The effect on the development of cerebral vasospasm in the rat of lesioning of the peripheral and central catecholamine systems

Na, Svendgaard; Brismar, J.; Tj, Delgado; Nh, Diemer

doi:10.1080/01616412.1985.11739697

Cited by 25 publications

(7 citation statements)

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“…Different mechanisms may underlie the 2 processes, 4 and a great variety have been implicated. [5][6][7][8][9][10][11] Recently we have shown that acute vasoconstriction is associated with decreased cerebral blood flow (CBF), ischemic glutamate release, and premature mortality after experimental SAH. 12 If acute vasoconstriction could be pharmacologically attenuated, then SAH-induced brain injury could potentially be reduced.…”

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confidence: 99%

Effects of S -Nitrosoglutathione on Acute Vasoconstriction and Glutamate Release After Subarachnoid Hemorrhage

Sehba

Ding

Chereshnev

et al. 1999

Stroke

101

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Background and Purpose-Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH. Methods-SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 mol/L/kg, nϭ31) or saline (nϭ21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 mol/L/kg, nϭ5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically. Results-GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6Ϯ26.6% versus saline 37. Key Words: cerebral blood flow Ⅲ glutamates Ⅲ nitric oxide Ⅲ subarachnoid hemorrhage Ⅲ vasoconstriction C erebral arteries respond to subarachnoid hemorrhage (SAH) with a biphasic contraction that begins minutes after the bleed and delayed vasospasm more than 48 hours later. 1-3 Although a great deal is known about the mechanisms and management of delayed vasospasm, less is known about the physiology, treatment, and importance of acute vasoconstriction. Different mechanisms may underlie the 2 processes, 4 and a great variety have been implicated. [5][6][7][8][9][10][11] Recently we have shown that acute vasoconstriction is associated with decreased cerebral blood flow (CBF), ischemic glutamate release, and premature mortality after experimental SAH. 12 If acute vasoconstriction could be pharmacologically attenuated, then SAH-induced brain injury could potentially be reduced.Resting cerebrovascular tone is maintained by a balance between opposing vasoconstrictive and vasodilatory forces, and both are pathologically altered in the acute phases of SAH. One of the most important of these is the resting vasodilatory influence of nitric oxide (NO). NO has been shown to induce endothelium-dependent vasodilatation via a cGMP-mediated See Editorial Comment, page 1961 mechanism. 13 Loss of endothelium-mediated vasodilatation 14,15 and decreased cGMP production 16,17 have been shown to contribute to vasospasm after SAH.Because administration of an NO donor after SAH should potentially restore c-GMP-dependent vasodilatation, a number of different NO donors have been tested for their ability to attenuate delayed vasospasm. 18 -21 Recent studies have suggested that sodium nitroprusside administered intrathecally 22 or intra-arterially 23 increases CBF acutely after SAH. In preliminary studies we have found that it also causes profound hypotension in this setting (J.B. Bederson, MD, et al, ...

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confidence: 99%

Effects of S -Nitrosoglutathione on Acute Vasoconstriction and Glutamate Release After Subarachnoid Hemorrhage

Sehba

Ding

Chereshnev

et al. 1999

Stroke

101

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“…7 - 10 Several recent investigations have used rats for experimental SAH, with results indicating that rats have many features found in the higher animal models. 79 " 12 Nonetheless, to be an exact model of a clinical condition, animals must reproduce the pathophysiologic defects found in patients.…”

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Subarachnoid hemorrhage fails to produce vasculopathy or chronic blood flow changes in rats.

Swift

Solomon

1988

Stroke

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Cerebral blood flow was measured by a [ l4 C]butanol indicator fractionation technique in rats subjected to subarachnoid hemorrhage, in control rats, and in rats given injections of buffered saline into the subarachnoid space (sham hemorrhage). Cerebral blood flow was significantly decreased in both the subarachnoid hemorrhage and sham hemorrhage rats 3 hours after injection. However, blood flow returned to control levels by 24 hours, and measurement for 14 days after subarachnoid hemorrhage failed to show any delayed decrease in cerebral blood flow. Electron microscopic studies of basilar arteries from rats subjected to subarachnoid hemorrhage 72 hours before killing failed to show any of the morphologic changes that have been associated with vasospasm in humans or in higher animal models. Our studies indicate that the rat model of subarachnoid hemorrhage has limited applicability to the study of subarachnoid hemorrhage following ruptured cerebral aneurysms in humans. However, although rats are not a perfect model of this clinical condition, some pathophysiologic changes similar to those observed in human subarachnoid hemorrhage have been demonstrated in this model and deserve further investigation. (Stroke 1988;19:878-882)

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“…This beneficious effect of periadventitial tissue stripping might just as well be due to the treatment of a supposed stiffening of non-contractile components; either as a mechanical release or by the sympathic "deafferentation" of the vessel [31]. It has already been shown that cranial sympathectomy relieves late vasoconstriction but not acute vasoconstriction [25]. As a conclusion it can be said that, by whatever mechanism, when periadventitial tissue is stripped away throughout surgery, subacute post-operative vasoconstriction and morphological changes are less serious although this immediate postoperative vasoconstriction is not prevented.…”

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confidence: 99%

Pharmacological and pathophysiological effects of periadventitial stripping on immediate and subacute postoperative vasoconstriction in Guinea pigs

et al. 1997

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Mechanically induced vasospasm observed in the immediate post-operative period was investigated, and the effect of factors such as temporary clip applications and post-operative intervals were studied. Guinea pig "cervical internal carotid arteries" were used and temporary clips, chosen according to the diameter of the artery and systolic pressure, were applied for a standard period. The same procedure was applied on arteries in which periadventitial tissue had been removed using appropriate microsurgical techniques. On postoperative days 1, 5, and 10, arterial rings were removed while the animals were still alive and Endothelium Dependent Relaxations were measured using a bioassay system. Morphological investigations were also performed using light microscopy on the same arterial preparations. We observed no difference between perioperative and first day postoperative results. The relaxations were minimum. The most striking pathological changes were observed on postoperative day 5, and the relaxation responses began to rise on day 10 together with morphological improvement. It was also found that periadventitial tissue stripping could be used to prevent subacute post-operative vasoconstriction, since its effect was marked on postoperative day 5 and began to resolve on day 10.

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The effect on the development of cerebral vasospasm in the rat of lesioning of the peripheral and central catecholamine systems

Cited by 25 publications

References 0 publications

Effects of S -Nitrosoglutathione on Acute Vasoconstriction and Glutamate Release After Subarachnoid Hemorrhage

Effects of S -Nitrosoglutathione on Acute Vasoconstriction and Glutamate Release After Subarachnoid Hemorrhage

Subarachnoid hemorrhage fails to produce vasculopathy or chronic blood flow changes in rats.

Pharmacological and pathophysiological effects of periadventitial stripping on immediate and subacute postoperative vasoconstriction in Guinea pigs

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