[Radionuclide angiocardiographic evaluation of the effect of isosorbide dinitrate in patients with Chagas' disease].
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Biomedical subjects
Publications and source records attributed to B C Maciel.
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Six normal subjects were submitted to dynamic exercise at workloads of 25, 50, 100 and 150 w for 4 min, intercalated by periods of rest, before and after an aerobic training period of 10 weeks. The heart rate response was fitted to 2 mathematical models, a 1st-order model and a 2nd-order model. The results indicate that these 2 models were not adequate to characterize the physiological response of heart rate induced by dynamic exercise.
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The relative contribution of the efferent components of the autonomic nervous system to the regulation of tachycardia induced by isometric exercise was assessed in 23 normal males. The isometric exercise (handgrip) was performed at the maximum intensity tolerated by the individual over a period of 10 s (maximal voluntary contraction-MVC) and at levels equivalent to 75, 50 and 25% of MVC for 20, 40 and 10 s, respectively. The study was performed both under control conditions and after pharmacological blockade with atropine (12 individuals) or propranolol (11 individuals). Under control conditions, the heart rate (HR) responses to isometric effort were dependent on the intensity and duration of the exercise, showing a tendency towards progressive elevation with the maintenance of muscular contraction at the levels studied. The tachycardia evoked by this effort was of considerable magnitude and of rapid onset, especially at the more intense levels of activity. Parasympathetic blockade markedly decreased tachycardia, which manifested itself during the first 10 s of exercise at all levels of intensity, whereas sympathetic blockade markedly modified the HR response after 10 s of effort at the 75 and 50% MVC levels. A slight depression of the tachycardiac response could be observed already after 10 s of maximum effort after propranolol. The present results suggest that the autonomic regulation of these responses is based on a biphasic mechanism, with the initial phase depending on the rapid withdrawal of the parasympathetic influence, followed by a marked sympathetic contribution to the induction of tachycardia after 10 s of isometric contraction or even a little before at maximum exertion.
In eight normal subjects we studied the effects of intravenous (i.v.) injection of 2 mg atropine sulfate on the static lung recoil pressure-volume (PV) curves, plethysmographic airway resistance (Raw), and maximum expiratory flow rates (Vmax). In addition, we determined the influence of atropine injection in esophageal elastance (Ees) by measuring the esophageal pressure with an esophageal balloon containing five different volumes (0.5 to 4 ml) of air and by calculating the change in esophageal pressure per unit change in balloon volume (delta Pes/delta Vb). This procedure allowed us to obtain static lung recoil pressure (Pst(1] at a balloon volume extrapolated to zero, thus avoiding the interference of changes in esophageal tone following atropine administration with the measurement of Pst(1). After vagal blockade with atropine, Pst(1) significantly decreased with a shift to the left of PV curves, Raw decreased, and Vmax increased mainly at lower lung volumes. Ees also decreased with parasympathetic blockade. We interpret these findings to indicate that inhibition of vagal tone results in dilatation of large and small airways, and also in the relaxation of smooth muscle in terminal lung units.
The mechanisms that control resting heart rate in hyperthyroidism were evaluated in six patients before and after treatment with propylthiouracil. The patients were subjected to pharmacological blockade under resting conditions in two experimental sessions: first session, propranolol (0.2 mg/kg body weight); second session, atropine (0.04 mg/kg body weight) followed by propranolol (0.2 mg/kg body weight). All drugs were administered intravenously. Resting heart rate was significantly reduced from 100 +/- 6.5 beats/min to 72 +/- 2.5 beats/min (P less than 0.005) after clinical and laboratory control of the disease. After double blockade, intrinsic heart rate was reduced from 105 +/- 6.8 beats/min before treatment to 98 +/- 6.0 beats/min after treatment (P less than 0.025). The reduction in heart rate caused by propranolol was not significantly different before (-13 +/- 1.4 beats/min) and after (-9 +/- 1.0 beats/min) propylthiouracil. In contrast, atropine induced a higher elevation of heart rate after treatment (45 +/- 8.6 beats/min) than before treatment (26 +/- 4.0 beats/min). The present results suggest no appreciable participation of the sympathetic component of the autonomic nervous system in the tachycardia of hyperthyroidism, at least under the conditions of the present study. The small change observed in intrinsic heart rate, although significant, seems to indicate that this is not the most important mechanism involved in this tachycardia. Our results suggest that an important reduction in the efferent activity of the parasympathetic component participates in the mechanisms that modify resting heart rte in hyperthyroidism.
Ten normal subjects and 14 patients with chronic Chagas' disease (seven with and seven without heart disease) underwent dynamic exercise on a cycle ergometer. Heart rate (HR), pulmonary ventilation (V), oxygen consumption (VO2), carbon dioxide production (VCO2), and respiratory quotient (RQ) were measured. Increasing workloads (25, 50, 100, and 150 W) were applied for 4 min and intercalated with resting periods. The main objective of this protocol was to analyse heart rate response in relation to the other cardiorespiratory variables in order to evaluate the functional conditions of the sympathetic and parasympathetic cardiac efferents. Analysis of the results showed that (a) the group of chagasic patients with heart disease had lower heart rates (p less than 0.05) than normal subjects during the initial 10 s (delta HR 0-10 s) of effort (fast component); (b) the difference between the normal subjects and chagasic patients without heart disease was not statistically significant; (c) the abnormalities in heart rate response were due to depression of parasympathetic efferent action on the sinus node; (d) the slow heart rate response (delta HR 1-4 min), which expresses the degree of sympathetic stimulation of the sinus node, was comparable in the three groups studied, thus showing unimpaired adrenergic responses during dynamic exercise in Chagas' disease; and (e) the V, VO2, VCO2, and RQ values were normal at all workloads in each group, suggesting that vagal dysfunction does not affect oxygen transport at these submaximal levels of dynamic exercise.
A 55-year-old man was admitted to our hospital because of progressive dyspnea, orthopnea and hemoptysis. Two-dimensional echocardiography multiple echo-dense images 1-4 mm in diameter were consistently seen crossing the tricuspid valve. A hypothesis of multiple pulmonary thromboembolism was raised. Clinical and postmortem evidence were later obtained to confirm this diagnosis.
Standardized handgrip at 100% of maximal voluntary capacity was used to study heart rate responses to isometric exercise in patients with the digestive form of Chagas' disease. The chronotropic responses of the group were significantly lower (P less than 0.001) than those exhibited by control subjects, and comparable to those observed in a group of cardiac chagasic patients. These results show that severe impairment of autonomic control of the heart may occur in chagasic patients apparently having only digestive tract involvement.
The relative contribution of the efferent components of the sympathetic and parasympathetic nervous systems to the heart rate (HR) response to dynamic physical exercise was evaluated in 23 normal males. The dynamic exercise was performed on a bicycle ergometer at work loads of 25, 50 and 100 W, before and after pharmacological blockade with atropine (13 individuals) or propranolol (10 individuals). Parasympathetic blockade significantly depressed the rapid HR response at the beginning of the exercise period at all levels of intensity, whereas sympathetic blockade only affected the slow-response phase (1-4 min), especially at the highest level of effort. The present results suggest that the tachycardia evoked by dynamic exercise is mediated by a biphasic mechanism initially depending on rapid vagal release, which increases progressively with increasing effort. An increased sympathetic activity manifests itself in a more delayed manner, especially at the higher levels of activity. Continuous monitoring of HR during the entire period of activity at different levels of intensity permits the utilization of dynamic exercise as a simple and non-invasive method for the functional evaluation of the two components of the autonomic nervous system of the heart.
Haemodynamic responses to sustained isometric exercise (handgrip at 30% of maximum voluntary capacity) were studied in 10 patients with Chagas's cardiopathy without previous or current heart failure. Five of the patients (group 1) had profound impairment of parasympathetic control of heart rate. They had no tachycardia in response to intravenous administration of atropine and no bradycardia during phase IV of the Valsalva manoeuvre. The other five (group 2) showed normal vagal regulation of heart rate, as judged by chronotropic responses to these tests. The heart rate change (mean (SD] elicited by the handgrip test was significantly lower in group 1 (from 93.0 (14.1) to 95.0 (16.7) beats/min) than in group 2 (from 78.2 (15.8) to 92.8 (18.1) beats/min). Pressor responses to handgrip were of similar magnitude (from 91.6 (7.8) to 109.0 (8.0) mm Hg in group 1 and from 88.6 (11.9) to 106.8 (20.9) mm Hg in group 2). In both groups no significant change in stroke index was detected during handgrip. Cardiac index increased during handgrip from 4.0 (1.2) to 4.8 (1.3) 1/min/m2 in group 2, but there was no significant change in group 1 (from 4.9 (0.7) to 4.8 (1.1) 1/min/m2). Changes in calculated systemic vascular resistance were significantly higher in group 1 (from 934 (175) to 1176 (383) dyn s cm-5) than in group 2 (from 1109 (404) to 1112 (424). This study shows that parasympathetic impairment adversely influences the haemodynamic pattern of response to isometric exercise in patients with Chagas's heart disease. In such conditions, the pressor response to handgrip is predominantly mediated by an increase in systemic vascular resistance rather than an increase in cardiac output.
Seven normal subjects of sedentary habits were submitted to a 10 week period of endurance physical training on a cycloergometer. The training programme produced a mean 15.6 +/- 1.4% (+/- SE) increase in VO2max (from 39.7 +/- 2.0 ml . kg-1 . min-1 to 45.9 +/- 2.4 ml . kg-1 . min-1) and a reduction in resting heart rate (HR) from 69 +/- 1.9 to 58 +/- 1.7 beats . min-1 in the supine position. After pharmacological blockade of the parasympathetic system with atropine sulphate, HR rose on average by 53 +/- 3.9 beats . min-1 before training and 47 +/- 3.6 beats . min-1 after training, the difference being statistically nonsignificant. The magnitude of respiratory sinus arrhythmia (RSA) was similar before and after the period of physical conditioning. The respiratory variation in HR ( Delta HR) at the 1 litre tidal volume was 20 +/- 2.4 beats . min-1 and 20 +/- 2.6 beats . min-1 before and after training, respectively. At the 2 litre tidal volume, these values were 25 +/- 3.2 and 27 +/- 4.5 beats . min-1. Similar results were obtained with the RSA test when a group of 13 sedentary individuals (VO2max = 39.4 +/- 1.3 ml . kg-1 . min-1) was compared with a group of 7 athletes who are medium distance runners (VO2max = 53.8 +/- 1.3 ml . kg-1 . min-1).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of parasympathetic blockade with intravenously administered atropine (0.04 mg/kg body weight) on the heart rate (HR) of 11 normal males was evaluated using a standardized isometric exercise (handgrip). This type of exercise, when maintained for 10 s at the maximum intensity tolerated by the volunteer, causes tachycardia mediated almost exclusively by parasympathetic withdrawal. The test was performed under baseline conditions and at 20 +/- 3, 33 +/- 3, 42 +/- 3, 52 +/- 3 and 61 +/- 3 min after atropine infusion. The heart rate of the subjects at rest in the supine position (mean +/- SEM) was 70 +/- 2 bpm, reaching values of 119 +/- 3 bpm after atropine. Under control conditions (sitting position), the increase in HR induced by isometric exercise was 22 +/- 1.8 bpm. After blockade, the increase was 4 +/- 0.8, 4 +/- 0.7, 5 +/- 0.6, 4 +/- 1.0 and 4 +/- 0.8 bpm, respectively, at each repetition of the test. These results suggest that the blockade induced by this dose of atropine is effective for at least 1 h. They also indicate the need for a more rigorous definition of the functional half-life of atropine in the heart, when considering physiological tests that either stimulate or withdraw parasympathetic activity upon the heart.
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The sensitivity of the baroreceptor reflex to transient hypertension was determined in 13 patients before (control) and after (72 hours) open cardiac operations with extracorporeal circulation (ECC). In all patients early postoperative values were appreciably decreased (p less than 0.01) as compared to the preoperative values. This decrease suggested severe impairment of baroreflex control of the sinoatrial node. These changes were not correlated with concurrent alterations in heart rate or systemic arterial, left atrial, or right atrial pressures. In addition, respiratory sinus node arrhythmia was absent in all subjects. In four patients, subsequent studies 4, 8, 10, and 12 months, respectively, after the operation revealed good recovery of baroreflex sensitivity and respiratory influences on beat-to-beat variation. No similar effects were observed in two patients studied before and after cardiac operations without ECC. It is possible that direct trauma to the nervous supply of the sinoatrial node is a major factor in that reversible dysfunction; in fact, in three patients evidence was obtained that while sinoatrial node responses were impaired, the reflex control of the atrioventricular region remained unaltered. These findings point to further impairment of the fine control of heart rate imposed by the conditions of cardiac operations with ECC in patients with previously curtailed cardiac reserve.
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