The pathogenesis of high-altitude pulmonary oedema (HAPE) is disputed. Recent reports show a strong correlation between the occurrence of HAPE and pulmonary artery pressure, and it is known that the oedema is of the high-permeability type. We have, therefore, proposed that HAPE is caused by ultrastructural damage to pulmonary capillaries as a result of stress failure of their walls. However, no satisfactory electron microscopy studies are available in patients with HAPE, and animal models are difficult to find. Madison strain Sprague-Dawley rats show a brisk pulmonary pressure response to acute hypoxia and are susceptible to HAPE. We exposed 13 Madison rats to a pressure of 294 torr for up to 12.5 h, or 4 rats to 236 torr for up to 8 h. Pulmonary arterial or right ventricular systolic pressures measured with a catheter increased from 30.5 +/- 0.5 (SEM) in controls (n = 4) to 48 +/- 2 torr (n = 11). The lungs were fixed for electron microscopy with intravascular glutaraldehyde. Frothy bloodstained fluid was seen in the trachea of three animals. Ultrastructural examination showed evidence of stress failure of pulmonary capillaries, including disruption of the capillary endothelial layer, or all layers of the wall, swelling of the alveolar epithelial layer, red blood cells (RBCs) and oedematous fluid in the alveolar wall interstitium, proteinaceous fluid and RBCs in the alveolar spaces, and fluid-filled protrusions of the endothelium into the capillary lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of extradural and general anaesthesia on the adrenocortical response to elective or emergency Caesarean section were studied in 72 patients. Maternal plasma concentrations of cortisol were measured before surgery, at delivery, and 30 and 60 min after skin incision. Umbilical vein and artery plasma cortisol concentrations at delivery were determined also. Maternal plasma cortisol concentrations in patients receiving extradural anaesthesia did not change significantly from control at any of the time intervals. In the general anaesthesia group concentrations were significantly increased from control, at 30 and 60 min after skin incision for elective Caesarean sections, and at 60 min after skin incision during emergency surgery. There were no significant differences between the mean umbilical vein and artery plasma cortisol concentrations compared within or between extradural or general anaesthesia groups. Extradural anaesthesia, in contrast to general anaesthesia, decreases the adrenocortical response to Caesarean section surgery by blocking afferent neurogenic pathways from the surgical site. The method of anaesthesia does not influence the fetal cortisol response.
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