Vascular control mechanisms have been studied extensively in mice. However, an in vitro characterization of penetrating intracerebral arterioles has not been reported. We describe methods for isolation and cannulation for mouse intracerebral arterioles. This technique allows analysis of mouse cerebral arteriolar physiology and pharmacology without the confounding influences of the surrounding brain elements. Penetrating intracerebral arterioles from adult C57/BL6 wild-type (WT) mice were isolated at 4 degrees C, transferred to an inverted microscope and cannulated at both ends using a dual glass micropipette system, wherein intraluminal flow (0.2 microl/min) and pressure (60 mmHg) were maintained. The arterioles developed spontaneous tone when the chamber was warmed to 37 degrees C, with the resulting diameter reaching 68.4+/-0.9% of passive diameter (29.8+/-1.1 microm). After the development of spontaneous tone, incremental changes in luminal pressure from 20 to 140 mmHg induced myogenic responses. Acidosis (pH 6.8) and alkalosis (pH 7.6) caused dilation (20.0+/-1.4%) and constriction (17.2+/-1.4%), respectively. Extraluminal adenosine (ADO (10 microM); 24.3+/-3.6%) and sodium nitroprusside (SNP (10 microM); 28.6+/-4.1%) and intraluminal adenosine 5'-triphosphate (ATP (10 microM); 20.0+/-3.9%) resulted in vasodilation similar in magnitude to that observed in rat arterioles. This information provides a foundation for elucidating cerebral vascular control mechanisms in genetically engineered mice.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s0165-0270(02)00197-8 | DOI Listing |
J Am Heart Assoc
December 2024
Division of Neurology, Rady Faculty of Health Sciences University of Manitoba Winnipeg MB Canada.
Background: About 25% of patients with acute ischemic stroke have lacunar infarct on follow-up imaging. In this secondary analysis from the AcT (Alteplase Compared With Tenecteplase) trial, we assessed if there is variation in safety or efficacy of intravenous thrombolysis by infarct type in patients with no visible occlusion. We also determined if this effect differed between tenecteplase and alteplase.
View Article and Find Full Text PDFNeuropharmacology
January 2025
School of Pharmacy and Bioengineering, Keele University, Staffordshire, ST5 5BG, UK. Electronic address:
Neurology
September 2024
From the Departments of Neurology (J.B., S.W., M.L., A.N.), Genetics (S.W.), and Ophthalmology (M-A. L.), Université Caen-Normandie, CHU de Caen-Normandie, Caen; NeuroDiderot (T.C.), Université Paris Cité, Inserm UMR 1141; and Service de Génétique Moléculaire Neurovasculaire (T.C.), AP-HP, Hôpital Saint-Louis, Paris, France.
A 50-year-old man presented with headache. Examination showed left sided ataxic hemiparesis and elevated blood pressure. Brain imaging revealed an acute intracerebral hemorrhage in the right lentiform nucleus, deep and periventricular white matter hyperintensities, and predominantly deep cerebral microbleeds.
View Article and Find Full Text PDFBackground: Cerebral amyloid angiopathy (CAA) is a cerebral small vessel disease in which amyloid-β accumulates in vessel walls. CAA is a leading cause of symptomatic lobar intracerebral hemorrhage and an important contributor to age-related cognitive decline. Recent work has suggested that vascular dysfunction may precede symptomatic stages of CAA, and that spontaneous slow oscillations in arteriolar diameter (termed vasomotion), important for amyloid-β clearance, may be impaired in CAA.
View Article and Find Full Text PDFbioRxiv
April 2024
Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, USA.
Cerebral amyloid angiopathy (CAA) is a vasculopathy characterized by vascular β-amyloid (Aβ) deposition on cerebral blood vessels. CAA is closely linked to Alzheimer's disease (AD) and intracerebral hemorrhage. CAA is associated with the loss of autoregulation in the brain, vascular rupture, and cognitive decline.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!