P Pu ur rp po os se e: : To compare the cardiovascular and sympathetic effects of a new ultra-short-acting, highly cardioselective ß-blocker, landiolol, with esmolol, using an in vivo rabbit model. ) were given intravenously, and the effects on heart rate (HR) mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were compared.R Re es su ul lt ts s: : Both landiolol and esmolol produced a dose-dependent decrease in HR. The maximum percent reductions of HR were similar with landiolol 3 mg·kg 1 and esmolol 5 mg·kg 1 (-14.0 ± 0.9% and -13.9 ± 1.4%, mean ± SE, respectively). HR decreased more rapidly with landiolol than with esmolol. Esmolol produced a dose-dependent decrease in MAP that was not observed with landiolol. The percent maximum reduction of MAP was -38.2 ± 3.2% with esmolol 5 mg·kg 1 . RSNA increased in a dose-dependent fashion with esmolol, but no changes were noted with landiolol.C Co on nc cl lu us si io on n: : These results suggest that, in rabbits, landiolol has slightly more potent negative chronotropic action than esmolol with significantly less effects on blood pressure.

The combination of fentanyl and diazepam significantly decreases systemic vascular resistance and blood pressure. We attempted to elucidate the reason the combination of these drugs can reduce blood pressure. In alpha-chloralose-anesthetized dogs, we investigated the effects of fentanyl and diazepam on mean arterial pressure (MAP) and arterial baroreflex control of renal sympathetic nerve activity (RSNA) in both intact (Study 1) and baroreflex-denervated dogs (Study 2). Study 1 included five dogs that received fentanyl 10 micrograms/kg followed by diazepam 0.4 mg/kg after a 10-min interval. Five more received both drugs in reversed sequence. The arterial baroreflex depressor test was performed with sodium nitroprusside before and after administration of each drug. Sensitivity of arterial baroreflex was examined by using the ratio of maximum increase of RSNA to maximum decrease of MAP (delta RSNA/delta MAP). RSNA and MAP significantly decreased only after both drugs had been administered (P < 0.05). Fentanyl alone did not attenuate arterial baroreflex sensitivity. Diazepam after fentanyl and diazepam alone attenuated baroreflex sensitivity to the same extent (P < 0.05). Study 2 comprised 14 dogs that underwent further surgical preparation of bilateral carotid sinus, aortic, and vagal nerve denervations. Seven received fentanyl, 5 and 10 micrograms/kg, and the other seven received diazepam, a total of 0.4 mg/kg. Fentanyl decreased both RSNA and MAP. Diazepam decreased only MAP significantly. The results indicate that fentanyl decreases mainly sympathetic outflow, whereas diazepam attenuates arterial baroreflex. We conclude that these combined effects of fentanyl and diazepam significantly decrease arterial blood pressure.

Loss of complexity (status of being complex behavior) of both heart rate and systolic blood pressure variability, indicated by increased fractal slopes, is one mechanism in attenuating baroreflex sensitivity after stellate ganglion block.

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Purpose: Whether or not right and left stellate ganglion blocks (SGB) affect blood pressure (BP) and heart rate (HR) differently has been controversial. The aim of this study was to analyze BP and HR changes after large numbers of right or left SGBs. Methods: A total of 16,404 right SGBs and 13,766 left SGBs were performed with 6 ml of 1% mepivacaine using the anterior paratracheal approach at C6. Changes in systolic BP and HR 30 min after SGBs were compared to the baseline values. Results: Systolic BP decreased by 25 to 49 mmHg in 10.93% and more than 50 mmHg in 0.67% of 16,404 right SGBs. Those percentages were significantly higher than corresponding percentages; 8.43% and 0.49% of 13,766 left SGBs (P < 0.0001 and P < 0.05, respectively). On the other hand, systolic BP increased by 25-49 mmHg in 5.74% and more than 50 mmHg in 0.52% of left SGBs, and in 4.15% and 0.18% of right SGBs (P < 0.0001and P < 0.0001 between left and right SGBs, respectively). Right SGB caused marked reduction in HR (greater than 30 beats/min), more than left SGB (4.22% versus 2.70%, P < 0.0001). Conclusions: Both right and left SGBs could produce clinically significant hypertension and hypotension, and also severe bradycardia. However, right SGB produces a higher incidence of significant reductions in systolic BP and HR, compared to left SGB. On the other hand, left SGB produces a significant increase in systolic BP compared to right SGB. Those differences likely stem from the hemispheric asymmetry in autonomic cardiovascular control.

One reason for the reported conflicting results of the effect of ketamine on hemodynamics and respiration may be variations in afferent inputs from peripheral receptors to the central nervous system. In order to evaluate unmasked direct effects of ketamine on sympathetic nerve and phrenic nerve outflow, totally deafferented (involving vagus, sinus nerve, aortic depressor nerve) rabbits (n = 18), rabbits with vagotomy (n = 21), and neuraxis-intact rabbits (n = 6) were used in this study. The animals were anesthetized with urethane and mechanically ventilated. Ketamine 0.5, 1, or 2 mg/kg was injected intravenously and mean arterial pressure (MAP), heart rate (HR), and integrated renal sympathetic nerve and phrenic nerve activity (IRSNA, IPNA) were recorded before, and 1, 2, 3, 5, and 10 min after injection. MAP and IRSNA were significantly decreased, even by the smallest dose of ketamine, in the totally deafferented group. IPNA was decreased by the largest dose of ketamine only in the totally deafferented group. On the other hand, spontaneous respiratory frequency was decreased in the totally deafferented and vagotomy groups, but more so in the totally deafferented group. In the neuraxis-intact group, the only significant change with the largest dose of ketamine, 2 mg/kg was a slight increase in HR. We conclude that ketamine can suppress vasomotor and respiratory centers directly, and that the suppression is counterbalanced by afferent inputs from peripheral receptors.

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The reason why adenine compounds when used as hypotensive agents are devoid of significant reflex sympathetic activity, such as rebound hypertension and tachycardia, is not clearly understood. This study, performed on alpha-chloralose-anesthetized dogs, examined, first, the effects of adenosine triphosphate (ATP) and adenosine as compared with those of sodium nitroprusside on efferent renal sympathetic nerve activity (RSNA), as an indicator of general reflex sympathetic activity, and second, whether vagal involvement could be demonstrated in the action of ATP and adenosine on RSNA. Renal sympathetic nerve activity increased progressively with increasing doses of sodium nitroprusside (5, 10, and 20 micrograms/kg) and adenosine (0.5, 2.0, and 4.0 mg/kg), whereas ATP suppressed RSNA at 2.0 and 4.0 mg/kg. High doses of ATP and adenosine (4.0 mg/kg) were injected into intact (n = 7) and vagotomized dogs (n = 7). Both ATP and adenosine induced rapid onset of hypotension without rebound hypertension and tachycardia. After vagotomy, the attenuation of RSNA by ATP was completely abolished and rebound hypertension and tachycardia were observed. Vagotomy did not alter the effect of adenosine on RSNA. It is concluded that ATP-induced hypotension is associated with attenuation of sympathetic efferent nerve activity mediated through vagal afferent pathways. Vagal afferent impulses are thought to be one of the mechanisms that inhibit reflex sympathetic activities, such as rebound hypertension after ATP-induced hypotension. The mechanisms by which adenosine inhibits reflex sympathetic activity are not, however, secondary to vagal afferent involvement and must be multifactorial.