HEMODYNAMIC BASIS OF OSCILLATIONS IN SYSTEMIC ARTERIAL-PRESSURE IN CONSCIOUS RATS

Citation
Bja. Janssen et al., HEMODYNAMIC BASIS OF OSCILLATIONS IN SYSTEMIC ARTERIAL-PRESSURE IN CONSCIOUS RATS, American journal of physiology. Heart and circulatory physiology, 38(1), 1995, pp. 62-71
Citations number
42
Categorie Soggetti
Physiology
ISSN journal
03636135
Volume
38
Issue
1
Year of publication
1995
Pages
62 - 71
Database
ISI
SICI code
0363-6135(1995)38:1<62:HBOOIS>2.0.ZU;2-3
Abstract
In conscious resting rats, beat-to-beat fluctuations in systemic mean arterial pressure (MAP) were compared with those in cardiac output and those in blood flow in the renal, mesenteric, and hindquarter vascula r beds. Spontaneous oscillations (lability) in MAP were observed in fr equency bands centered about 1.6 Hz (high: HF), 0.4 Hz (mid: MF), and 0.13 Hz (low: LF). Lability of MAP was confined within the LF (approxi mate to 8 s) band. Lability of cardiac output, on the other hand, show ed primary HF oscillations. LF oscillations in regional blood how were most prominent in the mesenteric and renal vascular beds. In these be ds, LF oscillations in blood flow showed negative phase angles with MA P, whereas those between MAP and hindquarter blood flow were positive. Cross correlation analysis indicated that similar to 2 s following a LF change in MAP, LF changes in mesenteric and renal blood flow occurr ed opposite to those of MAP. Changes in hindquarter flow were negative ly correlated with those in MAP about zero time delay. Admittance gain s were greater than or equal to 1 across all frequencies for all vascu lar beds, indicating the absence of autoregulation. This hemodynamic p attern suggests that myogenic mechanisms predominantly control mesente ric and renal blood flow in a nonautoregulatory but rather superregula tory manner, while autonomic mechanisms regulate hindquarter blood flo w. Thus, in conscious resting rats, spontaneous fluctuations in system ic arterial pressure predominantly exhibit slow (approximate to 8 s) o scillations, which do not arise from fluctuations in cardiac output, b ut originate from regionally specific myogenic oscillatory mechanisms contributing to resistance to flow.