José Mauro Goulart Brum

Sigma receptor activation does not mediate fentanyl-induced attenuation of muscarinic coronary contraction.

Our overall goal was to investigate the mechanism by which fentanyl attenuates acetylcholine-induced contraction in porcine coronary artery. We tested the hypothesis that fentanyl attenuates muscarinic coronary contraction via sigma receptor activation. Left coronary artery vascular rings were isolated from porcine hearts and were suspended in organ chambers for isometric tension recording. In untreated coronary vascular rings, acetylcholine administration resulted in dose-dependent contraction. Fentanyl attenuated acetylcholine-induced contraction. The sigma ligands--(+)-pentazocine, (+)-cyclazocine, haloperidol, and 1,3-di-o-tolylguanidine--also inhibited acetylcholine-induced contraction. In contrast, the selective sigma ligand, (+)-3-(3-hydroxyphenyl)-N-(1-propyl) piperidine failed to have an inhibitory effect on acetylcholine-induced contraction. Moreover, metaphit (1-[1(3-isothiocyanatophenyl)cyclohexyl]piperidine), which causes irreversible acylation of sigma receptors, only inhibited acetylcholine-induced contraction when it was present in the organ chamber. We also assessed the effects of inhibiting various points in the signal transduction pathway distal to naloxone-sensitive opioid receptor activation on acetylcholine-induced contraction. Selective (glybenclamide) and nonselective (tetraethylammonium) K+-channel inhibition, guanosine triphosphate-binding protein inactivation (pertussis toxin), and Type 1 and Type 2 dopamine receptor inhibition all failed to alter the attenuating effect of fentanyl on acetylcholine-induced contraction. Thus, neither sigma nor opioid receptor activation is a prerequisite for fentanyl-induced inhibition of muscarinic coronary contraction. (Anesth Analg 1996;82:982-7)

Cardioplegia retrógrada seqüencial

The distribution pattern of a cold (3-4oC), crystalloid cardioplegic solution (CS) in the myocardium was studied in 15 mongrel dogs, with 10-15 kg of body weight. Alter anesthesia and median sternal thoracotomy. The pericardium was opened and extracorporeal circulation established. The following routes were employed for cardioplegic perfusion: 1) Antegrade - through ascending aortic canullation bellow the aortic occlusion clamp;2) Selective retrograde - through coronary synus (Co.S - 25 mmHg) using a self-inflating ballooned cannula; 3) Total retrograde, (Co.S - 40 mmHg) - through a cannula inserted in the right atrium (RA); 4) Sequencial retrograde, Co.S-RA - with the CS flowing first through the coronary synus lowering the interventricular septal temperature to 16 oC and after through the RA cannula as in the total retrograde technique with the pulmonary artery occluded and;5) Sequencial retrograde, Co.S-RV - the RV chamber being directly cannulated through the tricuspid valve and perfused, instead of the RA in the latter technique. The temperature variation of the myocardium in the left ventricule (LV), RVt RA and sinus node region (SN) was controlled employing an Omega needle termistor and thermometer. With the antegrade technique (70 mmHg pressure) the most uniform myocardial cooling, the lowest CS volume and perfusion time duration was observed, followed In excelence by the Co.S-RA Sequencial retrograde technique and the Co.S-RV sequencial technique. The present data indicate that sequencial retrograde cardioplegic perfusion techinique is significantly better than the usual Co.S or RA total retrograde technique alone for myocardial protection when compared with the aortic root antegrade perfusion technique.