Search

We report on two patients who underwent bilateral lung transplantation (BLTx) combined with cardiac surgery. Patient 1 was a female whose pulmonary hypertension resulted from a congenital atrial septal defect (ASD) and idiopathic pulmonary arterial hypertension. She had a very small left ventricle (LV). We initiated venoarterial extracorporeal membrane oxygenation (ECMO) before induction of general anesthesia. She underwent ASD patch closure, pulmonary artery replacement, and BLTx under cardiopulmonary bypass (CPB). At the weaning from CPB, primary graft dysfunction and pulmonary edema induced by LV diastolic dysfunction was apparent. We gradually decreased the ECMO support and eventually weaned off the ECMO on the 4th postoperative day (POD) and the ventilator on the 29th POD. Patient 2 was a male with Eisenmenger syndrome, which resulted from ASD and ventricular septal defect (VSD). He had a normal LV. General anesthesia was induced smoothly without ECMO. He underwent ASD and VSD patch closure, pulmonary artery replacement, and BLTx under CPB. Weaning from CPB proceeded smoothly. These patients needed different management because of their different LV function. Especially, perioperative management of the BLTx patient with LV diastolic dysfunction was difficult. Assessment of perioperative cardiac function is very important in BLTx combined with cardiac surgery.

We evaluated the effects of an adenylate cyclase activator, N, N-dimetyl-beta-alanine[3R-(3alpha,4alphabeta,5beta+ ++,6beta,6aalpha, 10alpha,10abeta,10balpha)]-5(acetyloxy)-3-eth enyldodecahydro-10, 10b-dihydroxy-3,4a,7,7,10a-pentamethyl-1-oxo-1H-naphtho[2, 1-b]pyran-6-yl ester hydrochloride (NKH477), on neural control of renal functions in anesthetized dogs. Renal nerve stimulation (2 Hz) increased renal norepinephrine efflux and reduced renal blood flow, glomerular filtration rate, urine flow rate, urinary Na(+) excretion and fractional Na(+) excretion. Intrarenal arterial infusion of NKH477 (300 ng/kg/min) suppressed the stimulation-induced reductions in renal blood flow and glomerular filtration rate and attenuated the reductions in urine flow rate and urinary Na(+) excretion but not the changes in renal norepinephrine efflux and fractional Na(+) excretion. Infusion of NKH477 did not affect the urinary responses induced by renal nerve stimulation at a lower frequency (0.5-1 Hz) which had little influence on renal blood flow and glomerular filtration rate. The present results demonstrate that NKH477 inhibits renal vasoconstriction and hypofiltration but not the enhanced tubular Na(+) reabsorption during activation of the renal sympathetic nervous system.