Responses of cerebral arterioles to activation of beta-adrenergic receptors during diabetes mellitus.

Mayhan, William G.

doi:10.1161/01.str.25.1.141

Cited by 24 publications

(13 citation statements)

References 28 publications

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“…The diabetes induced vascular changes in l3-adrenergic receptor function may contribute to attenuation of the sympathetic stress response. Brain microvessels of streptozoto cin-induced diabetic rats have a decreased number of l3-adrenergic receptors and an attenuated CBF and pial arteriolar vasodilative response to isopro terenol (Mayhan, 1993(Mayhan, , 1994. Altered CBF re sponses to propranolol occur in our diabetic dogs as well (Sieber et aI., 1993a).…”

Section: Discussionmentioning

confidence: 90%

Poor Hemodynamic and Metabolic Recovery after Global Incomplete Cerebral Ischemia Associated with Short-Term Diabetes in Dogs

Palmon

Sieber

Brown

et al. 1995

J Cereb Blood Flow Metab

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Summary:We determined the effect of 4-5 weeks of di abetes on ATP recovery following global incomplete ce rebral ischemia. 31p magnetic resonance spectra of ATP, intracellular pH (pHj), and CBF (radiolabeled micro spheres) were measured in three groups of anesthetized dogs (n = 8/group): chronic hyperglycemic diabetes (pan createctomy followed by blood glucose of > to mM for 4-5 weeks); acute hyperglycemia (blood glucose of> to mM) during ischemia and reperfusion in nondiabetic dogs; and normoglycemic controls. Twenty minutes of incomplete ischemia was produced by ventricular fluid infusion to keep cerebral perfusion pressure (CPP) at to mm Hg during spontaneous variations in MABP. Intra cranial pressure was increased initially to similar levels, resulting in a similar Cushing response among the groups. However, during the final 8 min of ischemia, MABP de creased to a greater extent in diabetic (86 ± 42 mm Hg) than in hyperglycemic (162 ± 30 mm Hg) and normogly cemic (135 ± 54 mm Hg) groups and remained lower throughout 3 h of reperfusion. CPP was kept constant during ischemia, but was lower throughout reperfusion in diabetic dogs. During ischemia CBF was reduced simi larly among groups: 5 ± 3 ml . min -I • 100 g -1 in hyper glycemic and normoglycemic and 4 ± 3 ml . min -I . 100 g -I in diabetic dogs. During reperfusion early hyperemia During global cerebral ischemia, acute hypergly cemia is associated with increased neurologic dam age; however, the effects of chronic hyperglycemia secondary to diabetes on the cerebral ischemic re sponse are unclear. This is particularly true in aniReceived September 12, 1994; final revision received Novem ber 10, 1994; accepted November 11, 1994. Address correspondence and reprint requests to Dr. S. C. Palmon at Department of Anesthesiology and Critical Care Med icine, Johns Hopkins Hospital, 600 N. Wolfe St., Meyer 8-134, Baltimore, MD 21287-7834, U.S.A.Abbreviations used: CPP, cerebral perfusion pressure; ICP, intracranial pressure; MRS, magnetic resonance spectroscopy. 673was attenuated and delayed hypoperfusion was aug mented (7 ± 17 ml . min -I . 100 g-I by 180 min) as a result of low perfusion pressure in diabetics. However, medullary blood flow was similar among groups. End ischemic ATP was similar among groups (25 ± 34, 30 ± 25, and 4 ± 11% of baseline in normoglycemic, hypergly cemic and diabetic dogs, respectively). Following 180 min of reperfusion ATP was 87 ± 15,45 ± 38, and 7 ± 19% of control in normoglycemic, hyperglycemic and diabetic dogs, respectively. End-ischemic pHj was lower in hyper glycemic (5.94 ± 0.16) and diabetic (5.96 ± 0.08) than normoglycemic (6.32 ± 0.04) groups. By 45 min of reper fusion, pHi recovered in normoglycemic (7.02 ± 0.09) but not in diabetic (6.l3 ± 0.38) or hyperglycemic dogs (6.44 ± 0.28). This study shows that MABP, CBF, ATP, and pHi following global incomplete ischemia did not recover in diabetic dogs. In diabetics poor metabolic recovery was related to the MABP decreases during ischemia and reperfusion. These results contrast wi...

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Section: Discussionmentioning

confidence: 90%

Poor Hemodynamic and Metabolic Recovery after Global Incomplete Cerebral Ischemia Associated with Short-Term Diabetes in Dogs

Palmon

Sieber

Brown

et al. 1995

J Cereb Blood Flow Metab

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“…40 In diabetic humans as well as experimental animals, cerebral vasodilatory responses are impaired, presumably related to beta-adrenergic or sympathetic neuronal dysfunction. 41,42 In diabetic rats, the number of beta-adrenergic receptors is reduced in cerebral microvessels, 43 which can be attributed to the impaired beta-adrenergic receptor-mediated vasodilatory response in DM, resulting in enhanced pulsatility. Vessels in the posterior cerebral circulation, since they have fewer adrenergic neurons than in the anterior cerebral circulation, 40 may have a restricted vasodilatory response and enhance the susceptibility of DM-related neuronal dysregulation of cerebral vessels.…”

Section: Discussionmentioning

confidence: 99%

Arterial Pulsatility as an Index of Cerebral Microangiopathy in Diabetes

Lee

Sohn

Baik

et al. 2000

Stroke

143

110

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Background and Purpose-This study was designed to evaluate cerebral hemodynamic changes related to diabetes mellitus (DM) with transcranial Doppler ultrasonography (TCD). Methods-We measured the flow velocities and the Gosling pulsatility index (PI) of the middle cerebral artery (MCA), extracranial internal carotid artery (ICA), and basilar artery (BA) in 56 stroke-free, normotensive patients with type 2 DM and 70 age-and gender-matched healthy volunteers. Patients were divided into 2 groups according to the presence of microvascular complications such as retinopathy, nephropathy, and neuropathy. Results-Patients showed slightly lower hematocrit and higher serum fibrinogen levels than control subjects, but other clinical profiles, including stroke risk factors except for diabetes, were comparable between patients and controls. The flow velocity of the ICA but not the MCA and BA in patients regardless of the complication was significantly higher than that in controls. The PIs of the MCA and ICA were significantly higher in patients with complication than those without complication, as well as in controls. The PI of the BA was also significantly higher, even in patients without complication, than in controls. The PIs of the MCA and ICA but not the BA were closely correlated with the duration of DM (r 2 ϭ0.46 and 0.34, respectively). Conclusions-This study defines TCD findings of diabetes-related cerebral hemodynamic changes and suggests that the PI reflects microangiopathic changes of cerebral vessels.

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“…1 2 In contrast, ß-adrenergic blocking agents decrease cerebral blood flow in experimental study. 22 NTG and PGE1 have minimal effects on cerebral blood flow. 13 However, the results of the present study could not be explained by the known action of the drug on cerebral circulation under stable condition.…”

Section: Effect Of Each Anti-hypertensive Drug On Cerebral Hemodynamicsmentioning

confidence: 91%

Reduction of cerebral hyperemia with anti-hypertensive medication after electroconvulsive therapy

Saito

Kikuchi

Iriuchijima

et al. 2000

Can J Anesth/J Can Anesth

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REPORTS OF INVESTIGATION 767CAN J ANESTH 2000 / 47: 8 / pp [767][768][769][770][771][772][773][774] Purpose: Several different anti-hypertensive regimens have been introduced for the prevention of systemic hyperdynamic responses after electrically induced seizures. In the present study, the effects of anti-hypertensive medications on cerebral circulation were studied.Methods: Systemic blood pressure was controlled by several anti-hypertensive medications, nicardipine, prostaglandin E1, alprenolol and nitroglycerin, in 30 patients (150 electroconvulsive therapy trials). Changes in cerebral blood flow velocity were measured by transcranial Doppler sonography of the right middle cerebral artery from the start of anesthesia to 10 min after the electrical shock.Results: Administration of a Ca 2+ antagonist, nicardipine, or prostaglandin E1 did not alter the augmented cerebral blood flow velocity after the seizure. However, a ß-adrenergic blocking agent, alprenolol (P < 0.05) or nitroglycerin (P < 0.01) partially inhibited the increase in cerebral blood flow velocity. Maximal blood flow velocity was 133% larger than the pre-anesthesia value in the control group, 109% in the nicardipine group, 113% in the prostaglandin E1 group, 72% in the alprenolol group, and 45% in the nitroglycerin group, respectively. The increase in cerebral blood flow velocity after electrically induced seizure was independent of systemic blood pressure. Internal jugular venous saturation (SjO 2 ) was increased, and difference in arterial and venous concentrations of lactate was not altered in all groups.Conclusions: Cerebral hemodynamics is altered by ECT, even when systemic hemodynamics are stabilized by antihypertensive medication. Although the effects of antihypertensive medicine on cerebral hemodynamics are variable, systemic blood pressure control by these agents does not induce cerebral ischemia after ECT.Objectif : Différentes thérapies antihypertensives ont été proposées comme moyen de prévention des répon-ses hyperdynamiques généralisées à la suite d'électrochocs. Dans la présente étude, on a analysé les effets de médicaments antihypertenseurs sur la circulation cérébrale.Méthode : La pression sanguine générale a été contrôlée par différents médicaments antihypertenseurs, la nicardipine, la prostaglandine E 1 , l'alprénolol et la nitroglycérine, chez 30 patients lors de 150 essais d'électro-chocs. Les changements de vitesse circulatoire cérébrale ont été mesurés par échographie Doppler transcrâni-enne de l'artère cérébrale moyenne droite, du début de l'anesthésie jusqu'à 10 min après l'électrochoc.Résultats : L'administration d'un antagoniste de Ca 2 +, la nicardipine, ou la prostaglandine E 1 n'ont pas modifié la vitesse circulatoire cérébrale augmentée après les convulsions. Toutefois, un agent ß-bloquant, l'alprénolol (P < 0,05) ou la nitroglycérine (P < 0,01) ont partiellement inhibé l'augmentation de vitesse circulatoire cérébrale. La vitesse circulatoire maximale a été 133 % de la valeur préanesthésique mesurée dans le groupe tém...

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Responses of cerebral arterioles to activation of beta-adrenergic receptors during diabetes mellitus.

Cited by 24 publications

References 28 publications

Poor Hemodynamic and Metabolic Recovery after Global Incomplete Cerebral Ischemia Associated with Short-Term Diabetes in Dogs

Poor Hemodynamic and Metabolic Recovery after Global Incomplete Cerebral Ischemia Associated with Short-Term Diabetes in Dogs

Arterial Pulsatility as an Index of Cerebral Microangiopathy in Diabetes

Reduction of cerebral hyperemia with anti-hypertensive medication after electroconvulsive therapy

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