To determine the effect of left ventricular assist device (LVAD) pumping on sympathetic tone, renal sympathetic nerve activity (RSNA) was detected in acute animal experiments. Our TH-7B pneumatically driven, sac-type ventricular assist device was used in 7 adult mongrel dogs. RSNA was detected by the use of bipolar electrodes attached to the left renal sympathetic nerve. RSNA was amplified and integrated by use of an R-C integrator circuit. The area of the integrated nerve discharge per unit time was calculated in the computer system and expressed as RSNA per unit time. During LVAD pumping, RSNA decreased with increase in blood pressure, with an increase in pulmonary artery flow, and with a decrease in left atrial pressure. These data suggest that LVAD has an effect on the sympathetic nervous system which is mediated by the aortic and cardiopulmonary baroreflex system.

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In order to evaluate the effect of ventricular assist device (VAD) driving on the autonomic nervous system, sympathetic neurograms during left ventricular (LV) assistance were analyzed by power spectrum and coherence function. Our TH-7B pneumatically-driven sac-type VAD was used in seven adult mongrel dogs. VADs were inserted between the left atrium and the descending aorta. Renal sympathetic nerve activity (RSNA) was detected by use of bipolar electrodes attached to the left renal sympathetic nerve via a retroperitoneal approach. Values of squared coherence between the arterial pulse wave and RSNA were measured at the same frequency of cardiac and VAD pumping rhythms. During LV assistance, coherence at the cardiac rhythm frequency was decreased, and coherence at the VAD pumping rhythm frequency was increased. These results indicate that the arterial pulse wave, which was produced by the VAD assistance, contributed to postganglionic sympathetic nerve activity.

We describe a case of a 21-year-old man with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) who presented with hypoxic ventilatory depression. He had chronic hypoventilation, which was not explained by weakness of respiratory muscles. His hypercapnic ventilatory response was not impaired. In contrast, hypoxic ventilatory depression was observed in the isocapnic progressive hypoxic response test. After exposure to hypoxic conditions, his respiratory frequency decreased and tidal volume was unchanged. The hypoxic ventilatory depression was partially blocked by pretreatment with aminophylline. In conclusion, we need to be careful with patients with MELAS who are hypoxaemic because a vicious circle of hypoxia and hypoventilation can occur.

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