T. Shibamoto

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.

Effect of platelet-activating factor on hepatic capillary pressure in isolated dog liver

We determined the effects of platelet-activating factor (PAF), a potent vasoactive autacoid phospholipid, on the capillary pressure and liver weight (Wt) in isolated canine livers perfused with blood bivascularly via the portal vein and hepatic artery. PAF (0.01-33 microg) administered intraportally produced dose-dependent increases in the hepatic capillary pressure, as assessed by triple vascular occlusion pressure (Pto), and Wt. An intraportal injection of 10 microg PAF produced increases in Pto by 10 mmHg and Wt by 35 g/100 g liver weight. This hepatic vasoconstriction was attributed to a threefold increase in the portal vein resistance and a fourfold increase in the hepatic vein resistance. The hepatic arterial resistance was not changed when PAF was arterially or intraportally injected. In conclusion, in isolated perfused dog livers, PAF increases the hepatic capillary pressure and liver weight due to contraction of both the portal vein and hepatic vein, but not the hepatic artery.

Participation of nitric oxide in the sympathetic response to anaphylactic hypotension in anesthetized dogs

The role of nitric oxide (NO) was determined using a NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 20 mg/kg bolus and 0.05 mg/kg per min) in the renal sympathetic and hypotensive response to systemic anaphylaxis induced by Ascaris suum antigen (10 mg, i.v.) in naturally sensitized anesthetized dogs. Renal nerve activity (RNA) in animals pretreated with D-NAME, the biologically inactive enantiomer (n = 7), showed an initial increase (192 +/- 32%, (mean +/- SE) followed by a decrease (61 +/- 14%) after antigen. Pretreatment with L-NAME (n = 7) did not affect the initial sympathoexcitation but abolished the secondary sympathoinhibition (110 +/- 13%). However, the depressor response to antigen was not different between the L-NAME and D-NAME groups (-87 +/- 13 mmHg and -84 +/- 12 mmHg). In conclusion, NO is involved in the anaphylaxis-induced renal sympathoinhibitory response but not hypotension in anesthetized dogs.

Changes in tissue blood flow and sympathetic activities to various organs during prolonged hemorrhagic hypotension in monkeys

This experiment was designed to determine whether prolonged hemorrhagic hypotension in anesthetized monkeys produces differential control of tissue blood flow and sympathetic nerve activities to various organs (heart, kidney, liver, spleen, and hind-limb). We performed simultaneous multifiber recording of sympathetic nerve activity to the kidney (RNA), heart (CNA), spleen (SpNA), liver (HNA), and hind-limb (LNA) during sustained hemorrhagic hypotension at a mean blood pressure of 40 mmHg for 2 h. Immediately after bleeding, all of the sympathetic nerve activities increased significantly (Stage I) and then gradually decreased towards the prebleeding levels (Stage II). Thereafter, the secondary sympathetic excitation was observed (Stage III), followed by a gradual decrease in sympathetic activities below the prebleeding levels (Stage IV). The shed blood started to return to the animals at this final stage. Time course of changes in sympathetic nerve activities did not differ among organs innervated. However, tissue blood flow of the renal cortex, liver, skeletal muscle and spleen significantly decreased at Stage I and remained at low levels until the end of the experimental period. In contrast, blood flow of the renal medulla and heart was preserved until Stage III and Stage IV, respectively. These results indicate that although the sympathetic response to prolonged hemorrhagic hypotension of 40 mmHg did not differ among organs, changes in tissue blood flow were variable and blood flow to the heart and renal medulla was maintained at a steady level until a late stage of hemorrhage.

Differential regional sympathetic responses to somatic stimulation in anesthetized dogs

The present study was designed to determine whether regional differences exist in sympathetic responses to somatic nerve stimulation and whether the baroreceptor reflex modulates this somato-sympathetic reflex. The cardiac (CNA), renal (RNA), hepatic (HNA), splenic (SpNA) and adrenal (AdNA) sympathetic postganglionic nerve activities (SNA) were simultaneously recorded in anesthetized dogs with intact (n = 7) or bilaterally sectioned (n = 8) carotid sinus and vagus nerves. In the intact group, electrical stimulation of the left peroneal nerve at low intensity and low frequency (5 V, 5 Hz) produced a fall in mean arterial pressure (MAP) (-9.7 +/- 2.7 mmHg) and a decrease in each SNA with no regional differences RNA (79.2 +/- 8.5%), AdNA (82.7 +/- 5.4%), HNA (89.4 +/- 4.5%), CNA (87.5 +/- 3.5%), SpNA (84.2 +/- 3.2%). In contrast, stimulation at high intensity and high frequency (25 V, 50 Hz) produced a rise in MAP (+21.4 +/- 3.8 mmHg) and increases in SNA with quantitative predominance of RNA (178.6 +/- 13.6%) and AdNA (158.3 +/- 16.1%) over HNA (129.0 +/- 4.2%), CNA (117.7 +/- 7.6%), and SpNA (112.0 +/- 6.2%). Similar responses were observed when the left ulnar nerve was stimulated. The changes in SNA (delta SNA) at 10 s after the start of stimulation were plotted as a function of the changes in MAP (delta MAP) and the regression curves were determined. The best fit regression curve was a logistic sigmoid curve in the intact group and a linear one in the baroreceptor denervated group. Furthermore, delta RNA/delta MAP and delta AdNA/delta MAP during the somato-pressor response were significantly smaller in the intact group than in the denervated group. In conclusion, there are regional differences of sympathetic response during the somato pressor response but not during somato depressor response. The baroreceptor reflex may suppress the somato-sympathetic reflex of RNA and AdNA.