Measurement of nitric oxide in the rat cerebral cortex during hypercapnoea

Harada, Mikiko; Fuse, Akihisa; Tanaka, Yoshifumi

doi:10.1097/00001756-199703030-00036

Cited by 20 publications

(13 citation statements)

References 14 publications

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“…On the other hand, the blood flow response to hypercapnia was observed in endothelium-damaged arteries of rats (Wang et al, 1994a) and eNOS-knockout mice (Ma et al, 1996b), suggesting that NO derived from nNOS plays a crucial role in the response. The view has been supported by experiments with a relatively selective nNOS inhibitor, 7-nitroindazole (Harada et al, 1997;Okamoto et al, 1997).…”

Section: Pharmacology Of Neurogenic No In Blood Vesselmentioning

confidence: 97%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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Section: Pharmacology Of Neurogenic No In Blood Vesselmentioning

confidence: 97%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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“…The cellular sources of NO during hypercapnia remain to be established but some evidences suggest a role for nNOS-derived NO in vascular responses to hypercapnia. Hypercapnia increases nNOS-derived NO in rat brain (Harada et al, 1997). Administration of 7-NI reduces the vasodilator and CBF responses to hypercapnia in anesthetized rats, suggesting that NO synthesized by nNOS participates in hypercapnic hyperemia (Wang et al, 1995; Okamoto et al, 1997).…”

Section: Neurally-derived Nitric Oxide and Cerebrovascular Regulationmentioning

confidence: 99%

The complex contribution of NOS interneurons in the physiology of cerebrovascular regulation

Duchemin

Boily

Sadekova

et al. 2012

Front. Neural Circuits

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Following the discovery of the vasorelaxant properties of nitric oxide (NO) by Furchgott and Ignarro, the finding by Bredt and coll. of a constitutively expressed NO synthase in neurons (nNOS) led to the presumption that neuronal NO may control cerebrovascular functions. Consequently, numerous studies have sought to determine whether neuraly-derived NO is involved in the regulation of cerebral blood flow (CBF). Anatomically, axons, dendrites, or somata of NO neurons have been found to contact the basement membrane of blood vessels or perivascular astrocytes in all segments of the cortical microcirculation. Functionally, various experimental approaches support a role of neuronal NO in the maintenance of resting CBF as well as in the vascular response to neuronal activity. Since decades, it has been assumed that neuronal NO simply diffuses to the local blood vessels and produce vasodilation through a cGMP-PKG dependent mechanism. However, NO is not the sole mediator of vasodilation in the cerebral microcirculation and is known to interact with a myriad of signaling pathways also involved in vascular control. In addition, cerebrovascular regulation is the result of a complex orchestration between all components of the neurovascular unit (i.e., neuronal, glial, and vascular cells) also known to produce NO. In this review article, the role of NO interneuron in the regulation of cortical microcirculation will be discussed in the context of the neurovascular unit.

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“…It could be that NO and CBF are better linked when modulated by CO 2 , as CO 2 reactivity is exclusively mediated by neuronal NO synthase [10,21]. Hypercapnia increases the NO concentration and hyperventilation decreases it [24]. In the present study the pCO 2 levels were kept in a normal range to exclude these effects.…”

Section: Discussionmentioning

confidence: 92%

Nitric Oxide Synthesis Inhibition during Cerebral Hypoxemia and Reoxygenation with 100% Oxygen in Newborn Pigs

Kutzsche¹,

Solås

Lyberg³

et al. 2002

Neonatology

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The objective of our study was to evaluate the effects of N_σ-nitro-L-arginine methyl ester (L-NAME), an inhibitor of the nitric oxide (NO) pathway, on cerebral microcirculation during hypoxemia and reoxygenation with 100% oxygen in newborn pigs. Twenty-two pigs were randomized to hypoxemia [inspired fraction of oxygen (FIO₂) 0.08; 20 min] and reoxygenation (FIO₂ 1.0; 60 min) or normoxia. The hypoxemic animals were further randomized to receive either an intravenous bolus injection of 5 mg/kg L-NAME (n = 8) or a corresponding volume of isotonic saline (n = 8) 30 min before the onset of hypoxemia. The normoxemic group (n = 6) received the same pretreatment with L-NAME. Cerebral hemodynamics were assessed by laser Doppler flowmetry and intracranial pressure monitoring. The cerebral NO concentration was continuously measured using an electrochemical sensor. Pretreatment with L-NAME resulted in a more severe systemic hypotension and reduced cerebral microcirculation during the period of hypoxemia compared with the saline/hypoxemia group. NO synthesis inhibition during reoxygenation with 100% oxygen, however, blunted the increase in NO concentration (p < 0.05) without reduction of cerebral blood flow and cerebral perfusion pressure. In conclusion, in this newborn pig model, pretreatment with a bolus infusion of L-NAME induced severe hypotension and reduced cerebral microcirculation during hypoxemia. However, it appears to have no significant adverse effect on cerebral hemodynamics during the period of reoxygenation with 100% oxygen. This deleterious effect during hypoxemia limits the use of L-NAME as a preventive drug but suggests beneficial effects during reoxygenation with 100% oxygen.

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Measurement of nitric oxide in the rat cerebral cortex during hypercapnoea

Cited by 20 publications

References 14 publications

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

The complex contribution of NOS interneurons in the physiology of cerebrovascular regulation

Nitric Oxide Synthesis Inhibition during Cerebral Hypoxemia and Reoxygenation with 100% Oxygen in Newborn Pigs

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