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
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.