Neurovascular Coupling in Pregnancy and the Risk of Preeclampsia

Janzarik, Wibke G.; Ehmann, Renata; Ehlers, Elena; Allignol, Arthur; Mayer, Sebastian; Gabriel, Boris; Weiller, Cornelius; Prömpeler, H; Reinhard, Matthias

doi:10.1161/strokeaha.114.006272

Cited by 4 publications

(4 citation statements)

References 9 publications

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“…23 Abnormal functional hyperemia was not predictive of PE, as there was no association between changes in neurovascular coupling at 25–28 weeks of gestation and the occurrence of PE. 38 This finding suggests a potential causative role of PE in impaired functional hyperemia. It is possible that similar mechanisms underlie the impaired seizure-induced hyperemic response measured in the current study in experimental PE.…”

Section: Discussionmentioning

confidence: 89%

Altered hippocampal arteriole structure and function in a rat model of preeclampsia: Potential role in impaired seizure-induced hyperemia

Johnson

Cipolla

2016

J Cereb Blood Flow Metab

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We investigated the effect of experimental preeclampsia on hyperemia during seizure in the hippocampus and vascular function and structure of hippocampal arterioles using Sprague Dawley rats (n = 14/group) that were nonpregnant, pregnant (d20), or had experimental preeclampsia (induced by a high cholesterol diet d7-20). Hyperemia was measured via hydrogen clearance basally and during pentylenetetrazol-induced seizure (40-130 mg/kg i.v.). Reactivity of isolated and pressurized hippocampal arterioles to KCl, nitric oxide synthase inhibition with NG-nitro-L-arginine methyl ester and the nitric oxide donor sodium nitroprusside were investigated. Capillary density was quantified via immunohistochemistry. Cerebral blood flow increased during seizure vs. baseline in pregnant (118 ± 14 vs. 87 ± 9 mL/100 g/min; p < 0.05) and nonpregnant rats (106 ± 9 vs. 82 ± 9 mL/100 g/min; p < 0.05) but was unchanged in preeclamptic rats (79 ± 16 vs. 91 ± 4 mL/100 g/min; p > 0.05), suggesting impaired seizure-induced hyperemia in preeclampsia. Hippocampal arterioles from preeclamptic rats had less basal tone, and dilated less to 15 mM KCl (9 ± 8%) vs. pregnant (61 ± 27%) and nonpregnant rats (20 ± 11%). L-NAME had no effect on hippocampal arterioles in any group, but dilation to sodium nitroprusside was similar. Structurally, hippocampal arterioles from preeclamptic rats underwent inward hypotrophic remodeling and capillary rarefaction. Impaired seizure-induced hyperemia, vascular dysfunction, and limited vasodilatory reserve of hippocampal arterioles could potentiate hippocampal injury in preeclampsia especially during eclampsia.

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Section: Discussionmentioning

confidence: 89%

Altered hippocampal arteriole structure and function in a rat model of preeclampsia: Potential role in impaired seizure-induced hyperemia

Johnson

Cipolla

2016

J Cereb Blood Flow Metab

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“…Our present understanding of neurovascular coupling in humans is limited, and the available knowledge is generated from a small number of laboratories, using a variety of unstandardized assessments. [52][53][54][55][56][57][58][59][60][61][62][63] Although there is mechanistic insight provided by the isolated preparations of neurovascular coupling, 41 little is known about which mechanisms are sufficient versus necessary for a functional and effective neurovascular coupling response in humans. The available literature related to this topic is reviewed below.…”

Section: Human Neurovascular Couplingmentioning

confidence: 99%

Neurovascular coupling in humans: Physiology, methodological advances and clinical implications

Phillips

Chan

Zheng

et al. 2015

J Cereb Blood Flow Metab

341

364

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Neurovascular coupling reflects the close temporal and regional linkage between neural activity and cerebral blood flow. Although providing mechanistic insight, our understanding of neurovascular coupling is largely limited to nonphysiological ex vivo preparations and non-human models using sedatives/anesthetics with confounding cerebrovascular implications. Herein, with particular focus on humans, we review the present mechanistic understanding of neurovascular coupling and highlight current approaches to assess these responses and the application in health and disease. Moreover, we present new guidelines for standardizing the assessment of neurovascular coupling in humans. To improve the reliability of measurement and related interpretation, the utility of new automated software for neurovascular coupling is demonstrated, which provides the capacity for coalescing repetitive trials and time intervals into single contours and extracting numerous metrics (e.g., conductance and pulsatility, critical closing pressure, etc.) according to patterns of interest (e.g., peak/minimum response, time of response, etc.). This versatile software also permits the normalization of neurovascular coupling metrics to dynamic changes in arterial blood gases, potentially influencing the hyperemic response. It is hoped that these guidelines, combined with the newly developed and openly available software, will help to propel the understanding of neurovascular coupling in humans and also lead to improved clinical management of this critical physiological function.

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“…44 Studies utilizing a visual stimulation task and transcranial Doppler to assess neurovascular coupling in women with PE reported impaired coupling of blood flow and neuronal activity six years after the index pregnancy that was not present mid-gestation prior to PE onset. 44, 45 These findings suggest that cerebrovascular function is intact prior to development of PE, and that cerebrovascular dysfunction is a consequence of PE that may progress over time after the index pregnancy. 44 Although the findings of the current study support that PE exerts deleterious effects on cerebrovasculature function during the index pregnancy, a limitation is that WM integrity and cognitive function were not measured.…”

Section: Discussionmentioning

confidence: 88%

Impaired function of cerebral parenchymal arterioles in experimental preeclampsia

Johnson

Cipolla

2018

Microvascular Research

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Preeclampsia (PE), a dangerous hypertensive complication of pregnancy, is associated with widespread maternal vascular dysfunction. However, the effect of PE on the cerebral vasculature that can lead to stroke and cognitive decline is not well understood. We hypothesized that function of cortical parenchymal arterioles (PAs) would be impaired during PE. Using a high cholesterol diet to induce experimental PE in rats (ePE), we studied the function and structure of isolated and pressurized PAs supplying frontoparietal white matter (WM) tracts and cortex and compared to normal pregnant (Preg) and nonpregnant (Nonpreg) Sprague Dawley rats (n = 8/group). Myogenic reactivity and tone were similar between groups; however, constriction to intermediate-conductance calcium-activated potassium (IK) channel inhibition was diminished and dilation to inward-rectifying K (K) channel activation was impaired in PAs from ePE rats, suggesting altered ion channel function. Conducted vasodilation was significantly delayed in response to 12 mM KCl, but not 10 μM adenosine, in PAs from ePE rats versus Preg and Nonpreg rats (940 ± 300 ms vs. 70 ± 50 ms and 370 ± 90 ms; p < 0.05). Overall, dysfunction of PAs supplying frontoparietal WM and gray matter was present in ePE. If persistent these changes could potentiate neuronal injury that over time could contribute to WM lesions and early-onset cognitive decline.

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Neurovascular Coupling in Pregnancy and the Risk of Preeclampsia

Abstract: Neurovascular coupling was altered in women with impaired uteroplacentar vasoregulation but not a significant predictor of preeclampsia.

Cited by 4 publications

References 9 publications

Altered hippocampal arteriole structure and function in a rat model of preeclampsia: Potential role in impaired seizure-induced hyperemia

Altered hippocampal arteriole structure and function in a rat model of preeclampsia: Potential role in impaired seizure-induced hyperemia

Neurovascular coupling in humans: Physiology, methodological advances and clinical implications

Impaired function of cerebral parenchymal arterioles in experimental preeclampsia

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