Impacts of pulsatile systemic circulation on endothelium-derived nitric oxide release in anesthetized dogs

Nakano, Toshihide; Tominaga, Ryuji; Morita, Shigeki; Masuda, Mitsuharu; Nagano, Ichiro; Imasaka, Ken-ichi; Yasui, Hirofumi

doi:10.1016/s0003-4975(01)02644-3

Cited by 40 publications

(26 citation statements)

References 24 publications

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“…Weinberg et al (52) have also found a dose-dependent decrease in the relative height of the dicrotic notch or a/b after acetylcholine and SNP, both of which were abolished by L-NAME, and additionally confirmed an NO pathway-mediated effect. Others have found the rise of the a/b in humans after nitroglycerin administration (11,20,22,23,25,38,40,43). Our results are consistent and in close agreement with the aforementioned investigators.…”

Section: Discussionsupporting

confidence: 93%

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Uryash

Wu²,

Bassuk³

et al. 2009

Journal of Applied Physiology

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Uryash A, Wu H, Bassuk J, Kurlansky P, Sackner MA, Adams JA. Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation. J Appl Physiol 106: 1840 -1847, 2009. First published March 26, 2009 doi:10.1152/japplphysiol.91612.2008.-Low-amplitude pulses to the vasculature increase pulsatile shear stress to the endothelium. This activates endothelial nitric oxide (NO) synthase (eNOS) to promote NO release and endothelial-dependent vasodilatation. Descent of the dicrotic notch on the arterial pulse waveform and a-to-b ratio (a/b; where a is the height of the pulse amplitude and b is the height of the dicrotic notch above the end-diastolic level) reflects vasodilator (increased a/b) and vasoconstrictor effects (decreased a/b) due to NO level change. Periodic acceleration (pG z) (motion of the supine body head to foot on a platform) provides systemic additional pulsatile shear stress. The purpose of this study was to determine whether or not pG z applied to rats produced endothelial-dependent vasodilatation and increased NO production, and whether the latter was regulated by the Akt/phosphatidylinositol 3-kinase (PI3K) pathway. Male rats were anesthetized and instrumented, and pG z was applied. Sodium nitroprusside, N G -nitro-L-arginine methyl ester (L-NAME), and wortmannin (WM; to block Akt/PI3K pathway) were administered to compare changes in a/b and mean aortic pressure. Descent of the dicrotic notch occurred within 2 s of initiating pG z. Dose-dependent increase of a/b and decrease of mean aortic pressure took place with SNP. L-NAME produced a dose-dependent rise in mean aortic pressure and decrease of a/b, which was blunted with pG z. In the presence of WM, pGz did not decrease aortic pressure or increase a/b. WM also abolished the pG z blunting effect on blood pressure and a/b of L-NAME-treated animals. eNOS expression was increased in aortic tissue after pG z. This study indicates that addition of low-amplitude pulses to circulation through pG z produces endothelial-dependent vasodilatation due to increased NO in rats, which is mediated via activation of eNOS, in part, by the Akt/PI3K pathway. vascular resistance; N G -nitro-L-arginine methyl ester, wortmannin; nitric oxide ADDED LOW-AMPLITUDE PULSES to the vasculature were generated with periodic acceleration (pG z ). pG z is produced by a motorized platform that repetitively moves the horizontally oriented body sinusoidally in a head to foot direction. Inertia of fluid as the body accelerates and decelerates adds a small-amplitude pulse to the circulation that is superimposed on the natural pulse, increasing pulsatile shear stress to the endothelium (3, 6, 7). In large-animal models, increased pulsatile shear stress activates endothelial nitric oxide (NO) synthase (eNOS) to release NO into the circulation, which, in turn, induces endothelial-dependent pulmonary and systemic vasodilatation, as well as increasing organ blood flows (3,5,6). pG z applied to anesthetized swine increases serum nitrite, which is ...

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Section: Discussionsupporting

confidence: 93%

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Uryash

Wu²,

Bassuk³

et al. 2009

Journal of Applied Physiology

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“…These findings could be explained by improvements in elevated right heart and renal vein pressures, which increase interstitial pressures that in turn decrease cross-sectional area of intrarenal vessels and diastolic flow. Improvements in renal function by LVADs appears to be mediated by several factors, including reductions in vascular resistance within the kidney from changes in renal venous pressure, RAAS, and sympathetic activity, as well as improvements in cardiac output (48,(71)(72)(73).…”

Section: Improvement Of Rd After Lvad Placementmentioning

confidence: 99%

Renal Failure in Patients with Left Ventricular Assist Devices

Patel

Adeseun

Ahmed

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryImplantable left ventricular assist devices (LVADs) are increasingly being used as a bridge to transplantation or as destination therapy in patients with end stage heart failure refractory to conventional medical therapy. A significant number of these patients have associated renal dysfunction before LVAD implantation, which may improve after LVAD placement due to enhanced perfusion. Other patients develop AKI after implantation. LVAD recipients who develop AKI requiring renal replacement therapy in the hospital or who ultimately require longterm outpatient hemodialysis therapy present management challenges with respect to hemodynamics, volume, and dialysis access. This review discusses the mechanics of a continuous-flow LVAD (the HeartMate II), the effects of continuous blood flow on the kidney, renal outcomes of patients after LVAD implantation, dialysis modality selection, vascular access, hemodynamic monitoring during the dialytic procedure, and other issues relevant to caring for these patients.

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“…43 Similarly, in vivo studies reported that pulsatile flow enhanced endothelium-derived NO release in peripheral vasculature. 16, 17 Taken together, attenuation of pulsatility in blood flow could be a reason for the deterioration in endothelial function after CF-LVAD implantation. Stimulation of inflammatory cascade after CF-LVAD implantation in HF patients has been reported in several previous studies.…”

Section: Possible Mechanismsmentioning

confidence: 99%

“…13 Nitric oxide (NO) is the principal endothelium-derived relaxing factor, and its reduced release may be one of the mechanisms responsible for increased systemic vascular resistance in the setting of non-pulsatile blood flow. 14- 17 In contrast, pulsatile blood flow enhances basal and stimulated release of endothelium-derived NO, resulting in reduced resistance. 16, 17 In HF patients supported by continuous flow (CF) LVAD, although symptoms are largely alleviated, endothelial function may be eft ventricular assist devices (LVAD) are increasingly implanted in patients with end-stage heart failure (HF) as a bridge to transplantation and as destination treatment.…”

mentioning

confidence: 99%

“…14- 17 In contrast, pulsatile blood flow enhances basal and stimulated release of endothelium-derived NO, resulting in reduced resistance. 16, 17 In HF patients supported by continuous flow (CF) LVAD, although symptoms are largely alleviated, endothelial function may be eft ventricular assist devices (LVAD) are increasingly implanted in patients with end-stage heart failure (HF) as a bridge to transplantation and as destination treatment. 1-3 Over the past few decades, much progress has been made in the development and refinement of LVAD.…”

mentioning

confidence: 99%

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Attenuation in Peripheral Endothelial Function After Continuous Flow Left Ventricular Assist Device Therapy Is Associated With Cardiovascular Adverse Events

Hasin¹,

Matsuzawa²,

Guddeti³

et al. 2015

Circ J

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Background:Patients with heart failure (HF) have abnormal endothelial function. Although use of a continuous flow left ventricular assist device (CF-LVAD) results in significant hemodynamic improvement, the effects on systemic endothelial function are unclear. Methods and Results:Eighteen HF patients with CF-LVAD implantation were included in this prospective observational study. We measured reactive hyperemia index (RHI) before and after CF-LVAD implantation to evaluate sequential changes in endothelial function. Patients were followed clinically for the occurrence of adverse cardiovascular events, a composite of death, thrombosis, bleeding, HF, renal failure, and arrhythmia. Preoperative RHI was 1.77±0.39. Early in the postoperative period (7-14 days after operation) RHI significantly decreased to 1.19±0.31 (P<0.001, compared with preoperative RHI). At first and second follow-up (4-6 weeks and 3-7 months after operation) RHI remained lower at 1.48±0.50 (P=0.030) and 1.26±0.37 (P=0.002), respectively, compared with preoperative RHI. The decrease in early postoperative RHI relative to preoperative RHI was significantly associated with adverse cardiovascular events after CF-LVAD (age-adjusted risk ratio for 0.25 decrease in RHI, 1.35; 95% confidence interval: 1.13-1.62, P=0.001). Conclusions:Peripheral endothelial function had a significant and persistent decline up to 5 months following implantation of CF-LVAD, and this decline was associated with adverse cardiovascular events. These findings may provide insight into some of the vascular complications following CF-LVAD in HF patients. (Circ J 2015; 79: 770 -777)

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Impacts of pulsatile systemic circulation on endothelium-derived nitric oxide release in anesthetized dogs

Cited by 40 publications

References 24 publications

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Renal Failure in Patients with Left Ventricular Assist Devices

Attenuation in Peripheral Endothelial Function After Continuous Flow Left Ventricular Assist Device Therapy Is Associated With Cardiovascular Adverse Events

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