A NONINVASIVE EVALUATION OF BARORECEPTOR SENSITIVITY WITH THE VALSALVA MANEUVER AND PHENYLEPHRINE METHODS

Citation
Jp. Richter et al., A NONINVASIVE EVALUATION OF BARORECEPTOR SENSITIVITY WITH THE VALSALVA MANEUVER AND PHENYLEPHRINE METHODS, Methods and findings in experimental and clinical pharmacology, 17(6), 1995, pp. 423-428
Citations number
19
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
03790355
Volume
17
Issue
6
Year of publication
1995
Pages
423 - 428
Database
ISI
SICI code
0379-0355(1995)17:6<423:ANEOBS>2.0.ZU;2-S
Abstract
In a double-blind crossover study, we compared baroreceptor sensitivit y (BS) and latency, derived from the phenylephrine method with BS and latency derived from phase IV of the Valsalva maneuver(VM) using the F inapres(TM), a noninvasive blood pressure monitor Ten healthy voluntee rs were enrolled in the study and BS was determined with placebo, atro pine (0.03 mg/kg) and atenolol(10 mg) and was expressed as the linear relation between the change in RR interval following the blood pressur e vise induced by either phenylephrine or phase IV of the VM (i.e., af ter cessation of straining). Baseline baroreceptor sensitivity (p < 0. 001) and baroreceptor sensitivity in the presence of atropine (p < 0.0 2) was smaller with the VM but no differences in baroreceptor sensitiv ity between the two methods were evident after atenolol. Although no l inearity existed between the two methods under any of the experimental conditions, baroreceptor sensitivity in the presence of atropine was significantly smaller (p < 0.01) (and latency delayed(p < 0.08)) compa red to atenolol-induced changes with both methods. We found excellent correlation between baroreceptor sensitivity derived from the ECG trac ing and Finapres(TM) recorded beat-to-beat pulse intervals (p < 0.001; r > 0.8, under all conditions) although the correlation after atropin e was not as close (p < 0.01; r = 0.7). The smaller baroreceptor sensi tivity induced by the Valsalva maneuver with placebo and atropine, but not with atenolol, suggests a parasympathetically influenced vasodila tion, and sympathetically mediated tachycardia during phase IV of the VM.