{"id":{"repo_id":"ksu","oai_identifier":"oai:krex.k-state.edu:2097/19770"},"canonical_url":"https://search.dev.ndltd.org/etd/ksu/oai:krex.k-state.edu:2097/19770","repository":{"repo_id":"ksu","name":"Kansas State University","base_url":"https://krex.k-state.edu/server/oai/request"},"display":{"title":"Effects of nitrite infusion on skeletal muscle vascular control during exercise in rats with chronic heart failure","abstract":"Chronic heart failure (CHF) reduces nitric oxide (NO) bioavailability and impairs skeletal muscle vascular control during exercise. Reduction of nitrite (NO[subscript]2-) to NO may impact exercise-induced hyperemia particularly in muscles with pathologically-reduced O[subscript]2 delivery. We tested the hypothesis that NO[subscript]2- infusion would increase exercising skeletal muscle blood flow (BF) and vascular conductance (VC) in CHF rats with a preferential effect in muscles composed primarily of type IIb+IId/x fibers. CHF (coronary artery ligation) was induced in adult male, Sprague-Dawley rats. Following a >21 day recovery, mean arterial pressure (MAP, carotid artery catheter) and skeletal muscle BF (radiolabelled microspheres) were measured during treadmill exercise (20 m•min[superscript]-1, 5% incline) with and without NO[subscript]2- infusion. The myocardial infarct size (35 ± 3%) indicated moderate CHF. NO[subscript]2- infusion increased total hindlimb skeletal muscle VC (CHF: 0.85 ± 0.09, CHF+NO[subscript]2-: 0.93 ± 0.09 ml•min[superscript]-1•100g[superscript]-1•mmHg[superscript]-1, p<0.05) without changing MAP (CHF: 123 ± 4 mmHg, CHF+NO[subscript]2-: 120 ± 4 mmHg, p=0.17). Total hindlimb skeletal muscle BF was not significantly different (CHF: 102 ± 7, CHF+NO[subscript]2-: 109 ± 7 ml•min[superscript]-1•100g[superscript]-1, p>0.05). BF increased in 6 (~21%) and VC in 8 (~29%) of the 28 individual muscles and muscle parts. Muscles and muscle portions exhibiting greater BF and VC following NO[subscript]2- infusion were comprised of ≥63% type IIb+IId/x muscle fibers. These data demonstrate that NO[subscript]2- infusion can augment skeletal muscle vascular control during exercise in CHF rats. Given the targeted effects shown herein, a NO[subscript]2[superscript]--based therapy may provide an attractive “needs-based” approach for treatment of the vascular dysfunction in CHF.","abstract_html":"Chronic heart failure (CHF) reduces nitric oxide (NO) bioavailability and impairs skeletal muscle vascular control during exercise. Reduction of nitrite (NO[subscript]2-) to NO may impact exercise-induced hyperemia particularly in muscles with pathologically-reduced O[subscript]2 delivery. We tested the hypothesis that NO[subscript]2- infusion would increase exercising skeletal muscle blood flow (BF) and vascular conductance (VC) in CHF rats with a preferential effect in muscles composed primarily of type IIb+IId/x fibers. CHF (coronary artery ligation) was induced in adult male, Sprague-Dawley rats. Following a &gt;21 day recovery, mean arterial pressure (MAP, carotid artery catheter) and skeletal muscle BF (radiolabelled microspheres) were measured during treadmill exercise (20 m•min[superscript]-1, 5% incline) with and without NO[subscript]2- infusion. The myocardial infarct size (35 ± 3%) indicated moderate CHF. NO[subscript]2- infusion increased total hindlimb skeletal muscle VC (CHF: 0.85 ± 0.09, CHF+NO[subscript]2-: 0.93 ± 0.09 ml•min[superscript]-1•100g[superscript]-1•mmHg[superscript]-1, p&lt;0.05) without changing MAP (CHF: 123 ± 4 mmHg, CHF+NO[subscript]2-: 120 ± 4 mmHg, p=0.17). Total hindlimb skeletal muscle BF was not significantly different (CHF: 102 ± 7, CHF+NO[subscript]2-: 109 ± 7 ml•min[superscript]-1•100g[superscript]-1, p&gt;0.05). BF increased in 6 (~21%) and VC in 8 (~29%) of the 28 individual muscles and muscle parts. Muscles and muscle portions exhibiting greater BF and VC following NO[subscript]2- infusion were comprised of ≥63% type IIb+IId/x muscle fibers. These data demonstrate that NO[subscript]2- infusion can augment skeletal muscle vascular control during exercise in CHF rats. Given the targeted effects shown herein, a NO[subscript]2[superscript]--based therapy may provide an attractive “needs-based” approach for treatment of the vascular dysfunction in CHF.","abstract_has_math":false,"creators":["Glean, Angela A."],"institution":"Kansas State University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-08-01","date_published":"2015-08-01","updated_at":"2026-07-27T20:01:20Z","subjects":["Heart failure","Nitrite","Exercise","Muscle","Blood flow","Nitric oxide"],"languages":["en_US"],"rights":["© the author. This Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s)."],"rights_urls":["http://rightsstatements.org/vocab/InC/1.0/"],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2097/19770","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Glean, Angela A."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2015-07-06T16:52:27Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2015-07-06T16:52:27Z"]},{"key":"dc:date.issued","label":"Date","values":["2015-08-01"]},{"key":"dc:publisher","label":"Institution","values":["Kansas State University"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Heart failure","Nitrite","Exercise","Muscle","Blood flow","Nitric oxide"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_US"]},{"key":"dc:rights","label":"Dc Rights","values":["© the author. This Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s)."]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://rightsstatements.org/vocab/InC/1.0/"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/2097/19770"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Chronic heart failure (CHF) reduces nitric oxide (NO) bioavailability and impairs skeletal muscle vascular control during exercise. Reduction of nitrite (NO[subscript]2-) to NO may impact exercise-induced hyperemia particularly in muscles with pathologically-reduced O[subscript]2 delivery. We tested the hypothesis that NO[subscript]2- infusion would increase exercising skeletal muscle blood flow (BF) and vascular conductance (VC) in CHF rats with a preferential effect in muscles composed primarily of type IIb+IId/x fibers. CHF (coronary artery ligation) was induced in adult male, Sprague-Dawley rats. Following a >21 day recovery, mean arterial pressure (MAP, carotid artery catheter) and skeletal muscle BF (radiolabelled microspheres) were measured during treadmill exercise (20 m•min[superscript]-1, 5% incline) with and without NO[subscript]2- infusion. The myocardial infarct size (35 ± 3%) indicated moderate CHF. NO[subscript]2- infusion increased total hindlimb skeletal muscle VC (CHF: 0.85 ± 0.09, CHF+NO[subscript]2-: 0.93 ± 0.09 ml•min[superscript]-1•100g[superscript]-1•mmHg[superscript]-1, p<0.05) without changing MAP (CHF: 123 ± 4 mmHg, CHF+NO[subscript]2-: 120 ± 4 mmHg, p=0.17). Total hindlimb skeletal muscle BF was not significantly different (CHF: 102 ± 7, CHF+NO[subscript]2-: 109 ± 7 ml•min[superscript]-1•100g[superscript]-1, p>0.05). BF increased in 6 (~21%) and VC in 8 (~29%) of the 28 individual muscles and muscle parts. Muscles and muscle portions exhibiting greater BF and VC following NO[subscript]2- infusion were comprised of ≥63% type IIb+IId/x muscle fibers. These data demonstrate that NO[subscript]2- infusion can augment skeletal muscle vascular control during exercise in CHF rats. Given the targeted effects shown herein, a NO[subscript]2[superscript]--based therapy may provide an attractive “needs-based” approach for treatment of the vascular dysfunction in CHF."]},{"key":"dc:description.degree","label":"Dc Description Degree","values":["Master of Science"]},{"key":"dc:title","label":"Title","values":["Effects of nitrite infusion on skeletal muscle vascular control during exercise in rats with chronic heart failure"]}]}],"canonical_facts":{"dc:creator":["Glean, Angela A."],"dc:date.accessioned":["2015-07-06T16:52:27Z"],"dc:date.available":["2015-07-06T16:52:27Z"],"dc:date.issued":["2015-08-01"],"dc:description.abstract":["Chronic heart failure (CHF) reduces nitric oxide (NO) bioavailability and impairs skeletal muscle vascular control during exercise. Reduction of nitrite (NO[subscript]2-) to NO may impact exercise-induced hyperemia particularly in muscles with pathologically-reduced O[subscript]2 delivery. We tested the hypothesis that NO[subscript]2- infusion would increase exercising skeletal muscle blood flow (BF) and vascular conductance (VC) in CHF rats with a preferential effect in muscles composed primarily of type IIb+IId/x fibers. CHF (coronary artery ligation) was induced in adult male, Sprague-Dawley rats. Following a >21 day recovery, mean arterial pressure (MAP, carotid artery catheter) and skeletal muscle BF (radiolabelled microspheres) were measured during treadmill exercise (20 m•min[superscript]-1, 5% incline) with and without NO[subscript]2- infusion. The myocardial infarct size (35 ± 3%) indicated moderate CHF. NO[subscript]2- infusion increased total hindlimb skeletal muscle VC (CHF: 0.85 ± 0.09, CHF+NO[subscript]2-: 0.93 ± 0.09 ml•min[superscript]-1•100g[superscript]-1•mmHg[superscript]-1, p<0.05) without changing MAP (CHF: 123 ± 4 mmHg, CHF+NO[subscript]2-: 120 ± 4 mmHg, p=0.17). Total hindlimb skeletal muscle BF was not significantly different (CHF: 102 ± 7, CHF+NO[subscript]2-: 109 ± 7 ml•min[superscript]-1•100g[superscript]-1, p>0.05). BF increased in 6 (~21%) and VC in 8 (~29%) of the 28 individual muscles and muscle parts. Muscles and muscle portions exhibiting greater BF and VC following NO[subscript]2- infusion were comprised of ≥63% type IIb+IId/x muscle fibers. These data demonstrate that NO[subscript]2- infusion can augment skeletal muscle vascular control during exercise in CHF rats. Given the targeted effects shown herein, a NO[subscript]2[superscript]--based therapy may provide an attractive “needs-based” approach for treatment of the vascular dysfunction in CHF."],"dc:description.degree":["Master of Science"],"dc:identifier.uri":["http://hdl.handle.net/2097/19770"],"dc:language.iso":["en_US"],"dc:publisher":["Kansas State University"],"dc:rights":["© the author. This Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s)."],"dc:rights.uri":["http://rightsstatements.org/vocab/InC/1.0/"],"dc:subject":["Heart failure","Nitrite","Exercise","Muscle","Blood flow","Nitric oxide"],"dc:title":["Effects of nitrite infusion on skeletal muscle vascular control during exercise in rats with chronic heart failure"],"dc:type":["Thesis"]},"updated_at":"2026-07-27T20:01:20Z"}