Influence of Cerebral Vasoconstricting and Vasodilating Agents on Blood Flow in Regions of Focal Ischemia

Hanson, E. Jerome; Anderson, Robert E.; Sundt, Thoralf M.

doi:10.1161/01.str.6.6.642

Cited by 25 publications

(7 citation statements)

References 52 publications

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“…132 There are, however, examples of microcirculatory steal during hypercarbia or during administration of volatile anesthetic agents, such as halothane, in the setting of focal cerebral ischemia. 133,134 Unless vasodilator therapy is restricted to the arteries afflicted by cerebral vasospasm, intracarotid vasodilator therapy carries the theoretical risk of cerebral steal, due to vasodilation in the normal vascular beds.…”

Section: Clinical Use Of Intracarotid Drugsmentioning

confidence: 99%

Intracarotid Delivery of Drugs

Joshi¹,

Meyers

Ornstein³

2008

Anesthesiology

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The major efforts to selectively deliver drugs to the brain in the last decade have relied on smart molecular techniques to penetrate the blood brain barrier while intraarterial drug delivery has drawn relatively little attention. In the last decade there have been rapid advances in endovascular techniques. Modern endovascular procedures can permit highly targeted drug delivery by intracarotid route. Intracarotid drug delivery can be the primary route of drug delivery or it could be used to facilitate the delivery of smart-neuropharmaceuticals. There have been few attempts to systematically understand the kinetics of intracarotid drugs. Anecdotal data suggests that intracarotid drug delivery is effective in the treatment of cerebral vasospasm, thromboembolic strokes, and neoplasms. Neuroanesthesiologists are frequently involved in the care of such high-risk patients. Therefore, it is necessary to understand the applications of intracarotid drug delivery and the unusual kinetics of intracarotid drugs.

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Section: Clinical Use Of Intracarotid Drugsmentioning

confidence: 99%

Intracarotid Delivery of Drugs

Joshi¹,

Meyers

Ornstein³

2008

Anesthesiology

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“…First, and most obvious, is the general reduction in metabolic rate that occurs with high doses of barbiturates (Smith, 1979). Other beneficial effects of barbiturates theoretically include preferentially improved blood flow to injured areas (Hanson et al, 1975), decreased brain edema (Simeone et al, 1979), removal of harmful free radicals through an effective scavenger action, and stabilization of mitochondria1 systems that are particularly prone to disruption during any hypoxic state (Flamm et al, 1978).…”

Section: S29mentioning

confidence: 99%

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Lombroso

Burchfiel

1987

Epilepsia

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Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.

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“…It has been believed that PBT and other barbiturates exert direct constrictive effects on cerebral vessels. [25][26][27] However, the recent report of Marin et al 28 suggests that PBT decreases cerebrovascular reactivity and inhibits contractions elicited by various vasoconstrictor agents, such as noradrenalin, potassium chloride and 5-hydroxytryptamine, in insolated human cerebral arteries. As a possible explanation for the mechanism of the PBT-induced fall in ICP, they suggested that PBT relaxed the major cerebral arteries, but not the arterioles, thus triggering a vasoconstriction of the latter due to the increased hydrostatic pressure (the Bayliss effect).…”

Section: The Mechanisms Of Cerebral Protection By Pbt and Y-9179mentioning

confidence: 99%

Mechanisms of cerebral protection by pentobarbital and nizofenone correlated with the course of local cerebral blood flow changes.

Ochiai¹,

Asano²,

Takakura

et al. 1982

Stroke

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SUMMARY The effects of delayed administration of pentobarbital and a novel imidazole derivative (Nizofenone or Y-9179) on the infarction size following the regional cerebral ischemia were studied using the permanent middle cerebral artery (MCA) occlusion model in cats. The courses of local cerebral blood flow (€CBF) before and after drug administration were also studied using the hydrogen clearance method. The extent of infarction one week after MCA occlusion was significantly smaller in the drug-treated groups than in the control group. Regarding the time-course of (,CBF, there was no significant differences between the control and the Y-9179 groups. On the other hand, pentobarbital administration caused a significant €CBF increase in low-flow areas where the £CBF following MCA occlusion was below 40 ml/lOOg/min. In spite of this flow increase, the corresponding cortical areas underwent infarction. Histological examination of the state of vasogenic edema revealed that the perivascular exudation of plasma fluid in the infarcted area was definitely less in the Y-9179 treated group than in the other groups. Results indicate that redistribution of €CBF may not be involved in the mechanism of cerebral protection by pentobarbital or Y-9179.Stroke, Vol 13, No 6, 1982 IT WAS PREVIOUSLY REPORTED that pentobarbital (PBT) and a novel imidazole derivative (Y-9179 or Nizofenone*) reduced the size of infarction in the brain after permanent middle cerebral artery (MCA) occlusion in cats.1 The protective action of Y-9179 against hypoxia and ischemia had already been demonstrated with various models using rats and mice.2 In addition, Y-9179 has few side effects such as anesthetic or cardio-pulmonary depressant action. Although the mechanism of action of Y-9179 has not been fully elucidated, its moderate depressant action on the cerebral metabolic rate may be involved in its cerebral protective action.3 However, this effect is not so potent as with PBT,4 and the role of the decreased cerebral metabolic rate in the mechanism of cerebral protection is controversial. 5,6 In animal experiments it was shown that a barbiturate (methohexital) altered cerebral blood flow (CBF) so that local CBF (€CBF) in the severely ischemic area was increased and that in the unaffected area was decreased (inverse steal).7 Since such a hemodynamic effect might also be relevant to the action of Y-9179, we undertook the present experiments to evaluate i) effect of delayed administration of PBT or Y-9179 on €CBF as measured by the hydrogen clearance method and ii) overall effects of these drugs in terms of histological changes one week after the ischemic insult, using a permanent MCA occlusion model in cats. 8 -9 Materials and Methods Twenty-four adults cats of both sexes weighing 2.0-*From the Department of Neurosurgery, Faculty of Medicine, University of Tokyo, Tokyo, Japan.tAnd from Research Laboratories, Yoshitomi Pharmaceutical Industries, Fukuoka, Japan.Correspondence to: Chikayuki Ochiai, M.D., Department of Neurosurgery, University of Tokyo ...

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Influence of Cerebral Vasoconstricting and Vasodilating Agents on Blood Flow in Regions of Focal Ischemia

Cited by 25 publications

References 52 publications

Intracarotid Delivery of Drugs

Intracarotid Delivery of Drugs

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Mechanisms of cerebral protection by pentobarbital and nizofenone correlated with the course of local cerebral blood flow changes.

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