Changes in middle cerebral artery blood velocity in uremic patients after hemodialysis.

Postiglione, Alfredo; Faccenda, F.; Gallotta, Giovanni; Rubba, P.; Federico, Stefano

doi:10.1161/01.str.22.12.1508

Cited by 53 publications

(42 citation statements)

References 29 publications

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“…Indeed, a significant reduction in the middle cerebral artery and basilar blood flow velocity has been observed in uremic patients on dialysis. 48,49 Thus, the results of the present experiments further support the hypothesis that guanidino compounds should be considered as possible uremic toxins that may play a primary role in the cerebrovascular and neurological disorders observed in uremia. …”

supporting

confidence: 83%

Effects of Some Guanidino Compounds on Human Cerebral Arteries

Segarra

Medina

Ballester

et al. 1999

Stroke

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Background and Purpose-Accumulation of endogenous guanidino-substituted analogues of L-arginine in chronic renal failure might contribute to some of the vascular and neurological disorders of this pathology. We tested the hypothesis that in human cerebral arteries, some guanidino compounds may increase vascular tone, through nitric oxide (NO) synthase inhibition, and impair endothelium-dependent relaxation. Methods-Rings of human middle cerebral artery were obtained during autopsy of 26 patients who had died 3 to 12 hours before. The rings were suspended in organ baths for isometric recording of tension. We then studied the responses to N G -monomethyl-L-arginine (L-NMMA), N G ,N G -dimethyl-L-arginine (asymmetrical dimethylarginine; ADMA), aminoguanidine (AG), and methylguanidine (MG). Results-L-NMMA (10Ϫ6 to 3ϫ10 Ϫ4 mol/L) and ADMA (10 Ϫ6 to 3ϫ10 Ϫ4 mol/L) caused concentration-and endothelium-dependent contractions (median effective concentrations [EC 50 ]ϭ1.1ϫ10Ϫ5 and 1.6ϫ10 Ϫ5 mol/L, respectively; E max ϭ35.5Ϯ7.9% and 43.9Ϯ5.9% of the response to 100 mmol/L KCl). AG (10 Ϫ5 to 3ϫ10 Ϫ3 mol/L) and MG (10 Ϫ5 to 3ϫ10 Ϫ3 mol/L) produced endothelium-independent contractions (E max ϭ44.3Ϯ8.8% and 45.7Ϯ5.8% of the response to 100 mmol/L KCl, respectively). L-Arginine (10 Ϫ3 mol/L) prevented the contractions by L-NMMA and ADMA but did not change contractions induced by AG and MG. L-NMMA and ADMA inhibited endothelium-dependent relaxation induced by acetylcholine in a concentration-dependent manner; AG and MG were without effect. Conclusions-The results suggest that the contractions induced by L-NMMA and ADMA are due to inhibition of endothelial NO synthase activity, whereas AG and MG do not affect the synthesis of NO. An increase in the plasma concentration of L-NMMA and ADMA associated with uremia is likely to represent a diminished release or effect of NO, and consequently, an increased cerebrovascular tone in uremic patients is highly conceivable. (Stroke. 1999;30:2206-2211.)Key Words: cerebral arteries Ⅲ endothelium Ⅲ nitric oxide N itric oxide (NO) synthesized from L-arginine accounts for the powerful vasodilator effects of endotheliumderived relaxing factor 1,2 and consequently plays a decisive role in determining vasomotor tone in several vascular beds, including the cerebral circulation. [3][4][5][6][7] The synthesis of NO can be specifically and competitively antagonized by arginine analogues such as N G -monomethyl-L-arginine (L-NMMA). 4,8 Histochemical studies have demonstrated the presence of NO synthase immunoreactivity in the adventitia of rat and human cerebral arteries. 9,10 Consistent with these observations, several reports have shown that NO from perivascular nerve endings mediates dilatation in the cerebral arteries through a nonadrenergic, noncholinergic mechanism, 11-13 whereas NO of endothelial origin can modulate contractile responses of isolated human cerebral arteries to sympathetic stimulation. 6 Uremia is an established risk factor for cardiovascular disease and cerebrovascular acciden...

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supporting

confidence: 83%

Effects of Some Guanidino Compounds on Human Cerebral Arteries

Segarra

Medina

Ballester

et al. 1999

Stroke

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“…Significant decreases in cerebral perfusion and blood flow velocity after dialysis compared with before the session have been documented using Xenon inhalation scans of cerebral circulation (75) and transcranial Doppler ultrasound of the carotid, basilar, and middle cerebral arteries (76)(77)(78). Positron emission tomography (PET) scans also show decreased cerebral oxygen metabolism and regional blood flow in hemodialysis patients; cerebral blood flow in the frontal lobes and white matter is inversely related to dialysis vintage (79).…”

Section: The Dialysis Process and Cognitive Impairmentmentioning

confidence: 99%

“…The acute fluid shifts and intravascular volume loss that occur during dialysis induce cerebral edema and decreased intra-cerebral blood pressure, blood velocity and cerebral perfusion (76)(77)(78). If these hemodynamic factors increase the risk of recurrent transient ischemic accident and stroke, that risk may rise with the dialysis dose (Kt/V).…”

Section: The Dialysis Process and Cognitive Impairmentmentioning

confidence: 99%

Cognitive Impairment in the Aging Dialysis and Chronic Kidney Disease Populations: An Occult Burden

Murray

2008

Advances in Chronic Kidney Disease

348

241

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The heavy burden of cognitive impairment in hemodialysis and chronic kidney disease patients has only recently become recognized. Up to 70 percent of hemodialysis patients ages 55 years and older have moderate to severe chronic cognitive impairment, yet it is largely undiagnosed. Recent studies describe the strong graded relation between estimated glomerular filtration rate (eGFR) and cognitive function in CKD patients. The process of conventional hemodialysis may induce recurrent episodes of acute cerebral ischemia, which in turn may contribute to acute decline in cognitive function during dialysis. Thus the worst time to communicate with dialysis patients may be during the hemodialysis session. Both symptomatic and occult, subclinical ischemic cerebrovascular disease appear to play a large role in a proposed model of accelerated vascular cognitive impairment in these populations. Severe cognitive impairment or dementia among hemodialysis patients is associated with an approximately two-fold increased risk of both mortality and dialysis withdrawal. Pre-dialysis cognitive screening and adding dementia to the list of comorbidities on Form 2728 would provide critical information regarding the benefit versus risks of receiving dialysis. It could also improve quality of care and outcomes by raising clinician's awareness of the potential effects of cognitive impairment on medication, fluid, and dietary compliance, and ability to make advance directive decisions among dialysis patients. While much remains to be learned regarding the pathophysiology of cognitive impairment in kidney disease, the public health implications of this substantial burden are immediate.

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“…9 Different hemodynamic disturbances have been reported in patients with CKD. 10,11 Nevertheless, it is not clear whether impaired kidney function is associated with lower cerebral blood flow in the general population. Therefore, we aimed to investigate the association between different measures of kidney function and cerebral blood flow in a population-based cohort of individuals 45 years old and older.…”

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confidence: 99%

Kidney Function and Cerebral Blood Flow

Sedaghat¹,

Vernooij

Loehrer³

et al. 2016

Journal of the American Society of Nephrology

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CKD is linked with various brain disorders. Whereas brain integrity is dependent on cerebral perfusion, the association between kidney function and cerebral blood flow has yet to be determined. This study was performed in the framework of the population-based Rotterdam Study and included 2645 participants with mean age of 56.6 years (45% men). We used eGFR and albumin-to-creatinine ratio to assess kidney function and performed phase-contrast magnetic resonance imaging of basilar and carotid arteries to measure cerebral blood flow. Participants had an average (SD) eGFR of 86.3 (13.4) ml/min per 1.73 m 2 and a median (interquartile range) albumin-to-creatinine ratio of 3.4 (2.2-6.1) mg/g.In age-and sex-adjusted models, a higher albumin-to-creatinine ratio was associated with lower cerebral blood flow level (difference in cerebral blood flow [milliliters per minute per 100 ml] per doubling of the albumin-to-creatinine ratio, 20.31; 95% confidence interval, 20.58 to 20.03). The association was not present after adjustment for cardiovascular risk factors (P=0.10). Each 1 SD lower eGFR was associated with 0.42 ml/min per 100 ml lower cerebral blood flow (95% confidence interval, 0.01 to 0.83) adjusted for cardiovascular risk factors. Thus, in this population-based study, we observed that lower eGFR is independently associated with lower cerebral blood flow.

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Changes in middle cerebral artery blood velocity in uremic patients after hemodialysis.

Cited by 53 publications

References 29 publications

Effects of Some Guanidino Compounds on Human Cerebral Arteries

Effects of Some Guanidino Compounds on Human Cerebral Arteries

Cognitive Impairment in the Aging Dialysis and Chronic Kidney Disease Populations: An Occult Burden

Kidney Function and Cerebral Blood Flow

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