Hormonal Dependence of the Effects of Metabolic Encephalopathy on Cerebral Perfusion and Oxygen Utilization in the Rat

Koźniewska, Ewa; Roberts, Timothy P. L.; Vexler, Zinaida S.; Osęka, Maciej; Kucharczyk, John; Arieff, Allen I.

doi:10.1161/01.res.76.4.551

Cited by 23 publications

(17 citation statements)

References 36 publications

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“…Furthermore, ovariectomy with or without estrogen administration had no effect on these cerebrovascular responses. These findings are in agreement with previous reports that resting CBF and the increase in CBF produced by ACh or neural activity do not differ in male, female or OVX rodents (1,14,21,39). Similarly, no differences in resting CBF were observed in different estrous states (3).…”

Section: Effect Of Ovariectomy and Estrogen Administration On Cerebrosupporting

confidence: 93%

The neurovascular dysfunction induced by angiotensin II in the mouse neocortex is sexually dimorphic

Girouard

Lessard²,

Capone³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Women are less susceptible to the cerebrovascular complications of hypertension, such as a stroke and vascular dementia. The mechanism of such protection may be related to a reduced vulnerability of women to the cerebrovascular actions of hypertension. To test this hypothesis, we used a model of hypertension based on infusion of angiotensin II (ANG II), an octapeptide that plays a key role in hypertension and produces cerebrovascular dysregulation. Cerebral blood flow (CBF) was monitored by laser-Doppler flowmetry in anesthetized (urethane-chloralose) C57BL/6J male and female mice equipped with a cranial window. ANG II administration (0.25 mug.kg(-1).min(-1) iv x 30-45 min) elevated arterial pressure equally in both sexes but attenuated the CBF increase induced by whisker stimulation or by the endothelium-dependent vasodilator acetylcholine (ACh) in male but not in female mice. The administration of ANG II for 7 days (2.74 mg.kg(-1).day(-1)), using osmotic minipumps, also attenuated these cerebrovascular responses in male, but not female, mice. The reduced susceptibility to the effect of ANG II in female mice was abolished by ovariectomy and reinstated by estrogen administration to ovariectomized mice. Administration of estrogen to male mice abolished the ANG II-induced attenuation of CBF responses. We conclude that female mice are less susceptible to the cerebrovascular dysregulation induced by ANG II, an effect related to estrogen. Such protection from the deleterious cerebrovascular effects of hypertension may play a role in the reduced vulnerability to the cerebrovascular complications of hypertension observed in women.

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Section: Effect Of Ovariectomy and Estrogen Administration On Cerebrosupporting

confidence: 93%

The neurovascular dysfunction induced by angiotensin II in the mouse neocortex is sexually dimorphic

Girouard

Lessard²,

Capone³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…The main hormones involved in the regulation of water-electrolyte balance -antidiuretic hormone and natriuretic peptide, one of which is used to induce experimental hyponatremia in vivo [15,33] are vasoactive [30,37]. Their presence would complicate the interpretation of the data.…”

Section: Discussionmentioning

confidence: 99%

Original article Disturbed regulation of the isolated middle cerebral artery in acute hyponatremia

Aleksandrowicz¹,

Koźniewska²

2013

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A b s t r a c t Hyponatremia is a common disorder of water-electrolyte balance characterized by the decrease of plasma sodium ions concentration below 135 mM. Although water-electrolyte balance is regulated by a kidney, symptoms of hyponatremia are related to the disturbances of intracranial homeostasis and are attributed to brain swelling. Despite the importance of blood vessels function for the homeostasis of the brain, little is known about the influence of hyponatremia on cerebrovascular regulation. In the present study isolated, perfused and pressurized rat middle cerebral arteries (MCAs) were subjected to hyponatremia in the organ chamber by lowering the concentration of sodium ions from 145 to 121 mM. The response of the MCAs to the changes in intravascular pressure and to endothelium-dependent and independent vasodilators was compared in normo-and hyponatremia. The following results were obtained: the contraction of the MCA during progressive increases in intravascular pressure was similar in normo-and hyponatremia; the dilation in response to acetylcholine (10 -6 M, 10 -5 M and 10 -4 M), which is endothelium-and nitric oxide-dependent, was severely impaired in hyponatremia; the contraction after administration of the nonselective inhibitor of nitric oxide synthesis -NG-nitro-L-arginine methyl ester (L-NAME, 10 -5 M) was similar in normo-and hyponatremia; the nitric oxide donor -S-nitroso-N-acetylpenicillamine (SNAP,

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“…In addition the major importance of hyponatremia should be noted [69]. In rat experiments producing acute and chronic hyponatremia it could be proven that age, gender and the cerebral effects of vasopressin were major determinants of mortality in this type of experimental metabolic encephalopathy [70,71]. Chronic symptomatic hyponatremia of postmenopausal women can be assosiated with major morbidity and mortality.…”

Section: S Septic Encephalopathymentioning

confidence: 99%

Metabolic encephalopathies

Kunze¹

2002

Journal of Neurology

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Metabolic encephalopathies, usually multifactorial in origin, may be important complications of many diseases of patients treated in a critical care unit. In many cases these complications arise from more than one cause. Neurological signs of metabolic encephalopathies, ancillary tests and differential diagnosis, etiology and pathophysiology are discussed. In this context major single causes for metabolic encephalopathies are referred to. Metabolic encephalopathies as diseases per se (e. g. Wernicke's encephalopathy) and encephalopathies as consequences of deteriorating known diseases (e. g. renal or hepatic diseases) and encephalopathies as complications in patients treated with other diseases in the ICU have to be differentiated. Encephalopathies are known to be the most common complication of a large group of diseases treated in the ICU; on the other hand, manifestation of metabolic encephalopathy can be taken as a warning of deterioration or beginning organ dysfunction. So it would be misleading so far to reduce the clinical concept of metabolic encephalopathies in ICH to septic encephalopathy only.

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Hormonal Dependence of the Effects of Metabolic Encephalopathy on Cerebral Perfusion and Oxygen Utilization in the Rat

Cited by 23 publications

References 36 publications

The neurovascular dysfunction induced by angiotensin II in the mouse neocortex is sexually dimorphic

The neurovascular dysfunction induced by angiotensin II in the mouse neocortex is sexually dimorphic

Original article Disturbed regulation of the isolated middle cerebral artery in acute hyponatremia

Metabolic encephalopathies

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