Low glucose level and low pH alter the electrochemical function of human parietal pleura.

The aim of the present study was to investigate whether low glucose and pH level, which are usually measured in complicated pleural effusions, alter the electrochemical function of healthy human parietal pleura. Parietal pleural pieces were stripped from 66 patients during thoracic surgery and were mounted in Ussing chambers. Krebs' solutions containing different glucose levels (0, 40 and 100 mg) and balanced at different pH levels (7.4, 7.3 and 7.2) were added to the pleural cavity surface of the pieces. Transmesothelial potential difference was measured at various time-points as an electrophysiological variable and transmesothelial resistance (R(TM)) was calculated using Ohm's law. When normal-glucose Krebs at pH 7.45 was used, R(TM) remained unchanged over time, but when low-glucose Krebs was used, R(TM) decreased. Krebs without glucose caused the greatest decrease in R(TM). Use of low-pH Krebs decreased R(TM). The lower the pH of the Krebs, the faster the decrease in R(TM) and the greater the effect. The decrease in R(TM) was greater with low-pH than with low-glucose Krebs. Low glucose and low pH caused an additive decrease in R(TM). Low glucose concentration and low pH cause alteration of the electrochemical function of human parietal pleura and could act as agents that lead to further exudate progression.

Mediastinal cystic hygroma: report of a case with review of the literature.

Cystic hygroma is a developmental malformation of the lymphatic system. It is very uncommon for this type of tumor to arise from and grow exclusively in the mediastinum. Enlargement of such a lesion within this region often produces alarming respiratory symptoms requiring immediate medical attention.

Prevention of perioperative neurological dysfunction. A six year perspective of cardiac surgery.

Neurological dysfunction following cardiac surgical procedures is now well recognized. In order to minimise this serious complication, we instituted various protocols related to the potential causes of perioperative stroke such as: (1) components and use of the heart-lung machine; (2) air embolization; (3) intrinsic cerebro-vascular disease; (4) atheroemboli from the ascending aorta and (5) clot emboli from the left ventricle. We employed certain methods of operation of the heart-lung machine, air evacuation manoeuvres and a pharmacological brain protection protocol. These protocols were applied in a series of 1487 consecutive cardiac surgical procedures performed between 1984 and 1989; 127 patients died (8.54% mortality) and 16 patients (1.08%) suffered major neurological syndromes. Among the latter patients, 4 distinct groups were identified. Group A consisted of 6 patients who remained unresponsive after operation. In group B were 6 patients who awakened after operation but had clinical evidence of focal cerebral infarction. Group C included 3 patients who were initially intact neurologically but in whom neurological deficits developed later. Group D contained 1 patient who had severe mental aberration but no focal neurological deficits. Causative factors, including atheromatous embolism, perioperative hypotension and air embolism, were suspected in 12 of these 16 patients (75%) in groups A, B and C. The outcome was poor for unresponsive patients and 9 out of the 16 died or remained comatose (56.6%).