Effect of glycerol and intracarotid phenoxybenzamine on cerebral hemodynamics and metabolism after experimental subarachnoid hemorrhage

Hashi, Kazuo; Meyer, John Stirling; Shinmaru, S.; Welch, K. M. A.; Teraura, Tetsuaki

doi:10.1016/0022-510x(72)90018-4

Cited by 16 publications

(5 citation statements)

References 7 publications

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“…PBZ does not change MCBF though it significantly reduces arterial pressure. Similar observations were made by Hoff et al 18 and Sokoloff. 17 However, Hashi et al 18 found a significant increase in CBF induced by PBZ.…”

Section: Discussionsupporting

confidence: 79%

“…17 However, Hashi et al 18 found a significant increase in CBF induced by PBZ. The difference in the results could be accounted for by the design of the 2 sets of experiments in that Hoffet al 18 measured CBF 2-4 hours after giving the drug whereas Hashi et al 18 measured during infusion. PBZ does not change the sensitivity of CBF to changes in arterial Pco 2 .…”

Section: Discussionmentioning

confidence: 99%

“…The alterations during CO 2 inhalation were of the same order as found by Nyary et al 8 in untreated animals. Hoff et al 18 showed that there was no significant effect of PBZ upon CBF during hypo-or normocapnia. The reactivity of the cerebral vessels to CO 2 19 may account for the differences observed between the control flows.…”

Section: Discussionmentioning

confidence: 99%

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Effect of phenoxybenzamine on cerebral blood flow and metabolism in the baboon during hemorrhagic shock.

Hamar¹,

Kovách

Reivich

et al. 1979

Stroke

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Experiments were performed on 2 groups of baboons anesthetized with Sernylan. One group served as control and the other was premedicated with 5 mg/kg phenoxybenzamine (PBZ). A 2-step hypovolemic shock model was used followed by retransfusion of the shed blood. Cerebral blood flow was measured by the 133Xe clearance method. Arterial and cerebral venous samples were taken and analyzed for blood gases as well as glucose and lactate content. The cerebral metabolic rates of oxygen, glucose, and lactate were calculated. In addition, the effect of CO2 inhalation was studied before shock was induced. PBZ produced no effect on either CBF or the flow response to CO2 prior to bleeding. PBZ pretreatment prevented the fall in cerebral blood flow and CMRO2 produced by systemic hypotension due to bleeding. Lactic acid showed no evidence of change either in production or uptake by the brain during the experimental procedure. The cerebral metabolic pathway of glucose, however, seemed to be affected by PBZ both before and during shock.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

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Effect of phenoxybenzamine on cerebral blood flow and metabolism in the baboon during hemorrhagic shock.

Hamar¹,

Kovách

Reivich

et al. 1979

Stroke

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“…Both morphological and physiologi- 1 7 4 KUSCHINSKY, WAHL cal data (5) indicate the existence of sympathetic perivascular nerves at pial arteries, but under what conditions are these nerves activated? From studies using stimulation, denervation, and alphareceptor blockers, it has been suggested that the tone of cerebral arteries may be influenced by sympathetic constrictor nerves under conditions such as changes in arterial Pco 2 (26)(27)(28) or blood pressure (26) or during subarachnoidal hemorrhage or experimental spasm (12,29,30).…”

Section: Discussionmentioning

confidence: 99%

Alpha-receptor stimulation by endogenous and exogenous norepinephrine and blockade by phentolamine in pial arteries of cats.

Kuschinsky¹,

Wahl²

1975

Circ Res

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The question regarding the existence of an alpha-adrenergic component of pial arterial tone was investigated using a microapplication technique combined with the measurement of vascular diameter. Concentration-response curves for the alpha-receptor blocker, phentolamine, revealed no vascular reaction for a concentration range from 2.5 x 10(-11) to 2.5 x 10(-7) M. At higher concentrations (up to 1.3 x 10(-3) M) concentration-dependent dilations were observed. Constrictions of pial arteries induced by perivascular injection of 2.5 x 10(-6) M norepinephrine could be reduced by 38% and 73% when phentolamine was applied simultaneously in concentrations of 2.5 x 10(-7) and 2.5 x 10(-6) M, respectively, whereas constrictions due to 2.5 x 10(-4) M norepinephrine were not reduced by 2.5 x 10(-6) M phentolamine, indicating a competitive antagonism between norepinephrine and phentolamine for pial arteries. Stimulation of the cervical sympathetic chain (90 seconds, 10 v, 1.4 msec, 20 Hz) induced constrictions of pial arteries (mean 12%) which could be reduced by two-thirds during the simultaneous application of 2.5 x 10(-7) M phentolamine. Since the constriction induced by norepinephrine applied exogenously or released endogenously could be reduced by a concentration of phentolamine which had no vascular effect per se, we conclude that the resting tone of the pial arteries is not influenced by an alpha-adrenergic component under our experimental conditions. The dilations induced by high concentrations of phentolamine are believed to be nonspecific.

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“…A few works on cerebral edema in SAH that ever appeared in the literature were concerned mainly with the morphological evidence of cerebral edema. 27,28 In the present study, cerebral edema could be quantitatively documented with the aid of the recently developed microgravimetric technique 16 as well as by microdetermination of regional brain water content through vacuum freeze-drying. 17 Cerebral edema developed in grade II animals in which a temporary global cerebral ischemia was followed by reactive hyperemia and subsequent post-ischemic hypoperfusion.…”

Section: Cerebral Edema In Sahmentioning

confidence: 99%

Cerebral edema following experimental subarachnoid hemorrhage.

Shigeno¹,

Fritschka²,

Brock³

et al. 1982

Stroke

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The development of cerebral edema after experimental subarachnoid hemorrhage (SAH) was studied in cats by determining regional brain tissue water content with the microgravimetric technique as well as the drying-weighing method. SAH was induced by withdrawing needles previously pierced into one or both infraclinoid internal carotid arteries through a unilateral transorbital approach. Serial determinations of regional cerebral blood flow (rCBF) by labelled microspheres, and monitorings of vital signs such as intracranial pressure (ICP), blood pressure and EEG were carried out up to 24 h after SAH. Animals could be classified into three grades according to the severity of SAH. In grade I, the increase of ICP was transient and minor. In grade II, ICP increased up to 200 mm Hg with a marked reduction of rCBF below 20% of control in cerebral hemispheres. Following subsequent reduction of ICP, rCBF increased over control, indicating reactive hyperemia. Thereafter, a great reduction of rCBF was again observed. In grade III, rCBF was sustained at essentially zero flow with the presence of continuously increased ICP above 100 mm Hg. Cerebral edema was observed particularly in the parasagittal water-shed areas of all grade II animals. It is concluded that cerebral edema complicating SAH is caused by the combination of an initially induced global cerebral ischemia and the subsequent recovery of cerebral circulation. Post SAH hypertension is another factor to exacerbate the development of cerebral edema.

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Effect of glycerol and intracarotid phenoxybenzamine on cerebral hemodynamics and metabolism after experimental subarachnoid hemorrhage

Cited by 16 publications

References 7 publications

Effect of phenoxybenzamine on cerebral blood flow and metabolism in the baboon during hemorrhagic shock.

Effect of phenoxybenzamine on cerebral blood flow and metabolism in the baboon during hemorrhagic shock.

Alpha-receptor stimulation by endogenous and exogenous norepinephrine and blockade by phentolamine in pial arteries of cats.

Cerebral edema following experimental subarachnoid hemorrhage.

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