Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes
Background We determined the effects of NIDDM on haemodynamic parameters describing arterial wall elasticity and cardiac hypertrophy in rats administered streptozotocin (STZ) and nicotinamide (NA), using the aortic impedance analysis. Methods Male Wistar rats at 2 months were administered intraper...
Gespeichert in:
| Veröffentlicht in: | European journal of clinical investigation 2006-01, Vol.36 (1), p.1-7 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 7 |
|---|---|
| container_issue | 1 |
| container_start_page | 1 |
| container_title | European journal of clinical investigation |
| container_volume | 36 |
| creator | Chang, K.-C. Tseng, C.-D. Chou, T.-F. Cho, Y.-L. Chi, T.-C. Su, M.-J. Tseng, Y.-Z. |
| description | Background We determined the effects of NIDDM on haemodynamic parameters describing arterial wall elasticity and cardiac hypertrophy in rats administered streptozotocin (STZ) and nicotinamide (NA), using the aortic impedance analysis.
Methods Male Wistar rats at 2 months were administered intraperitoneally 180 mg kg−1 of NA, 30 min before an intravenous injection of 50 mg kg−1 STZ, to induce type 2 diabetes. The STZ‐NA rats were divided into two groups, 4 weeks and 8 weeks after induction of diabetes, and compared with untreated age‐matched controls. Pulsatile aortic pressure and flow signals were measured by a high‐fidelity pressure sensor and electromagnetic flow probe, respectively, and were then subjected to Fourier transformation for the analysis of aortic input impedance.
Results In each diabetic group, the experimental syndrome was characterized by a moderate and stable hyperglycaemia and a relative deficiency of insulin secretion. However, the 8‐week but not the 4‐week STZ‐NA diabetic rats showed a decrease in cardiac output in the absence of any significant changes in mean aortic pressure, having increased total peripheral resistance. The diabetic syndrome at 8 weeks also contributed to an increase in aortic characteristic impedance, from 1·49 ± 0·33 (mean ± SD) to 1·95 ± 0·28 mmHg s mL−1 (P |
| doi_str_mv | 10.1111/j.1365-2362.2006.01588.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70686460</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70686460</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4358-fa156c039011e78e0eaaeb2fdda9e7fe4e44d153af5f4754fb9a7628616f3243</originalsourceid><addsrcrecordid>eNqNkM9v0zAUgC0EYmXwLyBf4Jbw_CO2e-AwRVuZNIGQJsHNek2emUuaFDvV2v-ehFbbFV9syd9nP32McQGlmNanTSmUqQqpjCwlgClBVM6Vhxds8XTxki0AhC7k0soL9ibnDQA4oeRrdiGMBgWgFuz7VRopRex4HmMI1Mf-F8e-5Q2mNmLDH447SmMadg9HHnuOvKdHnnDk26Gljg-BjxPBJZ_oNY2U37JXAbtM7877Jbu_ub6vvxR331a39dVd0WhVuSKgqEwDaglCkHUEhEhrGdoWl2QDadK6FZXCUAVtKx3WS7RGOiNMUFKrS_bx9OwuDX_2lEe_jbmhrsOehn32Fowz2sAEuhPYpCHnRMHvUtxiOnoBfq7pN36O5udofq7p_9X0h0l9f_5jv95S-yye803AhzOAucEuJOybmJ85q61xeh7284l7jB0d_3sAf13fzqfJL05-zCMdnnxMv72xylb-x9eVl7X-qWq38rX6CzhenoY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>70686460</pqid></control><display><type>article</type><title>Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Chang, K.-C. ; Tseng, C.-D. ; Chou, T.-F. ; Cho, Y.-L. ; Chi, T.-C. ; Su, M.-J. ; Tseng, Y.-Z.</creator><creatorcontrib>Chang, K.-C. ; Tseng, C.-D. ; Chou, T.-F. ; Cho, Y.-L. ; Chi, T.-C. ; Su, M.-J. ; Tseng, Y.-Z.</creatorcontrib><description>Background We determined the effects of NIDDM on haemodynamic parameters describing arterial wall elasticity and cardiac hypertrophy in rats administered streptozotocin (STZ) and nicotinamide (NA), using the aortic impedance analysis.
Methods Male Wistar rats at 2 months were administered intraperitoneally 180 mg kg−1 of NA, 30 min before an intravenous injection of 50 mg kg−1 STZ, to induce type 2 diabetes. The STZ‐NA rats were divided into two groups, 4 weeks and 8 weeks after induction of diabetes, and compared with untreated age‐matched controls. Pulsatile aortic pressure and flow signals were measured by a high‐fidelity pressure sensor and electromagnetic flow probe, respectively, and were then subjected to Fourier transformation for the analysis of aortic input impedance.
Results In each diabetic group, the experimental syndrome was characterized by a moderate and stable hyperglycaemia and a relative deficiency of insulin secretion. However, the 8‐week but not the 4‐week STZ‐NA diabetic rats showed a decrease in cardiac output in the absence of any significant changes in mean aortic pressure, having increased total peripheral resistance. The diabetic syndrome at 8 weeks also contributed to an increase in aortic characteristic impedance, from 1·49 ± 0·33 (mean ± SD) to 1·95 ± 0·28 mmHg s mL−1 (P < 0·05), suggesting a detriment to the aortic distensibility in NIDDM. Meanwhile, the STZ‐NA diabetic animals after 8 weeks had an increased wave reflection factor (0·46 ± 0·09 vs. 0·61 ± 0·13, P < 0·05) and decreased wave transit time (25·8 ± 3·8 vs. 20·6 ± 2·8 ms, P < 0·05). Ratio of the left ventricular weight to body weight was also enhanced in the 8‐week STZ‐NA diabetic rats.
Conclusion The heavy intensity with early return of the pulse wave reflection may augment systolic load of the left ventricle coupled to the arterial system, leading to cardiac hypertrophy in the rats at 8 weeks after following STZ and NA administration.</description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1111/j.1365-2362.2006.01588.x</identifier><identifier>PMID: 16403003</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Aorta - physiopathology ; Aortic distensibility ; aortic input impedance ; Biological and medical sciences ; Cardiomegaly - physiopathology ; diabetes mellitus type 2 ; Diabetes Mellitus, Experimental - physiopathology ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetes. Impaired glucose tolerance ; Diabetic Angiopathies - physiopathology ; Elasticity ; Electrophoresis, Polyacrylamide Gel ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; General aspects ; Hemodynamics ; Male ; Medical sciences ; Pulsatile Flow ; pulse wave reflection ; Rats ; Rats, Wistar ; streptozotocin-nicotinamide diabetic rats ; Vascular Resistance</subject><ispartof>European journal of clinical investigation, 2006-01, Vol.36 (1), p.1-7</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4358-fa156c039011e78e0eaaeb2fdda9e7fe4e44d153af5f4754fb9a7628616f3243</citedby><cites>FETCH-LOGICAL-c4358-fa156c039011e78e0eaaeb2fdda9e7fe4e44d153af5f4754fb9a7628616f3243</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2362.2006.01588.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2362.2006.01588.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,4010,27900,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17476844$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16403003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, K.-C.</creatorcontrib><creatorcontrib>Tseng, C.-D.</creatorcontrib><creatorcontrib>Chou, T.-F.</creatorcontrib><creatorcontrib>Cho, Y.-L.</creatorcontrib><creatorcontrib>Chi, T.-C.</creatorcontrib><creatorcontrib>Su, M.-J.</creatorcontrib><creatorcontrib>Tseng, Y.-Z.</creatorcontrib><title>Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description>Background We determined the effects of NIDDM on haemodynamic parameters describing arterial wall elasticity and cardiac hypertrophy in rats administered streptozotocin (STZ) and nicotinamide (NA), using the aortic impedance analysis.
Methods Male Wistar rats at 2 months were administered intraperitoneally 180 mg kg−1 of NA, 30 min before an intravenous injection of 50 mg kg−1 STZ, to induce type 2 diabetes. The STZ‐NA rats were divided into two groups, 4 weeks and 8 weeks after induction of diabetes, and compared with untreated age‐matched controls. Pulsatile aortic pressure and flow signals were measured by a high‐fidelity pressure sensor and electromagnetic flow probe, respectively, and were then subjected to Fourier transformation for the analysis of aortic input impedance.
Results In each diabetic group, the experimental syndrome was characterized by a moderate and stable hyperglycaemia and a relative deficiency of insulin secretion. However, the 8‐week but not the 4‐week STZ‐NA diabetic rats showed a decrease in cardiac output in the absence of any significant changes in mean aortic pressure, having increased total peripheral resistance. The diabetic syndrome at 8 weeks also contributed to an increase in aortic characteristic impedance, from 1·49 ± 0·33 (mean ± SD) to 1·95 ± 0·28 mmHg s mL−1 (P < 0·05), suggesting a detriment to the aortic distensibility in NIDDM. Meanwhile, the STZ‐NA diabetic animals after 8 weeks had an increased wave reflection factor (0·46 ± 0·09 vs. 0·61 ± 0·13, P < 0·05) and decreased wave transit time (25·8 ± 3·8 vs. 20·6 ± 2·8 ms, P < 0·05). Ratio of the left ventricular weight to body weight was also enhanced in the 8‐week STZ‐NA diabetic rats.
Conclusion The heavy intensity with early return of the pulse wave reflection may augment systolic load of the left ventricle coupled to the arterial system, leading to cardiac hypertrophy in the rats at 8 weeks after following STZ and NA administration.</description><subject>Animals</subject><subject>Aorta - physiopathology</subject><subject>Aortic distensibility</subject><subject>aortic input impedance</subject><subject>Biological and medical sciences</subject><subject>Cardiomegaly - physiopathology</subject><subject>diabetes mellitus type 2</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Angiopathies - physiopathology</subject><subject>Elasticity</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>General aspects</subject><subject>Hemodynamics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pulsatile Flow</subject><subject>pulse wave reflection</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>streptozotocin-nicotinamide diabetic rats</subject><subject>Vascular Resistance</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkM9v0zAUgC0EYmXwLyBf4Jbw_CO2e-AwRVuZNIGQJsHNek2emUuaFDvV2v-ehFbbFV9syd9nP32McQGlmNanTSmUqQqpjCwlgClBVM6Vhxds8XTxki0AhC7k0soL9ibnDQA4oeRrdiGMBgWgFuz7VRopRex4HmMI1Mf-F8e-5Q2mNmLDH447SmMadg9HHnuOvKdHnnDk26Gljg-BjxPBJZ_oNY2U37JXAbtM7877Jbu_ub6vvxR331a39dVd0WhVuSKgqEwDaglCkHUEhEhrGdoWl2QDadK6FZXCUAVtKx3WS7RGOiNMUFKrS_bx9OwuDX_2lEe_jbmhrsOehn32Fowz2sAEuhPYpCHnRMHvUtxiOnoBfq7pN36O5udofq7p_9X0h0l9f_5jv95S-yye803AhzOAucEuJOybmJ85q61xeh7284l7jB0d_3sAf13fzqfJL05-zCMdnnxMv72xylb-x9eVl7X-qWq38rX6CzhenoY</recordid><startdate>200601</startdate><enddate>200601</enddate><creator>Chang, K.-C.</creator><creator>Tseng, C.-D.</creator><creator>Chou, T.-F.</creator><creator>Cho, Y.-L.</creator><creator>Chi, T.-C.</creator><creator>Su, M.-J.</creator><creator>Tseng, Y.-Z.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200601</creationdate><title>Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes</title><author>Chang, K.-C. ; Tseng, C.-D. ; Chou, T.-F. ; Cho, Y.-L. ; Chi, T.-C. ; Su, M.-J. ; Tseng, Y.-Z.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4358-fa156c039011e78e0eaaeb2fdda9e7fe4e44d153af5f4754fb9a7628616f3243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Aorta - physiopathology</topic><topic>Aortic distensibility</topic><topic>aortic input impedance</topic><topic>Biological and medical sciences</topic><topic>Cardiomegaly - physiopathology</topic><topic>diabetes mellitus type 2</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Angiopathies - physiopathology</topic><topic>Elasticity</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>General aspects</topic><topic>Hemodynamics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pulsatile Flow</topic><topic>pulse wave reflection</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>streptozotocin-nicotinamide diabetic rats</topic><topic>Vascular Resistance</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, K.-C.</creatorcontrib><creatorcontrib>Tseng, C.-D.</creatorcontrib><creatorcontrib>Chou, T.-F.</creatorcontrib><creatorcontrib>Cho, Y.-L.</creatorcontrib><creatorcontrib>Chi, T.-C.</creatorcontrib><creatorcontrib>Su, M.-J.</creatorcontrib><creatorcontrib>Tseng, Y.-Z.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, K.-C.</au><au>Tseng, C.-D.</au><au>Chou, T.-F.</au><au>Cho, Y.-L.</au><au>Chi, T.-C.</au><au>Su, M.-J.</au><au>Tseng, Y.-Z.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2006-01</date><risdate>2006</risdate><volume>36</volume><issue>1</issue><spage>1</spage><epage>7</epage><pages>1-7</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract>Background We determined the effects of NIDDM on haemodynamic parameters describing arterial wall elasticity and cardiac hypertrophy in rats administered streptozotocin (STZ) and nicotinamide (NA), using the aortic impedance analysis.
Methods Male Wistar rats at 2 months were administered intraperitoneally 180 mg kg−1 of NA, 30 min before an intravenous injection of 50 mg kg−1 STZ, to induce type 2 diabetes. The STZ‐NA rats were divided into two groups, 4 weeks and 8 weeks after induction of diabetes, and compared with untreated age‐matched controls. Pulsatile aortic pressure and flow signals were measured by a high‐fidelity pressure sensor and electromagnetic flow probe, respectively, and were then subjected to Fourier transformation for the analysis of aortic input impedance.
Results In each diabetic group, the experimental syndrome was characterized by a moderate and stable hyperglycaemia and a relative deficiency of insulin secretion. However, the 8‐week but not the 4‐week STZ‐NA diabetic rats showed a decrease in cardiac output in the absence of any significant changes in mean aortic pressure, having increased total peripheral resistance. The diabetic syndrome at 8 weeks also contributed to an increase in aortic characteristic impedance, from 1·49 ± 0·33 (mean ± SD) to 1·95 ± 0·28 mmHg s mL−1 (P < 0·05), suggesting a detriment to the aortic distensibility in NIDDM. Meanwhile, the STZ‐NA diabetic animals after 8 weeks had an increased wave reflection factor (0·46 ± 0·09 vs. 0·61 ± 0·13, P < 0·05) and decreased wave transit time (25·8 ± 3·8 vs. 20·6 ± 2·8 ms, P < 0·05). Ratio of the left ventricular weight to body weight was also enhanced in the 8‐week STZ‐NA diabetic rats.
Conclusion The heavy intensity with early return of the pulse wave reflection may augment systolic load of the left ventricle coupled to the arterial system, leading to cardiac hypertrophy in the rats at 8 weeks after following STZ and NA administration.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>16403003</pmid><doi>10.1111/j.1365-2362.2006.01588.x</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0014-2972 |
| ispartof | European journal of clinical investigation, 2006-01, Vol.36 (1), p.1-7 |
| issn | 0014-2972 1365-2362 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70686460 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Aorta - physiopathology Aortic distensibility aortic input impedance Biological and medical sciences Cardiomegaly - physiopathology diabetes mellitus type 2 Diabetes Mellitus, Experimental - physiopathology Diabetes Mellitus, Type 2 - physiopathology Diabetes. Impaired glucose tolerance Diabetic Angiopathies - physiopathology Elasticity Electrophoresis, Polyacrylamide Gel Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance General aspects Hemodynamics Male Medical sciences Pulsatile Flow pulse wave reflection Rats Rats, Wistar streptozotocin-nicotinamide diabetic rats Vascular Resistance |
| title | Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T06%3A29%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Arterial%20stiffening%20and%20cardiac%20hypertrophy%20in%20a%20new%20rat%20model%20of%20type%202%20diabetes&rft.jtitle=European%20journal%20of%20clinical%20investigation&rft.au=Chang,%20K.-C.&rft.date=2006-01&rft.volume=36&rft.issue=1&rft.spage=1&rft.epage=7&rft.pages=1-7&rft.issn=0014-2972&rft.eissn=1365-2362&rft_id=info:doi/10.1111/j.1365-2362.2006.01588.x&rft_dat=%3Cproquest_cross%3E70686460%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=70686460&rft_id=info:pmid/16403003&rfr_iscdi=true |