SYMPATHETIC NEURAL BLOCKADE BY THORACIC EPIDURAL-ANESTHESIA SUPPRESSES RENIN RELEASE IN RESPONSE TO ARTERIAL-HYPOTENSION

Citation
Hb. Hopf et al., SYMPATHETIC NEURAL BLOCKADE BY THORACIC EPIDURAL-ANESTHESIA SUPPRESSES RENIN RELEASE IN RESPONSE TO ARTERIAL-HYPOTENSION, Anesthesiology, 80(5), 1994, pp. 992-999
Citations number
38
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
80
Issue
5
Year of publication
1994
Pages
992 - 999
Database
ISI
SICI code
0003-3022(1994)80:5<992:SNBBTE>2.0.ZU;2-7
Abstract
Background: The renin-angiotensin and vasopressin systems, in addition to the sympathetic system, are important backup mechanisms for mainta ining arterial blood pressure during circulatory challenges. We tested the hypothesis that preganglionic sympathetic blockade by thoracic ep idural anesthesia interferes with the functional integrity of the reni n-angiotensin system. Methods: Renin concentrations were assessed in a wake nonsedated patients in response to induced arterial hypotension b oth before and during sympathetic blockade by thoracic epidural anesth esia (n=10). Heart rate (electrocardiogram) and mean arterial blood pr essure (electromanometry) were recorded continuously. Active renin (ra dioimmunoassay), vasopressin (radioimmunoassay), and osmolality (osmom etry) in arterial blood were measured intermittently: (1) at baseline, (2) during a hypotensive challenge (15 min) induced by sodium nitropr usside (titrated to decrease mean arterial blood pressure by at least 25%) with the sympathetic system intact, (3) during recovery, (4) with epidural anesthesia alone (sensory blockade T1-T11), and (5) during a second hypotensive challenge and sympathetic blockade with sodium nit roprusside titrated to the same mean arterial blood pressure as with t he sympathetic system intact. Results: With the sympathetic system int act hypotension almost doubled renin concentration (34+/-32 SD to 60+/ -58 pg.ml(-1), P=0.019), while vasopressin concentration remained unch anged. In contrast, during sympathetic blockade and despite identical hypotension (mean arterial blood pressure 68+/-8 vs. 67+/-5 mmHg), ren in concentration did not change (35+/-27 vs. 35+/-29 pg.ml(-1), P=0.5) , whereas vasopressin concentration increased (4.6+/-2.5 to 13.4+/-9.4 pg.ml(-1), P=0.01). Osmolality remained unchanged. Conclusion: Our re sults Indicate a key role of renal sympathetic fibers in mediating ren in release during hypotension in humans, and that epidural anesthesia interferes with the functional integrity of the renin-angiotensin syst em.