Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood

Martins, Albert N.; Newby, N; Doyle, Thomas F.; Kobrine, Arthur I.; Ramirez, Archimedes

doi:10.3171/jns.1976.44.3.0353

Cited by 4 publications

(2 citation statements)

References 21 publications

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“…Based on the abovementioned findings, inhibition of SN activity using α1 receptor antagonists and α2 receptor agonists to treat SAH has long been studied, and while some studies have shown favorable results (Bunc et al, 2003;Walter et al, 1982,) others have reported negative effects (Lambert et al, 2002;Martins et al, 1976;Toda et al, 1980) on SAH prognosis. A recent meta-analysis has revealed that β blocker can improve the post-SAH mortality rate, although other SAH-related complications remained unaffected (Ramesh et al, 2020).…”

Section: B R Ain Inj Ury In Hyper Acute Pha S E Involving the C S N Sys Tem In Sahmentioning

confidence: 99%

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Central sympathetic nerve activation in subarachnoid hemorrhage

Hasegawa

Uchikawa

Kajiwara

et al. 2021

Journal of Neurochemistry

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Subarachnoid hemorrhage (SAH) is a life-threatening condition, and although its two main complications-cerebral vasospasm (CVS)/delayed cerebral ischemia (DCI) and early brain injury (EBI)-have been widely studied, prognosis has not improved over time. The sympathetic nerve (SN) system is important for the regulation of cardiovascular function and is closely associated with cerebral vessels and the regulation of cerebral blood flow and cerebrovascular function; thus, excessive SN activation leads to a rapid breakdown of homeostasis in the brain. In the hyperacute phase, patients with SAH can experience possibly lethal conditions that are thought to be associated with SN activation (catecholamine surge)-related arrhythmia, neurogenic pulmonary edema, and irreversible injury to the hypothalamus and brainstem. Although the role of the SN system in SAH has long been investigated and considerable evidence has been collected, the exact pathophysiology remains undetermined, mainly because the relationships between the SN system and SAH are complicated, and many SNmodulating factors are involved. Thus, research concerning these relationships needs to explore novel findings that correlate with the relevant concepts based on past reliable evidence. Here, we explore the role of the central SN (CSN) system in SAH pathophysiology and provide a comprehensive review of the functional CSN network; brain injury in hyperacute phase involving the CSN system; pathophysiological overlap between the CSN system and the two major SAH complications, CVS/DCI and EBI; CSN-modulating factors; and SAH-related extracerebral organ injury. Further studies are warranted to determine the specific roles of the CSN system in the brain injuries associated with SAH.

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Section: B R Ain Inj Ury In Hyper Acute Pha S E Involving the C S N Sys Tem In Sahmentioning

confidence: 99%

“…In CVS/DCI of SAH, there have been conflicting results on the prognosis of using a single anti-adrenergic drug. Phentolamine, a non-selective α antagonist, was insufficient for reduction of vasoconstriction and reduced CBF without changing cerebrovascular resistance (Martins et al, 1976;Toda et al, 1980). However, Walter…”

Section: Cvs/dcimentioning

confidence: 99%

Central sympathetic nerve activation in subarachnoid hemorrhage

Hasegawa

Uchikawa

Kajiwara

et al. 2021

Journal of Neurochemistry

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Reversal of cerebral arterial spasm by intrathecal administration of a calcium antagonist (nimodipine)

et al. 1984

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Specific antagonists to the influx of calcium, necessary for the excitation-contraction coupling process in arterial smooth muscle, are potentially useful in the treatment of cerebral vasospasm but systemic hypotension might limit their clinical applicability. We studied the effect of the calcium antagonist nimodipine (BAY e 9736) on cerebral arterial spasm, intraventricular pressure and blood pressure (BP), when administered into the cerebral ventricles of the dog. Cerebral vasospasm was produced by the injection of autologous blood into the cisterna magna. In a group of 8 dogs, 100 micrograms of nimodipine was injected into the lateral ventricle. The effect of the drug on the basilar artery was monitored angiographically. Nimodipine always relieved spasm, and often the relaxation surpassed the resting vessel diameter. In a control group, the injection of placebo did not relax the spastic arteries. Determinations using gas chromatography of nimodipine in CSF and blood demonstrated that a concentration of 1 microgram/ml in cisternal CSF was sufficient to reduce spasm while concomitant plasma concentrations of 0.004 micrograms/ml did not result in significant BP reduction.

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Early effects of experimental arterial subarachnoid haemorrhage on the cerebral circulation part I: Experimental subarachnoid haemorrhage in cat and its pathophysiological effects methods of regional cerebral blood flow measurement and evaluation of microcirculation

Trojanowski

1984

Acta neurochir

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Studies of pathophysiological changes, regional cerebral blood flow (rCBF) and cerebral microcirculation were performed in cats subjected to arterial subarachnoid haemorrhage (SAH). An original method for SAH imitating aneurysm rupture was developed. The bleeding was induced by puncturing of the internal carotid artery approached tranpresphenoidally and followed by immediate closure of the skull opening. It was found, that arterial subarachnoid bleeding elevates intracranial pressure and results in a transitory fall in cerebral perfusion pressure which is not prevented by elevation of arterial blood pressure (Cushing reflex). A depression in brain electrical activity and respiration rate were present in the course of subarachnoid haemorrhage.

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Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood

Cited by 4 publications

References 21 publications

Central sympathetic nerve activation in subarachnoid hemorrhage

Central sympathetic nerve activation in subarachnoid hemorrhage

Reversal of cerebral arterial spasm by intrathecal administration of a calcium antagonist (nimodipine)

Early effects of experimental arterial subarachnoid haemorrhage on the cerebral circulation part I: Experimental subarachnoid haemorrhage in cat and its pathophysiological effects methods of regional cerebral blood flow measurement and evaluation of microcirculation

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