dogs.
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To determine the increment in cardiac output and in O2 consumption (Vo2) from quiet breathing to maximal sustained ventilation, Vo2 and cardiac output were measured using an acetylene rebreathing technique in five subjects. Cardiac output and Vo2 were measured multiple times in each subject at rest and during sustained maximal ventilation. During maximal ventilation subjects breathed 5% CO2 to prevent hypocapnia. The increase in cardiac output from rest to maximal breathing was taken as an estimate of respiratory muscle blood flow and was used to calculate the arteriovenous O2 content difference across the respiratory muscles from the Fick equation. Cardiac output increased by 4.3 +/- 1.0 l/min (mean +/- SD), from 5.6 +/- 0.7 l/min at rest to 9.9 +/- 1.1 l/min, during maximal ventilations ranging from 127 to 193 l/min. Vo2 increased from 312 +/- 29 to 723 +/- 69 ml/min during maximal ventilation. O2 extraction across the respiratory muscles during maximal breathing was 9.6 +/- 1.0 vol% (range 8.5 to 10.7 vol%). These values suggest an upper limit of respiratory muscle blood flow of 3-5 l/min during unloaded maximal sustained ventilation.
The purpose of these experiments was to determine the effects of a spontaneously generated inspiration on the size and shape of the left ventricle (LV) in anesthetized supine dogs. We implanted markers in the LV to establish three perpendicular axes and recorded the motion of these markers using biplane cinefluoroscopy at 60 Hz. The primary changes in LV size that accompanied inspiration occurred at end diastole (ED). The largest change in LVED dimension was a 2.46-mm narrowing of the septal-lateral wall dimension, but the apex-base dimension decreased also, by 0.74 mm. The anteroposterior dimension actually widened by 1.07 mm. The septal-lateral narrowing was caused by both a 1.0-mm narrowing of the distance between the septal marker and the apex-base axis, as well as by a 1.4-mm narrowing between the apex-base axis and the lateral wall marker. Narrowing of the septal portion seemed expected because of presumed enhanced right ventricular filling during inspiration. Narrowing of the lateral portion of the LV, while the anteroposterior dimension widened, was surprising because a change in LVEDV shape is implied. Assuming ventricular homogeneity, this change in LVED shape implies that the forces applied to the epicardial surface were not uniform. There must have been a retraction on the anterior and posterior surface that was not experienced by the lateral LV wall. The net effect of these dimensional changes of the LV at end diastole (estimated from the product of the three ED axes) was a 3.5-cm3 reduction in LVED volume.(ABSTRACT TRUNCATED AT 250 WORDS)
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