José Carlos Manço

Limitations of facial immersion as a test of parasympathetic activity in man.

1. The heart rate response to immersion of the face in water, as an isolated manoeuvre or in combination with apnoea, was studied in eight normal volunteers to establish the conditions under which it could be used as a standardized, simple, non‐invasive and reproducible test of parasympathetic activity. 2. The following procedures were evaluated: (a) 10 s apnoea in air at different lung volumes; (b) facial immersion in water for 2 min at various temperatures (5, 15 and 25 degrees C), with respiration maintained through a closed circuit; (c) combination of immersion and apnoea at different lung volumes. Three volunteers were re‐evaluated after pharmacological blockade with atropine sulphate (0.04 mg/kg body weight). 3. The results showed that: (a) apnoea in air triggered lung volume‐dependent heart rate responses; (b) facial immersion in water induced transient bradycardia which was maximum between 20 and 30 s of immersion; (c) there was no appreciable difference in the bradycardia evoked by immersion at different temperatures; (d) the combination of immersion and apnoea caused heterogeneous heart rate responses with no potentiation of bradycardia in relation to each manoeuvre as performed separately; (e) atropine did not reduce the magnitude of bradycardia induced by immersion in two of the subjects studied. 4. The variability of responses observed in the present study was probably due to the multiple receptors and afferent pathways that are simultaneously excited during these manoeuvres. As a consequence, the autonomic efferent response will depend on the unpredictable net effect of interaction of these mechanisms. This is a limiting factor for the standardization of this test as a simple and reproducible method for the assessment of parasympathetic activity. 5. Furthermore, the results obtained under pharmacological blockade indicate that the vagal efferent mechanism is not the only factor responsible for the bradycardia caused by facial immersion without apnoea.

The use of isometric exercise as a means of evaluating the parasympathetic contribution to the tachycardia induced by dynamic exercise in normal man.

Fourteen normal subjects were submitted to isometric exercise (IE), dynamic exercise (DE) and a combination of the two (IE+DE). The main purpose of the present study was to use IE as a means of evaluating the mechanism of the heart rate (HR) increase induced by DE. To this end, the magnitude of the IE (handgrip) was standardized so as to cause an elevation of HR almost exclusively by vagal withdrawal: IE was performed using a dynamometer straingauge system with a linear response at 75% of maximum voluntary contraction (MVC) for 10s, repeated at 1 min intervals. The change in HR evoked by IE under control conditions was compared with that evoked during DE, and during the corresponding recovery period. DE was performed by the legs, with the subject in the seated position for 4 min, at workloads of 55 and 105 watts, separated by a rest period. In the combined protocol, IE was performed at the beginning of DE, as well as at 1, 2 and 3 min during DE, and at 0, 1, 2, 3 and 5 min during recovery period. The following results were obtained: (1) IE associated with DE always induced smaller increase in heart rate than IE alone, and this effect was more marked at 105 than at 55W; this finding suggested a workload-dependent vagal withdrawal at the very beginning of DE that was sustained until the end of effort. (2) During DE, each IE induced a similar increase in HR, even at workload of 105 W, when the HR increased gradually in response to DE itself; these results suggest that, this gradual tachycardia (from the 1st to the 4th min of DE) was not vagus dependent. (3) The standardized IE used here permitted functional evaluation of the dynamics of vagal withdrawal without resorting to pharmacological blockade of the autonomic nervous system.

Evaluation of the Autonomic Nervous System of the Heart in Male Patients with Mitral Valve Prolapse Syndrome Using Respiratory Sinus Arrhythmia and Dynamic Exercise

The autonomic nervous system of the heart was evaluated in two male groups composed of 11 patients with mitral valve prolapse and of 10 normal subjects, using the heart rate response in two types of tests: respiratory sinus arrhythmia at rest and dynamic exercise. Sinus arrhythmia was of higher magnitude in patients with mitral valve prolapse when compared to the control group; however, the differences reached statistical significance only at a respiratory frequency of 7 cycles/min. With respect to dynamic exercise (25, 50, 100, 150 W during 4 min), the heart rate response, either in terms of the early, vagus-dependent fast tachycardia (first 10 s), or the late, sympathetic-dependent tachycardia (1-4 min) was normal in both groups studied, the same occurring with aerobic exercise capacity evaluated by measurement of the anaerobic threshold. Thus, our results show that in the group of male patients with mitral valve prolapse studied here, the parasympathetic abnormalities, if present, are of questionable physiological significance and do not affect the sympathetic and parasympathetic control of heart rate during dynamic exercise.

Effects of intravenous atropine on static P-V curves of the lung in normal man

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.

Mass on chest X-ray.

Accepted 30 October 1996 A 22-year-old man was admitted to hospital with a 14-kg weight-loss over the last 14 months, and an abnormal chest X-ray. Physical examination revealed signs of consolidation over the left hemithorax, fever, tachypnoea and tachycardia. Computed tomography (CT) was performed (figure 1) and one liter of bloody fluid was drained by thoracentesis. Abdominal CT scan was normal.