Functional Heterogeneity in Canine Coronary Resistance Arteries

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dc.contributor.advisorPeter B. Raven
dc.contributor.committeeMemberPatricia A. Gwirtz
dc.contributor.committeeMemberJames Caffrey
dc.creatorParker, James Bruce
dc.date.accessioned2019-08-22T21:13:51Z
dc.date.available2019-08-22T21:13:51Z
dc.date.issued1994-06-01
dc.date.submitted2013-09-23T13:42:07-07:00
dc.description.abstractParker, James B., Functional Heterogeneity in Canine Coronary Resistance Arteries. Doctor of Philosophy (Biomedical Sciences), June, 1994, 89 pages, 21 illustrations, bibliography, 82 titles. Two thirds of the coronary vascular resistance resides in the smallest arteries and investigators have hypothesized that they may respond differently to endogenous vasoactive substances. The arterial responses to norepinephrine, acetylcholine, and adenosine were evaluated in large ([greater than] 700 μm, n=24), intermediate (400 600 μm, n=24), and small arteries (μm, n=24). Maximal vessel lumen diameter (Dmax) was determined in CA++ free medium. A reference diameter (84 ± 4.3% of Dmax) was established by re-equilibration in medium containing 2.0 mM Ca++. Arterial maximal responses as a percentage of Dmax to norepinephrine, acetylcholine, and adenosine are given in table 1: Table 1; Large % of Dmax; Inter. % of Dmax; Small % of Dmax; Norepinephrine; 41 ± 2.3; 50 ± 4.2; 83 ± 2.4; Acetylcholine; 96 ± 2.7; 88 ± 3.9; 78 ± 1.9; Adenosine; 71 ± 1.8; 81 ± 4.2; 96 ± 1.4. The sensitivity of canine coronary arteries to norepinephrine, acetylcholine, and adenosine in terms of ED50’s are given in table 2: Table 2; Agonists; Large ED50 μM; Inter. ED50 μM; Small ED50 μM; Norepinephrine; 0.037 ± 0.002; 0.078 ± 0.004; no response; acetylcholine; 0.028 ± 0.003; 0.087 ± 0.005; 0.309 ± 0.03; Adenosine; 0.295 ± 0.002; 0.095 ± 0.004; 0.035 ± 0.03. These data indicate that canine arterial responses to the native agonists norepinephrine, acetylcholine, and adenosine are heterogeneous and that neural control predominates in the larger “transport” arteries while local control predominates in the smaller “distributive” arteries. Responses of small and intermediate isolated canine coronary arteries (lumen diameter 147±42μm, and 531±37μm respectively) to norepinephrine were evaluated after pharmacological or mechanical interruption of endothelial relaxing activity. Following with the nitric oxide synthase inhibitor N-Nitro-L-Arginine Methylester (L-NAME) 10^-5 M the small and intermediate vessels spontaneously constricted to 73±4.1% of Dmax indicating a significant basal release of nitric oxide. After L-NAME or endothelial disruption graded additions of norepinephrine now reduced the vessel diameter in previously unresponsive small arteries. These data suggest that the weak and equivocal response of coronary resistance arteries to norepinephrine results from the competitive dilatory influence of endothelial derived nitric oxide production and not to the absence of norepinephrine receptors.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12503/29173
dc.language.isoen
dc.provenance.legacyDownloads0
dc.subjectAnimal Sciences
dc.subjectCardiovascular Diseases
dc.subjectCardiovascular System
dc.subjectCirculatory and Respiratory Physiology
dc.subjectComparative and Laboratory Animal Medicine
dc.subjectLife Sciences
dc.subjectMedical Physiology
dc.subjectMedical Sciences
dc.subjectMedicine and Health Sciences
dc.subjectSmall or Companion Animal Medicine
dc.subjectVeterinary Medicine
dc.subjectVeterinary Physiology
dc.subjectHeterogeneity
dc.subjectcanine
dc.subjectcoronary resistance arteries
dc.subjectcoronary vascular resistance
dc.subjectendogenous vasoactive substances
dc.subjecttransport arteries
dc.subjectdistributive arteries
dc.subjectnorepinephrine
dc.subjectdilatory influence
dc.subjectendothelial derived nitric oxide production
dc.titleFunctional Heterogeneity in Canine Coronary Resistance Arteries
dc.typeDissertation
dc.type.materialtext
thesis.degree.departmentGraduate School of Biomedical Sciences
thesis.degree.disciplineBiomedical Sciences
thesis.degree.grantorUniversity of North Texas Health Science Center at Fort Worth
thesis.degree.nameDoctor of Philosophy

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