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Flow Autoregulation (flow + autoregulation)

Distribution by Scientific Domains
Medical Sciences80%

Kinds of Flow Autoregulation

  • blood flow autoregulation
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    Selected Abstracts

    Nitric oxide, superoxide and renal blood flow autoregulation in SHR after perinatal L -arginine and antioxidants

    ACTA PHYSIOLOGICA, Issue 4 2007
    M. P. Koeners
    Abstract Aim:, Nitric oxide (NO) and superoxide are considered to be regulatory in renal blood flow (RBF) autoregulation, and hence may contribute to development of hypertension. To extend our previous observations that dynamic NO release is impaired in the spontaneously hypertensive rat (SHR) we investigated, firstly, if superoxide dependency of RBF autoregulation is increased in SHR and, secondly, if the beneficial effect of perinatal supplementation in SHR is partly as a result of early correction of RBF autoregulation. We hypothesized that perinatal supplementation by restoring dynamic NO release and/or decreasing superoxide dependency and would improve life-long blood pressure regulation. Methods:, Autoregulation was studied using stepwise reductions in renal perfusion pressure in anaesthetized male SHR, SHR perinatally supplemented with arginine and antioxidants (SHRsuppl) and Wistar-Kyoto (WKY), prior to and during i.v. N, -nitro- l -arginine (NO synthase inhibitor) or tempol (superoxide dismutase mimetic). Results:, Spontaneously hypertensive rat displayed a wider operating range of RBF autoregulation as compared with WKY (59 ± 4 vs. 33 ± 2 mmHg, respectively; P < 0.01). Perinatal supplementation in SHR decreased mean arterial pressure, renal vascular resistance and the operating range of RBF autoregulation (43 ± 3 mmHg; P < 0.01). In addition autoregulation efficiency decreased. RBF autoregulation characteristics shifted towards those of normotensive WKY. However, dynamic NO release was still impaired and no clear differences in superoxide dependency in RBF autoregulation between groups was observed. Conclusion:, Perinatal supplements shifted RBF autoregulation characteristics of SHR towards WKY, although capacity of the SHRsuppl kidney to modulate NO production to shear stress still seems impaired. The less strictly controlled RBF as observed in perinatally supplemented SHR could result in an improved long-term blood pressure control. This might partly underlie the beneficial effects of perinatal supplementation. [source]

    Regional cerebral blood flow autoregulation in patients with fulminant hepatic failure

    LIVER TRANSPLANTATION, Issue 6 2000
    Fin Stolze Larsen
    The absence of cerebral blood flow autoregulation in patients with fulminant hepatic failure (FHF) implies that changes in arterial pressure directly influence cerebral perfusion. It is assumed that dilatation of cerebral arterioles is responsible for the impaired autoregulation. Recently, frontal blood flow was reported to be lower compared with other brain regions, indicating greater arteriolar tone and perhaps preserved regional cerebral autoregulation. In patients with severe FHF (6 women, 1 man; median age, 46 years; range, 18 to 55 years), we tested the hypothesis that perfusion in the anterior cerebral artery would be less affected by an increase in mean arterial pressure compared with the brain area supplied by the middle cerebral artery. Relative changes in cerebral perfusion were determined by transcranial Doppler,measured mean flow velocity (Vmean), and resistance was determined by pulsatility index in the anterior and middle cerebral arteries. Cerebral autoregulation was evaluated by concomitant measurements of mean arterial pressure and Vmean in the anterior and middle cerebral arteries during norepinephrine infusion. Baseline Vmean was lower in the brain area supplied by the anterior cerebral artery compared with the middle cerebral artery (median, 47 cm/s; range, 21 to 62 cm/s v 70 cm/s; range 43 to 119 cm/s, respectively; P < .05). Also, vascular resistance determined by pulsatility index was greater in the anterior than middle cerebral artery (median, 1.02; range 1.00 to 1.37 v 0.87; range 0.75 to 1.48; P < .01). When arterial pressure was increased from 84 mm Hg (range 57 to 95 mm Hg) to 115 mm Hg (range, 73 to 130 mm Hg) during norepinephrine infusion, Vmean remained unchanged in 2 patients in the anterior cerebral artery, whereas it increased in the middle cerebral artery in all 7 patients. In the remaining patients, Vmean increased approximately 25% in both the anterior and middle cerebral arteries. Thus, this study could only partially confirm the hypothesis that autoregulation is preserved in the brain regions supplied by the anterior cerebral artery in patients with FHF. Although the findings of this small study need to be further evaluated, one should consider that autoregulation may be impaired not only in the brain region supplied by the middle cerebral artery, but also in the area corresponding to the anterior cerebral artery. [source]

    Ocular blood flow autoregulation and the clinical implications of its alteration

    ACTA OPHTHALMOLOGICA, Issue 2009
    G GARHOFER
    Autoregulation is commonly defined as the ability of a vascular bed to adapt blood flow to changes in ocular perfusion pressure (pressure autoregulation) or to adapt to changes in metabolic need (metabolic autoregulation). Considering the high metabolic turnover of the eye, its intact function is strongly dependent on a stable blood supply, assured by an intact vascular autoregulation. However, it has been shown that in the recent years that several ocular diseases such as glaucoma, diabetic retinopathy or age related macula degeneration are associated with an impaired autoregulation. This vascular dysregulation may lead to an under- or overperfusion of the tissue and in turn to ischemia and/or oxidative stress. This talk seeks to summarize our current knowledge of autoregulation in the ocular vascular beds. Furthermore, the possible reasons of impaired autoregulation and how this may relate to ocular pathologies will be discussed. [source]

    Hypertension, vascular cognitive disorders and neuroprotection

    ACTA NEUROPSYCHIATRICA, Issue 5 2007
    Dimiter Hadjiev
    Objective:, The role of the antihypertensive therapy in preventing vascular cognitive disorders in elderly persons without a history of stroke is a matter of debate. This review focuses on cognitive disorders in elderly hypertensive patients. Methods:, Relevant papers were identified by searches in PubMed from 1946 until February 2007 using the keywords ,cerebral blood flow autoregulation', ,vascular cognitive disorders', ,neuroimaging in hypertension', ,antihypertensive treatment' and ,neuroprotection in cerebral ischemia'. Results:, Excessive blood pressure lowering in patients with long-standing hypertension may increase the risk of cerebral hypoperfusion, white matter lesions and consequent cognitive decline. White matter lesions have been found in the majority of patients with long-standing hypertension. They correlate with vascular cognitive disorders, particularly impairments of attention and executive function, while memory is relatively preserved. Cerebral small vessel disease in elderly patients should be taken into account when antihypertensive treatment is considered. Renin,angiotensin blockade, some calcium channel blockers and statins are thought to possess neuroprotective action. Conclusion:, For prevention of cerebral hypoperfusion in elderly hypertensives blood pressure lowering should be cautiously controlled. The increased risk of white matter lesions is an indication for early neuroprotection. The combination of renin,angiotensin blockade or calcium channel blockers with statins may become a promising preventive strategy against cognitive decline in elderly hypertensives. Cerebral white matter protection is a future challenge. [source]