Increased cerebral blood flow but no reversal or prevention of vasospasm in response to l-arginine infusion after subarachnoid hemorrhage

Pluta, Ryszard; Afshar, John K. B.; Thompson, B. Gregory; Boock, Robert J.; Harvey−White, Judith; Oldfield, Edward H.

doi:10.3171/jns.2000.92.1.0121

Cited by 40 publications

(26 citation statements)

References 64 publications

(112 reference statements)

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“…Cerebral blood flow measurements in rabbits revealed resolution of vasospasm after SAH with short-term intracisternal and intracarotid L-arginine infusion (Ozü m et al, 2007). On the other hand, in cynomolgus monkeys, brief intracarotid and continuous intravenous infusion of L-arginine did not influence the incidence or degree of 84 cerebral vasospasm after SAH (Pluta et al, 2000). Whether the discrepancy in effectiveness of L-arginine is due to differences in animal species, route of drug administration, or dosage has not been determined.…”

Section: Therapeutic Measures In Animalsmentioning

confidence: 92%

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Toda

Ayajiki²,

Okamura³

2009

Pharmacol Rev

336

248

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Section: Therapeutic Measures In Animalsmentioning

confidence: 92%

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Toda

Ayajiki²,

Okamura³

2009

Pharmacol Rev

336

248

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“…7 Similarly, IA infusion of L-arginine has been shown to markedly increase CBF in a primate model of SAH, despite the lack of any angiographic changes. 20 Changes in perfusion at the microvasculature level probably account for this clinicoangiographic dissociation. Therefore, assessment of cerebral perfusion as opposed to angiographic results alone should be considered when evaluating novel therapies for vasospasm.…”

Section: Discussionmentioning

confidence: 99%

Intra-Arterial Nicardipine Infusion Improves CT Perfusion–Measured Cerebral Blood Flow in Patients with Subarachnoid Hemorrhage–Induced Vasospasm

Nogueira¹,

Lev²,

Roccatagliata³

et al. 2008

AJNR Am J Neuroradiol

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“…Infusion of the NO precursor L-arginine or NO donors were shown to increase CBF after experimental stroke 52,53 ; however, so far, none of these promising approaches could be translated into the clinic because of various reasons. 54 Some approaches impaired the endogenous NO production, 55 whereas others lacked a clinically feasible mode of administration 56 or, most importantly, caused significant reduction of systemic blood pressure, eg, L-arginine infusion. 57 As compared to previous attempts that tried to utilize NO-based strategies for the treatment of tissue ischemia, the main advantages of iNO are its specific effect on hypoperfused tissue without any effect on systemic blood pressure, its immediate action, simple and well-investigated route of administration, its efficacy across species, and its excellent safety profile that is based on the use of iNO in several thousand patients with pulmonary disorders.…”

Section: Discussionmentioning

confidence: 99%

Inhalation of Nitric Oxide Prevents Ischemic Brain Damage in Experimental Stroke by Selective Dilatation of Collateral Arterioles

Terpolilli

Kim

Thal

et al. 2012

Circulation Research

176

134

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Rationale: Stroke is the third most common cause of death in industrialized countries. The main therapeutic target is the ischemic penumbra, potentially salvageable brain tissue that dies within the first few hours after blood flow cessation. Hence, strategies to keep the penumbra alive until reperfusion occurs are needed.Objective: To study the effect of inhaled nitric oxide on cerebral vessels and cerebral perfusion under physiological conditions and in different models of cerebral ischemia. Methods and Results:This experimental study demonstrates that inhaled nitric oxide (applied in 30% oxygen/70% air mixture) leads to the formation of nitric oxide carriers in blood that distribute throughout the body. This was ascertained by in vivo microscopy in adult mice. Although under normal conditions inhaled nitric oxide does not affect cerebral blood flow, after experimental cerebral ischemia induced by transient middle cerebral artery occlusion it selectively dilates arterioles in the ischemic penumbra, thereby increasing collateral blood flow and significantly reducing ischemic brain damage. This translates into significantly improved neurological outcome. These findings were validated in independent laboratories using two different mouse models of cerebral ischemia and in a clinically relevant large animal model of stroke. Key Words: collateral blood flow Ⅲ ischemic penumbra Ⅲ ischemic stroke Ⅲ nitric oxide inhalation E very year stroke is responsible for the death of 5.5 million people. 1 Despite its high incidence and mortality, clinical therapeutic options are still limited. 2 Research efforts to find novel treatment strategies focus primarily on rescuing the ischemic penumbra, the viable tissue surrounding the nonviable infarct core. In the penumbra, blood flow is critically reduced but still suffices to sustain neuronal integrity for several hours. The delayed nature of cell death in the penumbra leaves a unique window of opportunity for therapeutic interventions. If adequate cerebral perfusion is re-established sufficiently fast, then penumbral tissue can be effectively saved. 3 Therefore, penumbral reperfusion at the earliest possible time is the most critical factor in determining neurological outcome and in preventing mortality after stroke. 4 Conclusions:

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Increased cerebral blood flow but no reversal or prevention of vasospasm in response to l-arginine infusion after subarachnoid hemorrhage

Cited by 40 publications

References 64 publications

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Intra-Arterial Nicardipine Infusion Improves CT Perfusion–Measured Cerebral Blood Flow in Patients with Subarachnoid Hemorrhage–Induced Vasospasm

Inhalation of Nitric Oxide Prevents Ischemic Brain Damage in Experimental Stroke by Selective Dilatation of Collateral Arterioles

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