RESUMO
Endothelial cells [ECs] contribute to the regulation of blood pressure and blood flow by releasing vasodilators such as nitric oxide [NO], substance P [SP], prostacyclin [PGI [2]] and adrenomedullin, as well as vasoconstrictors including endothelin [ET] and platelet-activating factor [PAF]. Several previous studies have discussed the relation between anaesthetics and the vascular endothelium in vitro only and demonstrated that volatile anaesthetics [halothane and isoflurane] can alter endothelium-dependant vasodilatation in vitro. In vivo studies are scarce in that field. This could be attributed to the radical nature of NO and its very short half-life and involvement of labor-intensive assay and handling of radioactive isotopes. Consequently, determination of the more stable end products of NO, nitrite and nitrate, was used as a measure for NO production. It is the aim of the current study to make use of this technique to ascertain whether NO, as well as SP and ET, is actually involved in the circulatory effects of isoflurane/halothane, in the clinical context. The study was conducted on 40 patients of [ASA classes I and II], scheduled for open abdominal and/or pelvic procedures of minimum 1 hour duration. Reduction of MBP more than 20% of the preoperative level was considered hypotension. Induction in both groups was done by IV fentanyl [2 micro g/ kg], sodium thiopentone [4-7mg/kg] followed by vecuronium [0.1mg/kg] for intubation and long acting muscle relaxation. Anaesthesia was maintaied using 100% oxygen and halothane 0.5-1%, or isoflurane 0.6-1-2%, in groups Land II respectively. Mechanical ventilation was adjusted to maintain normocapnia. Nitrous oxide was omitted and increments of fentanyl and vecuronium were titrated to the patients' needs. Monitoring of arterial blood pressure and heart rate was done every 5 minutes. Reversal was done using prostigmine [0.08mg/kg] and atropine sulphate [0.02mg/kg]. Venous blood samples were collected before induction, 15, 30 and 60 minutes after initiation of anaesthesia [T0, T1, T2, T3], at cessation of anesthesia and fifteen minutes later [T4 and T5]. Plasma endothelin concentration was determined by enzyme immunoassay technique. Plasma substance P was measured by radioimmunoassay. Determination of serum nitrite and nitrate was done by a colorimetric assay. We have succeeded in ascertaining the role of nitric oxide in isoflurane-induced hypotension, but not halothane. The hypotensive effect of isoflurane which is known to be basically related to peripheral vasodilator mechanism may be via its stimulatory effect on vasodilator mediator [NO]. The role of ET and SP could be related to the short-term changes, mediated by the endothelium, in vasomotor tone in response to alterations in shear stress, in face of the significant hypertension that follows cessation of isoflurane anaesthesia