Y. Saeki

The effects of sevoflurane, enflurane, and isoflurane on baroreceptor-sympathetic reflex in rabbits

This study was designed to determine the effects of sevoflurane, enflurane, and isoflurane ranging from 0.5 to 1.25 minimum alveolar anesthetic concentration (MAC) on spontaneous efferent renal sympathetic nerve activity (RNA) and the baroreceptor-sympathetic reflex in rabbits. Enflurane produced significant decreases in spontaneous RNA by 22.5% +/- 6.6% at 1.0 MAC, while sevoflurane and isoflurane, at the equivalent MAC, did not. All of the anesthetics attenuated the baroreflex gain similarly when mean blood pressure (MBP) was changed by sodium nitroprusside or phenylephrine intravenously. However, the sensitivity of baroreceptors at the aortic wall was not changed by any anesthetic, because no changes in the relationship between aortic nerve activity and MBP were obtained in anesthetic concentration even at 1.25 MAC. Furthermore, these anesthetics suppressed the sympathoinhibitory response to aortic nerve stimulation above 1.0 MAC. In conclusion, enflurane inhibits RNA to a greater degree than sevoflurane or isoflurane. However, all three anesthetics depress the reflex regulation of RNA to the same degree. The suppression on the baroreceptor-sympathetic reflex does not appear to be related to a change in the receptor sensitivity on the aorta, but is mediated by suppression of the central or peripheral sympathetic integrating system. (Anesth Analg 1996;82:342-8)

Effects of thromboxane A2 analogue on vascular resistance distribution and permeability in isolated blood-perfused dog lungs

This study was designed to determine the effects of thromboxane A2 (TxA2) on the distribution of vascular resistance, lung weight, and microvascular permeability in isolated dog lungs perfused at a constant pressure with autologous blood. The stable TxA2 analogue (STA2; 30 μg, n = 5) caused an increase in pulmonary capillary pressure (Pc) assessed as double-occlusion pressure to 14.0 ± 0.4 mmHg from the baseline of 7.9 ± 0.3 mmHg with progressive lung weight gain. Pulmonary vascular resistance increased threefold exclusively due to pulmonary venoconstriction. Pulmonary venoconstriction was confirmed in lungs perfused in a reverse direction from the pulmonary vein to the artery (n = 5), as evidenced by marked precapillary vasoconstriction and a sustained lung weight loss. Furthermore, in lungs perfused at a constant blood flow (n = 5), STA2 also caused selective pulmonary venoconstriction. Vascular permeability measured by the capillary filtration coefficient and the isogravimetric Pc at 30 and 60 min after STA2 infusion did not change significantly from baseline in any lungs studied. Moreover, elevation of Pc by raising the venous reservoir of the intact lobes (n = 5) to the same level as the STA2 lungs caused a greater or similar weight gain compared with the STA2 lungs. Thus, we conclude that TxA2 constricts selectively the pulmonary vein resulting in an increase in Pc and lung weight gain without significant changes in vascular permeability in isolated blood-perfused dog lungs.

Renal vascular and sympathetic nerve responses to hypotension induced by platelet-activating factor in anesthetized dogs

This experiment was designed to determine renal sympathetic and renal vascular responses to platelet-activating factor (PAF)-induced hypotension in anesthetized dogs with and without systemic baroreceptor denervation. The left kidney was perfused at a constant flow, and renal perfusion pressure and efferent left renal sympathetic nerve activity were measured simultaneously. Intrarenal injection of PAF (1.25-5.0 x 10(-2) micrograms/kg, n = 6) produced a dose-dependent increase in renal perfusion pressure without any change in systemic blood pressure. An intravenous injection of PAF (10 micrograms/kg) to intact animals (n = 7) caused an initial increase in renal nerve activity (157 +/- 14%) followed by a gradual reduction below baseline (72 +/- 7%) with concomitant systemic hypotension (from 116 +/- 7 to 46 +/- 6 mmHg). Renal perfusion pressure increased significantly from 84 +/- 2 to 161 +/- 33 mmHg concomitant with an increase in renal nerve activity at 1 min and was maintained at this elevated level throughout the experiment. Similar responses of renal nerve activity and renal perfusion pressure were found in animals with complete systemic baroreceptor denervation (n = 7). These results suggest that renal vascular response during PAF-induced hypotension may presumably be mediated by a direct vasoconstrictor effect of PAF on the renal vasculature and that baroreceptor reflex is not involved in either renal sympathetic or renal vascular changes.