{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/72406"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/72406","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Cellular Calcium Movements and Excitation-Contraction Coupling in Guinea Pig Atria","abstract":"Guinea pig left atria were suspended in a tissue bath of normal Krebs-Henseleit solution which was aerated with 95% O$\\sb2$/5% CO$\\sb2$ and maintained at 27$\\sp\\circ$C. The atria were attached to a force transducer and impaled with calcium sensitive micro-electrodes. The tissue was stimulated through 2 AgCl electrodes at 2 pulses per second (pps). When the tissue had reached a steady-state of contraction strength, rest intervals of 1 minute were introduced and the changes in the paracellular calcium levels were measured with the calcium sensitive micro-electrodes. The control condition produced an average increase during the interval in paracellular calcium concentration of 23.6 + 1.33 uM. Following treatment of the tissue with 8uM $3\\sp\\prime, 4\\sp\\prime$-di-chlorobenzamil (DCB), the average increase in paracellular calcium was 9.02 + 1.25 uM. DCB reduces the normal calcium efflux by 61.6 + 7.3%, n = 4, p $<$ 0.005. (Statistical analysis used paired one tail T-test.) 10 nM Ryanodine treated-tissue showed an increased efflux of calcium as measured by increased para-cellular calcium concentration of 9.8 + 1.9 uM over the control condition. 8uM DCB decreased the ryanodine treated tissues calcium efflux by 53.6 + 8.0%, n = 6, p $<$ 0.005, as measured by a decrease in the paracellular calcium concentration of 10.4 + 1.8 uM compared to the ryanodine treated condition. The cellular calcium efflux may be calculated from the measured changes in paracellular calcium concentration assuming an extracellular space of 47.8 ml/100 gm tissue. 8 uM DCB decreased the calcium efflux by 11.6 nmoles/sec per 100 gm tissue in non-ryanodine treated atria, and by 8.3 nmoles/sec per 100 gm of tissue in ryanodine treated atria. We conclude that DCB is an inhibitor of sodium-calcium exchange in guinea pig atria and that a measurable increase in paracellular calcium occurs during rest due to efflux of calcium from the cells via sodium-calcium exchange. In addition, we have shown that DCB decreases post-rest beat potentiation and this may indicate that sodium-calcium exchange plays a role in post-rest beat potentiation as well as the excitation-contraction coupling process.","abstract_html":"Guinea pig left atria were suspended in a tissue bath of normal Krebs-Henseleit solution which was aerated with 95% O$\\sb2$/5% CO$\\sb2$ and maintained at 27$\\sp\\circ$C. The atria were attached to a force transducer and impaled with calcium sensitive micro-electrodes. The tissue was stimulated through 2 AgCl electrodes at 2 pulses per second (pps). When the tissue had reached a steady-state of contraction strength, rest intervals of 1 minute were introduced and the changes in the paracellular calcium levels were measured with the calcium sensitive micro-electrodes. The control condition produced an average increase during the interval in paracellular calcium concentration of 23.6 + 1.33 uM. Following treatment of the tissue with 8uM $3\\sp\\prime, 4\\sp\\prime$-di-chlorobenzamil (DCB), the average increase in paracellular calcium was 9.02 + 1.25 uM. DCB reduces the normal calcium efflux by 61.6 + 7.3%, n = 4, p $<$ 0.005. (Statistical analysis used paired one tail T-test.) 10 nM Ryanodine treated-tissue showed an increased efflux of calcium as measured by increased para-cellular calcium concentration of 9.8 + 1.9 uM over the control condition. 8uM DCB decreased the ryanodine treated tissues calcium efflux by 53.6 + 8.0%, n = 6, p $<$ 0.005, as measured by a decrease in the paracellular calcium concentration of 10.4 + 1.8 uM compared to the ryanodine treated condition. The cellular calcium efflux may be calculated from the measured changes in paracellular calcium concentration assuming an extracellular space of 47.8 ml/100 gm tissue. 8 uM DCB decreased the calcium efflux by 11.6 nmoles/sec per 100 gm tissue in non-ryanodine treated atria, and by 8.3 nmoles/sec per 100 gm of tissue in ryanodine treated atria. We conclude that DCB is an inhibitor of sodium-calcium exchange in guinea pig atria and that a measurable increase in paracellular calcium occurs during rest due to efflux of calcium from the cells via sodium-calcium exchange. In addition, we have shown that DCB decreases post-rest beat potentiation and this may indicate that sodium-calcium exchange plays a role in post-rest beat potentiation as well as the excitation-contraction coupling process.","abstract_has_math":true,"creators":["Burton, John Todd"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Biophysics","degree_department":null,"school":null,"contributors":["Sleator, William,"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-12-17T22:22:50Z","date_published":"2014-12-17T22:22:50Z","updated_at":"2026-07-22T22:26:06Z","subjects":["Biology, Cell","Biology, Animal Physiology","Biophysics, Medical"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(UMI)AAI9328985"],"render_values":[{"text":"(UMI)AAI9328985","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/72406","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Sleator, William,"]},{"key":"dc:creator","label":"Author","values":["Burton, John Todd"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2014-12-17T22:22:50Z","10000-01-01","1993"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biophysics"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Cell","Biology, Animal Physiology","Biophysics, Medical"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/72406","(UMI)AAI9328985"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Guinea pig left atria were suspended in a tissue bath of normal Krebs-Henseleit solution which was aerated with 95% O$\\sb2$/5% CO$\\sb2$ and maintained at 27$\\sp\\circ$C. The atria were attached to a force transducer and impaled with calcium sensitive micro-electrodes. The tissue was stimulated through 2 AgCl electrodes at 2 pulses per second (pps). When the tissue had reached a steady-state of contraction strength, rest intervals of 1 minute were introduced and the changes in the paracellular calcium levels were measured with the calcium sensitive micro-electrodes. The control condition produced an average increase during the interval in paracellular calcium concentration of 23.6 + 1.33 uM. Following treatment of the tissue with 8uM $3\\sp\\prime, 4\\sp\\prime$-di-chlorobenzamil (DCB), the average increase in paracellular calcium was 9.02 + 1.25 uM. DCB reduces the normal calcium efflux by 61.6 + 7.3%, n = 4, p $<$ 0.005. (Statistical analysis used paired one tail T-test.) 10 nM Ryanodine treated-tissue showed an increased efflux of calcium as measured by increased para-cellular calcium concentration of 9.8 + 1.9 uM over the control condition. 8uM DCB decreased the ryanodine treated tissues calcium efflux by 53.6 + 8.0%, n = 6, p $<$ 0.005, as measured by a decrease in the paracellular calcium concentration of 10.4 + 1.8 uM compared to the ryanodine treated condition. The cellular calcium efflux may be calculated from the measured changes in paracellular calcium concentration assuming an extracellular space of 47.8 ml/100 gm tissue. 8 uM DCB decreased the calcium efflux by 11.6 nmoles/sec per 100 gm tissue in non-ryanodine treated atria, and by 8.3 nmoles/sec per 100 gm of tissue in ryanodine treated atria. We conclude that DCB is an inhibitor of sodium-calcium exchange in guinea pig atria and that a measurable increase in paracellular calcium occurs during rest due to efflux of calcium from the cells via sodium-calcium exchange. In addition, we have shown that DCB decreases post-rest beat potentiation and this may indicate that sodium-calcium exchange plays a role in post-rest beat potentiation as well as the excitation-contraction coupling process.","Made available in DSpace on 2014-12-17T22:22:50Z (GMT). No. of bitstreams: 1 9328985.pdf: 3213932 bytes, checksum: e713db419f97d52cc141a0e71dbb5f13 (MD5) Previous issue date: 1993","Embargo set by: Seth Robbins for item 72574 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","86 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1993."]},{"key":"dc:title","label":"Title","values":["Cellular Calcium Movements and Excitation-Contraction Coupling in Guinea Pig Atria"]}]}],"canonical_facts":{"dc:contributor":["Sleator, William,"],"dc:creator":["Burton, John Todd"],"dc:date":["2014-12-17T22:22:50Z","10000-01-01","1993"],"dc:description":["Guinea pig left atria were suspended in a tissue bath of normal Krebs-Henseleit solution which was aerated with 95% O$\\sb2$/5% CO$\\sb2$ and maintained at 27$\\sp\\circ$C. The atria were attached to a force transducer and impaled with calcium sensitive micro-electrodes. The tissue was stimulated through 2 AgCl electrodes at 2 pulses per second (pps). When the tissue had reached a steady-state of contraction strength, rest intervals of 1 minute were introduced and the changes in the paracellular calcium levels were measured with the calcium sensitive micro-electrodes. The control condition produced an average increase during the interval in paracellular calcium concentration of 23.6 + 1.33 uM. Following treatment of the tissue with 8uM $3\\sp\\prime, 4\\sp\\prime$-di-chlorobenzamil (DCB), the average increase in paracellular calcium was 9.02 + 1.25 uM. DCB reduces the normal calcium efflux by 61.6 + 7.3%, n = 4, p $<$ 0.005. (Statistical analysis used paired one tail T-test.) 10 nM Ryanodine treated-tissue showed an increased efflux of calcium as measured by increased para-cellular calcium concentration of 9.8 + 1.9 uM over the control condition. 8uM DCB decreased the ryanodine treated tissues calcium efflux by 53.6 + 8.0%, n = 6, p $<$ 0.005, as measured by a decrease in the paracellular calcium concentration of 10.4 + 1.8 uM compared to the ryanodine treated condition. The cellular calcium efflux may be calculated from the measured changes in paracellular calcium concentration assuming an extracellular space of 47.8 ml/100 gm tissue. 8 uM DCB decreased the calcium efflux by 11.6 nmoles/sec per 100 gm tissue in non-ryanodine treated atria, and by 8.3 nmoles/sec per 100 gm of tissue in ryanodine treated atria. We conclude that DCB is an inhibitor of sodium-calcium exchange in guinea pig atria and that a measurable increase in paracellular calcium occurs during rest due to efflux of calcium from the cells via sodium-calcium exchange. In addition, we have shown that DCB decreases post-rest beat potentiation and this may indicate that sodium-calcium exchange plays a role in post-rest beat potentiation as well as the excitation-contraction coupling process.","Made available in DSpace on 2014-12-17T22:22:50Z (GMT). No. of bitstreams: 1 9328985.pdf: 3213932 bytes, checksum: e713db419f97d52cc141a0e71dbb5f13 (MD5) Previous issue date: 1993","Embargo set by: Seth Robbins for item 72574 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","86 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1993."],"dc:identifier":["http://hdl.handle.net/2142/72406","(UMI)AAI9328985"],"dc:subject":["Biology, Cell","Biology, Animal Physiology","Biophysics, Medical"],"dc:title":["Cellular Calcium Movements and Excitation-Contraction Coupling in Guinea Pig Atria"],"dc:type":["text"],"thesis:degree_discipline":["Biophysics"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:26:06Z"}