Effect of Beta-Adrenergic Blockade With Propranolol on Cerebral Blood Flow, Autoregulation

نویسندگان

  • MINORU AQYAGI
  • VINOD D. DESHMUKH
  • JOHN STIRLING MEYER
  • YASUO KAWAMURA
  • YUKIO TAGASHIRA
چکیده

Cerebral autoregulation and vasomotor responsiveness to carbon dioxide were measured quantitatively in normal baboons before and after intravertebral or intravenous infusion of the beta-adrenergic blocking agent, propranolol hydrochloride (Inderal®). Continuous measurements were made of cerebral blood flow (CBF: measured as bilateral internal jugular venous outflow using an electromagnetic flowmeter), cerebral perfusion pressure (CPP), arterial Po, and Pco2 and venous Po2, cerebral arteriovenous oxygen difference and endotracheal Pco2. The autoregulation index (A.I. = ACBF/ACPP) and the chemical index (C.I. = ACBF/APaco2) were used as quantitative measures. The effect of intravertebral infusion of propranolol (0.01 mg per kilogram of body weight) was compared to intravenous infusion of identical doses of propranolol so that any specific action of the drug on a possible vasomotor center in the brain stem may be assessed. Significant reductions (-25%) in CBF and CPP followed both intravertebral and intravenous infusion of propranolol. Cerebral metabolic rate for oxygen (CMRO2) decreased significantly ( — 18%) and cerebrovascular resistance (CVR) increased significantly ( + 19%) after intravertebral infusion of propranolol while less significant changes ensued following intravenous infusion of propranolol. Cerebral autoregulatory vasoconstriction during increases in CPP was significantly enhanced following both intravertebral and intravenous propranolol. Cerebral autoregulatory vasodilatation during decrease in CPP was not influenced by propranolol. Cerebral vasodilatory responsiveness to CO2 inhalation was significantly inhibited following intravertebral propranolol while no significant change resulted from intravenous propranolol. Cerebral vasoconstrictive responsiveness to hyperventilation was not influenced by propranolol. These results indicate that the CBF and CMRO2 are reduced by a pharmacological beta adrenergic blockade with propranolol hydrochloride.

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

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تاریخ انتشار 2005