Five soldiers were injured by inhalation of hexite smoke (ZnCl2) during military training. Two soldiers, not wearing gas masks breathed hexite for 1 or 2 min, they slowly developed severe adult respiratory distress syndrome (ARDS) over the ensuing 2 weeks. This slow, progressive clinical course has not been previously described. In both patients, an increased plasma zinc concentration was measured 3 weeks after the incident. Intravenous and nebulized acetylcysteine increased the urinary excretion of zinc, and briefly decreased the plasma levels. In an attempt to arrest collagen deposition in the lungs, L-3,4 dehydroproline was administered. Both patients died of severe respiratory failure (25 and 32 days after inhalation). At autopsy diffuse microvascular obliteration, widespread occlusion of the pulmonary arteries and extensive interstitial and intra-alveolar fibrosis was observed. Three soldiers wearing ill fitting gas masks, immediately developed severe coughing and dyspnea. They improved, and 12 months after exposure their lung function tests were nearly normal, but they still had slight dyspnea on exercise.
1. The aim of this study was to provide direct evidence that sympathetic outflow to the skin in humans is governed by central neural mechanisms. 2. Microneurographic measurements of skin sympathetic nerve activity (SNA) from the peroneal nerve was performed in nine subjects during: (1) static hand grip at 10, 20 and 30% maximal voluntary contraction (MVC); and (2) attempted static hand grip during partial neuromuscular blockade produced by injection of vecuronium. 3. Two minutes of static hand grip at 20 and 30% MVC (force output, 9-6 + 0X2 and 14A4 + 0.3 kg, respectively) evoked significant increases in skin SNA that were graded to the intensity of the exercise. Static hand grip at 10% MVC (force output, 4-8 + 0.1 kg) caused a small but insignificant increase in skin SNA. 4. During vecuronium-induced neuromuscular blockade, subjects failed to maintain a force output equivalent to the output produced during 10% MVC before vecuronium (force output: 1st min, 4-4 + 0-6 kg; 2nd min, 21 + 0 4 kg), in spite of maximal effort being applied. This attempted hand grip exercise consistently evoked considerable increases in skin SNA that did not significantly differ from the responses produced by hand grip at 30% MVC; total skin SNA increased by 246 + 93% during 2 min of attempted hand grip and increased by 243 + 77% during 2 min of static hand grip at 30% MVC (means+ S.E.M., P < 0 05). These increases in skin SNA were not due to activation of resting muscles because measurements of surface electromyography showed no activity in resting forearm muscles during static or attempted hand grip exercise. 5. This study provides direct neurophysiological evidence that central motor command can activate sympathetic outflow. During static hand grip, central motor command is the primary mechanism that stimulates sympathetic outflow to skin.
Plasma cortisol and glucose were measured in 24 patients undergoing abdominal hysterectomy during spinal anaesthesia with 0.5% hyperbaric tetracaine or neurolept anaesthesia. The sensory level of analgesia to pinprick extended to at least T4 before skin incision in the spinal group. The mean sensory analgesic level regressed almost linearly, reaching the fourth lumbar segment 4 h after incision. Plasma cortisol and glucose measurements from before to 9 h after skin incision showed significant increases in both parameters during and after surgery. Plasma cortisol and glucose levels were significantly lower during and immediately after surgery in the spinal group, but later postoperatively the mean levels were similar in the two groups. The increase in plasma cortisol 1 h after skin incision in the spinal group correlated to the segmental level of analgesia at that time (r = 0.77, P less than 0.01) and a similar correlation was found with regard to plasma glucose changes (r = 0.60, P less than 0.05). The regression lines showed that maintenance of a sensory analgesic level about the fourth thoracic segment prevented the adrenocortical and hyperglycaemic response to surgery. These findings are in accordance with the anatomical assumption that the upper segmental level of visceral afferent input to the spinal cord is about the fourth thoracic segment. Our results further demonstrate that the inhibitory effect of spinal anaesthesia on the stress response to surgery is transient, and correlates to the regression of sensory analgesia.
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