Subservient relationship of the peripheral second systolic pressure peak to the central hemodynamic parameters is preserved, irrespective of atherosclerosis progression in hypercholesterolemic rabbits.
We investigated whether the subservient relationship of peripheral to central hemodynamic parameters, such as the augmentation index (AI) and the second systolic (SBP2) and pulse pressures, were preserved with the progression of atherosclerosis in the Kurosawa and Kusanagi-hypercholesterolemic (KHC) rabbit, an animal model for hypercholesterolemia and atherosclerosis. Male KHC rabbits, aged 12 and 24 months, were anesthetized with pentobarbital sodium. Two catheter-tip transducers were introduced to the central (ascending aorta) and peripheral (distal region of the right brachial artery) arteries through the left common carotid and the right radial arteries, respectively. Pressure waves were simultaneously recorded under regular atrial pacing to investigate changes in response to the intravenous infusion of angiotensin II (Ang II) (30-40 ng kg(-1) min(-1)) and sodium nitroprusside (NTP) (20-30 μg kg(-1) min(-1)). Central systolic blood pressure (cSBP) and diastolic blood pressure (DBP), peripheral systolic blood pressure (pSBP) and DBP, and peripheral second systolic blood pressure (pSBP2) showed no significant difference between the 12- and 24-month-old groups before the administration of vasoactive drugs. There was no significant difference in central AI (cAI) between the two age groups before the drug infusion, even though atherosclerosis progressed with aging. Peripheral AI (pAI) changed in parallel with cAI in response to vasopressor and depressor actions due to the infusion of Ang II and NTP, respectively. We conclude that the subservience of pSBP2 to cSBP and pAI to cAI, in addition to the regression relationship of these parameters between peripheral and central arteries, were well preserved, irrespective of the progression of atherosclerosis.
Department of Cellular and Integrative Physiology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Shin-ichiro
S
Katsuda
Jichi Medical University Health Care Center, Tochigi, Japan.
Hiroshi
H
Miyashita
Shin-Oyama City Hospital, Tochigi, Japan.
Kazuyuki
K
Shimada
Research and Development Department, Omron Healthcare Co., Ltd., Kyoto, Japan.
Yoshinori
Y
Miyawaki
Research and Development Department, Omron Healthcare Co., Ltd., Kyoto, Japan.
Iwao
I
Kojima
Research and Development Department, Omron Healthcare Co., Ltd., Kyoto, Japan.
Yuri
Y
Shiogai
Department of Cellular and Integrative Physiology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Akihiro
A
Hazama
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D050197:Atherosclerosis / Q000209:etiology / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology*; D018450:Disease Progression; D006439:Hemodynamics / Q000502:physiology; D006937:Hypercholesterolemia / Q000150:complications / Q000503:physiopathology*; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D011817:Rabbits; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D009599:Nitroprusside