Effect of beta-adrenergic blockade with propranolol on cerebral blood flow, autoregulation and CO2 responsiveness.

Aqyagi, M; Deshmukh, Vinod D.; Meyer, John Stirling; Kawamura, Yasuo; Tagashira, Yukio

doi:10.1161/01.str.7.3.291

Cited by 47 publications

(16 citation statements)

References 33 publications

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“…This responsiveness is impaired by many factors, such as atherosclerosis with aging (Yamaguchi et aI., 1979; Yamamoto et aI., 1980), severe head trauma, and subarachnoid hemorrhage (Enevoldsen and Jensen, 1978;Mendelow et aI., 1981) Pharmacologi cal agents have also been demonstrated to influence cerebral vasomotor reactivity to CO2, Propranolol decreased the vasodilatory effect of hypercarbia without affecting cerebrovasoconstriction induced by hypocarbia (Aoyagi et al, 1976). The influence of anesthetic agents seems to depend on the condi tions of the experiments.…”

Section: Discussionmentioning

confidence: 99%

Effects of Midazolam on Cerebral Hemodynamics and Cerebral Vasomotor Responsiveness to Carbon Dioxide

Forster

Juge

Morel

1983

J Cereb Blood Flow Metab

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Although it is known that hypercarbia increases and benzodiazepines decrease cerebral blood flow (CBF), the effects of benzodiazepines on CBF responsiveness to CO2 are not well documented. The influence on CBF and CBF-C02 sensitivity of placebo or midazolam, which is a new water-soluble benzodiazepine, was measured in eight healthy volunteers using the noninvasive 133Xe inhalation method for CBF determination. Under normocarbia, midazolam decreased CBF from 40.6 ± 3.2 to 27.0 ± 5.0 ml 100 g−1 min−1 (x̄ ± SD). At a later session under hypercarbia, CBF was 58.8 ± 4.4 ml 100 g−1 min−1 after administration of placebo, and 49.1 ± 10.2 ml 100 g−1 min−1 after midazolam. The mean of the slopes correlating Paco2 and CBF was significantly steeper with midazolam (2.5 ± 1.2 ml 100 g−1 min−1 mm Hg−1) than with placebo (1.5 ± 0.4 ml 100 g−1 min−1 mm Hg−1). Our results suggest that midazolam may be a safe agent to use in patients with intracranial hypertension, since it decreases CBF and thus cerebral blood volume; however, it should be administered with caution in nonventilated patients with increased intracranial pressure, since its beneficial effects on cerebrovascular tone can be readily counteracted by the increase in arterial CO2 tension induced by this drug.

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Section: Discussionmentioning

confidence: 99%

Effects of Midazolam on Cerebral Hemodynamics and Cerebral Vasomotor Responsiveness to Carbon Dioxide

Forster

Juge

Morel

1983

J Cereb Blood Flow Metab

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“…It has been reported (Aoyagi et al, 1976;Hares et al, 1977) that CBF falls when ,B-adrenergic blocking drugs are administered acutely. We wondered if in a more chronic setting this might also occur and be reflected clinically in the lethargy and lightedness which are known to occur on occasion in association with these drugs (Petrie, Galloway, Jeffers & Webster, 1976).…”

Section: Discussionmentioning

confidence: 99%

The effect of beta‐adrenergic receptor blocking drugs on cerebral blood flow.

Griffith¹,

Im²,

Newbury³

et al. 1979

Brit J Clinical Pharma

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1 Cerebral blood flow (CBF) was measured by the 133xenon inhalation method in 33 newly‐diagnosed hypertensive patients prior to commencing therapy. 2 Blood pressure was treated by using a varying sequence of four different drugs, namely labetalol, metoprolol, oxprenolol and sotalol, each of which is a beta‐adrenergic receptor blocking agent, but with differing additional properties. 3 CBF measurements were repeated when blood pressure was controlled. No significant change in CBF was found with any of the four drugs, in contrast to the fall which has been reported when drugs of this type are administered acutely.

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“…Other investigators have reported minimal or no effect 15 18 or a deleterious effect 62 "" of propranolol on cerebral blood flow. Studies have differed however as to species, route of administration, dosage, and modes of measurement.…”

Section: Comparison Of Results Of 3 Hour and 6 Hour Right Mca Occlusimentioning

confidence: 96%

Treatment of acute focal cerebral ischemia with propranolol.

ACapraro¹,

PReedy²,

PLatchaw³

et al. 1984

Stroke

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Propranolol's potential as a protective agent against tissue injury has been noted in experimental myocardial, renal and early acute focal cerebral ischemia. The purpose of the present investigation was to study further the effects of racemic (d,l) propranolol on blood-brain barrier permeability, morphological changes, cortical electrical activity, and regional cerebral blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult cats, anesthetized with nitrous oxide, underwent 6 hours of right middle cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion, both directly into the right carotid artery. Right Sylvian rCBF did not significantly differ in the treated and untreated groups. Carbon filling defects and vital dye (i.e., Evans blue and fluorescein) extravasation were less severe in the propranolol treated animals. Light microscopic findings demonstrated no difference in infarct size between the two groups. The findings suggest that at doses given, racemic propranolol does not exert a protective effect upon cerebral tissue subjected to 6 hours of incomplete ischemia.

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Effect of beta-adrenergic blockade with propranolol on cerebral blood flow, autoregulation and CO2 responsiveness.

Cited by 47 publications

References 33 publications

Effects of Midazolam on Cerebral Hemodynamics and Cerebral Vasomotor Responsiveness to Carbon Dioxide

Effects of Midazolam on Cerebral Hemodynamics and Cerebral Vasomotor Responsiveness to Carbon Dioxide

The effect of beta‐adrenergic receptor blocking drugs on cerebral blood flow.

Treatment of acute focal cerebral ischemia with propranolol.

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