Endothelial injury following experimental subarachnoid hemorrhage in rats: Effects on brain blood flow

Clower, Ben R.; Yamamoto, Yoshihiro; Cain, Loretta; Haines, Duane E.; Smith, Robert R.

doi:10.1002/ar.1092400110

Cited by 41 publications

(24 citation statements)

References 31 publications

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“…This endothelial injury impairs the equilibrium between NO and prostacylin whose balance is critical for the maintenance of vascular tone 24,25 . Previous reports have indicated that CVS is observed as early as 30 minutes (the acute phase) 26 after SAH, and reaches a peak at days 3-7 (the chronic phase) 27 .…”

Section: Discussionmentioning

confidence: 99%

Effect of cervical sympathetic block on cerebral vasospasm after subarachnoid hemorrhage in rabbits

Liu

et al. 2013

Acta Cir. Bras.

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PURPOSE:Cerebral vasospasm (CVS) is a major complication after subarachnoid hemorrhage (SAH) induced by the rupture of intracranial aneurysms. The aim of the present study was to investigate the effect and mechanism of cervical sympathetic block on cerebral vasospasm of the rabbits after SAH. METHODS:After successful modeling of cervical sympathetic block, 18 healthy male white rabbits were randomly divided into three groups (n=6), ie, sham operation group (Group A), SAH group (Group B) and SAH with cervical sympathetic block group (Group C).Models of delayed CVS were established by puncturing cisterna magna twice with an injection of autologous arterial blood in Groups B and C. A sham injection of blood through cisterna magna was made in Group A. 0.5 ml saline was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 3 d in Group B (bilateral alternating). 0.5 ml of 0.25% bupivacaine was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 7 d in Group B. 2 ml venous blood and cerebrospinal fluid were obtained before (T1), 30 min (T2) and 7 d (T3) after the first injection of blood, respectively, and conserved in a low temperature refrigerator. Basilar artery value at T1, T2 and T3 was measured via cerebral angiography. The degree of damage to nervous system at T1 and T3 was recorded. RESULTS:There was no significant difference in diameter of basilar artery at T1 among three groups. The diameters of basilar artery at T2 and T3 of Groups B and C were all smaller than that in Group A, which was smaller than Group C, with a significant difference.There was no significant difference in NO and NOS in plasma and cerebrospinal fluid among three groups. The NO and NOS contents at T2 and T3 of Groups B and C were all lower than Group A; Group C was higher than Group B, with a significant difference. The nerve function at T3 of Groups B and C were all lower than Group A and that of Group C higher than Group B, with a significant difference. CONCLUSION:Cervical sympathetic block can relieve cerebral vasospasm after subarachnoid hemorrhage and increase NO content and NOS activity in plasma and cerebrospinal fluid to promote neural functional recovery.

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Section: Discussionmentioning

confidence: 99%

Effect of cervical sympathetic block on cerebral vasospasm after subarachnoid hemorrhage in rabbits

Liu

et al. 2013

Acta Cir. Bras.

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“…Their individual portion of effect on the CBF decrease is still object of discussion. The immediate reason for CBF decrease is endothelial damage [56] and vasoconstriction [38,57]. Various experimental studies of traumatic brain injury showed strong evidence for an increase of CBF after an administration of hypertonic saline [26,27].…”

Section: Cerebral Blood Flow Cerebral Perfusion Pressure and Mabpmentioning

confidence: 99%

Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats: A comparison between small volume resuscitation and mannitol

Bermueller

Thal

Plesnila

et al. 2006

Journal of the Neurological Sciences

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“…The term “no-reflow” was coined by Ames in 1968 to describe a period of lack of blood filling the vessels directly after ischemia (Ames et al , 1968) and was first used by Asano and Sano in 1977, to describe early perfusion deficits due to increased ICP in SAH animals (Asano and Sano, 1977). Other factors that contribute to the initial CBF fall in humans include presence of subarachnoid blood (Clower et al , 1994; Ebel et al , 1996; Solomon et al , 1985; Umansky et al , 1983), hypovolemia caused by cerebral salt wasting and excessive urinary output (Solomon et al , 1988), and disturbed autoregulation (Ebel et al , 1996; Jakubowski et al , 1982; Kamiya et al , 1983; Rasmussen et al , 1992). The early CBF reduction after aSAH is accompanied by reduced cerebral metabolic rate of oxygen (Frykholm et al , 2004; Hayashi et al , 2008; Hayashi et al , 2000; Jakobsen et al , 1990; Kawamura et al , 2000) and signs of clinical deterioration (Kobayashi et al , 1979; Miranda et al , 2006).…”

Section: Early Events After Asahmentioning

confidence: 99%

The importance of early brain injury after subarachnoid hemorrhage

Sehba

Hou

Pluta

et al. 2012

Progress in Neurobiology

494

392

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Aneurysmal subarachnoid hemorrhage (aSAH) is a medical emergency that accounts for 5% of all stroke cases. Individuals affected are typically in the prime of their lives (mean age 50 years). Approximately 12% of patients die before receiving medical attention, 33% within 48 hours and 50% within 30 days of aSAH. Of the survivors 50% suffer from permanent disability with an estimated lifetime cost more than double that of an ischemic stroke. Traditionally, spasm that develops in large cerebral arteries 3-7 days after aneurysm rupture is considered the most important determinant of brain injury and outcome after aSAH. However, recent studies show that prevention of delayed vasospasm does not improve outcome in aSAH patients. This finding has finally brought in focus the influence of early brain injury on outcome of aSAH. A substantial amount of evidence indicates that brain injury begins at the aneurysm rupture, evolves with time and plays an important role in patients’ outcome. In this manuscript we review early brain injury after aSAH. Due to the early nature, most of the information on this injury comes from animals and few only from autopsy of patients who died within days after aSAH. Consequently, we began with a review of animal models of early brain injury, next we review the mechanisms of brain injury according to the sequence of their temporal appearance and finally we discuss the failure of clinical translation of therapies successful in animal models of aSAH.

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Endothelial injury following experimental subarachnoid hemorrhage in rats: Effects on brain blood flow

Abstract: The results indicate a direct correlation between changes in LCBF and the structural integrity of endothelial cells in the early stages following SAH. The lack of chronically depressed LCBF (after 1 day) may be related to the quick structural repair of endothelium.

Cited by 41 publications

References 31 publications

Effect of cervical sympathetic block on cerebral vasospasm after subarachnoid hemorrhage in rabbits

Effect of cervical sympathetic block on cerebral vasospasm after subarachnoid hemorrhage in rabbits

Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats: A comparison between small volume resuscitation and mannitol

The importance of early brain injury after subarachnoid hemorrhage

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