Résumé
Septic shock is the most frequent cause of death in intensive care units. Despite major advances in antimicrobial therapy, critical care and surgical techniques, there has been little improvement in morbidity or mortality due to sepsis or septic shock. The aim of this study was to evaluate the role of vascular cell adhesion molecule-1 [VCAM-1] and intercellular adhesion molecule-1 [ICAM-1] in sepsis, septic shock, haemodynamic changes and outcome. Thirty intensive care unit patients suffering from sepsis with or without shock were subjected to blood culture, culture from the site of infection if possible, blood gases analysis, acute physiology and chronic health evaluation score [APACHE II] at baseline, multiple organ failure score on day one [MOF1], cummulative organ failure score [MOFC] on day 5, haemodynamic measurements, as well as serum VCAM-1 and ICAM-1 levels for 5 days after admission. Ten healthy control subjects were also included in the study. The most common site of infection was the chest, the isolates were mostly Gram negative [60%of cases], 9 patients [30%] had positive blood cultures. Serum ICAM-1 and VCAM-1 levels gradually increased from a baseline till day 5 of the study and were significantly higher in patients on admission [62 +/- 20.21, 404.67 +/- 130.85 ng/ml, respectively] than in the control group [14.0 +/- 4.71, 128.0 +/- 34.9 ng/ml respectively], [P=0.00]. They were higher in shocked than in non-shocked patients, and significantly so in non-survivors than in survivors and in patients with positive blood cultures than in those with negative blood cultures, throughout the study period [P=0.00]. A significant positive correlation was observed between serum ICAM-1 and VCAM-1 levels on one hand, and APACHE II as well as both organ failure scores for the 1st day or cumulative on the other hand. We conclude that these adhesion molecules could be measured in critically ill septic patients to predict prognosis and guide therapy
Résumé
This work was performed on 12 asthmatic patients who showed a 15% improvement or more in the forced expiratory flow [FEF] between 25-75% of the forced vital capacity [FVC] following 2.5 mg isoproterenol inhalation. An alpha-blocker phentolamine [regitine] was administered in ascending [1, 2.5, 5, 7.5 and 10 mg] doses by inhalation on separate days after performing a baseline spirometric study. A placebo dose was administered randomly between the phentolamine doses. Spirometric recordings were performed at 1, 5, 30, 60, 90 and 120 minutes. Pulse rate and blood pressure recordings were obtained for each trial. Arterial blood samples were obtained as a baseline and at 10 and 60 minutes of the optimum 10 mg phentolamine dose for arterial pH, oxygen tension [PaO2] and carbon dioxide tension [PaCO2]. The results generally indicated a failure of the alpha-blocker phentolamine in reproducing bronchodilatation. It had a significant effect on PaCO2 levels. The response of pulse rate and blood pressure was variable