Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments
Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments. Rats were subjected to 25 min of unilateral renal artery occlusion and were studied at 5, 15, and 30 min and at 1, 2, 4, 8, 16, 24, and 48 hr following ischemia. The patterns of epithelial injury an...
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| description | Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments. Rats were subjected to 25 min of unilateral renal artery occlusion and were studied at 5, 15, and 30 min and at 1, 2, 4, 8, 16, 24, and 48 hr following ischemia. The patterns of epithelial injury and repair in proximal tubule (PT) segments S1, S2, and S3 were followed, and associated changes in renal function were determined. We found that S1 and S2 cells alike are only reversibly injured and recover completely to normalcy within 4 hr, whereas S3 cells selectively undergo progressive cell injury and death and are exfoliated into tubular lumina. The necrotic S3 cells are replaced by mitotic division of survivor cells 24 to 48 hr following the ischemic insult. In addition, there was selective damage within tubular cells. Within 5 min of blood reflow following ischemia, the majority of brush border microvilli (MV) in all three PT segments underwent coalescence by membrane fusion and thus were interiorized into the cytoplasm of PT cells. A minority of MV fragmented and were shed into PT lumina, but nephron obstruction by shed membranes was only mild and transient, unlike in the 1-hr ischemia model. Loss of MV reached a maximum at 15 min. By 30 min, MV began to reappear; by 2 hr, large numbers of MV had been regenerated; and by 4 hr, S1 and S2 cells appeared normal. The regenerative process included the luminal repositioning of previously interiorized MV membrane. MV regeneration occurred in S3 segments also, but before the process was complete, the cells developed features of irreversible cellular injury. Glomerular nitration rate (GFR) was 22% of control at 30 min of reflow, rose progressively to 55% of normal by 7 to 8 hr, and was normal at 24 hr. Single nephron filtration rate (SNGFR) was not significantly different from normal throughout. Proximal tubular sodium reabsorption was depressed and urinary sodium excretion increased at 30 min and at 2 to 3 hr, i.e., at times when MV alterations were prominent, but both were normal by 7 to 8 hr when MV in S1 and S2 cells had been fully reconstituted. Our major conclusions are: 1) There is differential susceptibility by cell type to ischemic injury in rat PT. 2) A rapid brush border loss/ regeneration cycle occurs after ischemic injury. 3) Intact brush border may be required for normal sodium reabsorption by PT. Reasons for the GFR/SNGFR discrepancy are unclear, but tubular malfunction may partly explain the pheno |
| doi_str_mv | 10.1038/ki.1978.87 |
| format | Article |
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Lésions ischémiques et réparation dans le tube proximal du rat: Différences entre les segments S1, S2, et S3. Des rats ont été soumis à une occlusion unilatérale de l'artère rénale de 25 min puis étudiés 5, 15, 30 min, 1, 2, 4, 8, 16, 24, et 48 hr après l'ischémie. Les modalités des lésions épithéliales et de leur réparation dans les segments S1, S2, et S3 du tube proximal (PT) ont été suivies et les modifications associées du fonctionnement rénal ont été évaluées. Nous avons constaté que les cellules S1 et S2 ne sont lésées que de façon réversible et paraissent à nouveau normales après 4 hr, alors que les cellules S3 subissent un processus progressif de destruction qui aboutit à la mort suivie d'exfoliation dans la lumière tubulaire. Les cellules S3 nécrotiques sont remplacées par des divisions mitotiques des cellules survivantes 24 à 48 hr après l'ischémie. De surcroît il existe une lésion sélective des cellules tubulaires. Dans les 5 min qui suivent le rétablissement de la circulation, la majorité des microvillosités (MV) de la bordure en brosse des trois segments de PT subissent une coalescence par fusion des membranes et sont incluses è l'intérieur du cytoplasme des cellules du PT. Une minorité des MV se fragmentent et sont déversées dans la lumière tubulaire, mais l'obstruction néphronique qu'elles réalisent est modérée et transitoire, à la différence de ce qui se produit dans l'ischémie d'une durée d'une heure. La perte des MV atteint un maximum à 15 min. A 30 min, les MV commencent à réapparaître; à 2 hr un grand nombre de MV ont été régénérées et à 4 hr les cellules S1 et S2 paraissent normales. Le processus de régénération inclue la reposition luminale des MV antérieurement en position intra-cellulaire. La régénération des MV se produit aussi dans les segments S3 mais avant que ce processus ne soit achevé les dextructions cellulaires irréversibles apparaissent. La filtration glomérulaire (GFR) est 22% des contrôles 30 min après le rétablissement de la circulation et augmente progressivement jusqu'a 55% des valeurs normales è 7–8 hr, et redevient normale è 24 hr. Les nitrations glomérulaires individuelles (SNGFR) ne sont pas significativement différentes de la normale tout au long de cette évolution. La réabsorption proximale du sodium est diminuée et 1'excrétion urinaire du sodium augmente à 30 min et à 2–3 hr, c'est-à-dire quand les lésions de MV sont importantes, mais réabsorption proximale et excrétion urinaire redeviennent normales à 7–8 hr, c'est-à-dire quand les MV des cellules S1 et S2 sont complètement reconstituées. Nos conclusions sont: 1) il existe une différence de sensibilité à l'ischémie selon le type cellulaire du tube proximal du rat. 2) Un cycle rapide de destruction et régénération de la bordure en brosse survient après l'ischémie 3) L'intégrité de la bordure en brosse est nécessaire pour une réabsorption normale du sodium par PT. Les raisons de l'absence de correspondance entre GFR et SNGFR ne sont pas claires, un dysfonctionnement tubulaire, cependant, pourrait expliquer en partie ce phénomène.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.1978.87</identifier><identifier>PMID: 682423</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cytoplasm - ultrastructure ; Glomerular Filtration Rate ; Ischemia - etiology ; Kidney - blood supply ; Kidney Tubules, Proximal - metabolism ; Kidney Tubules, Proximal - pathology ; Kidney Tubules, Proximal - physiopathology ; Kidney Tubules, Proximal - ultrastructure ; Male ; Microscopy, Electron ; Microvilli - ultrastructure ; Rats ; Renal Artery Obstruction - physiopathology ; Sodium - metabolism ; Time Factors</subject><ispartof>Kidney international, 1978-07, Vol.14 (1), p.31-49</ispartof><rights>1978 International Society of Nephrology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-d9ad4e65f21fa29ac6ab48a1955631604ebacaf1090e372566b8f7dc6b1cc16f3</citedby><cites>FETCH-LOGICAL-c469t-d9ad4e65f21fa29ac6ab48a1955631604ebacaf1090e372566b8f7dc6b1cc16f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/682423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Venkatachalam, Manjeri A.</creatorcontrib><creatorcontrib>Bernard, David B.</creatorcontrib><creatorcontrib>Donohoe, John F.</creatorcontrib><creatorcontrib>Levinsky, Norman G.</creatorcontrib><title>Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments. Rats were subjected to 25 min of unilateral renal artery occlusion and were studied at 5, 15, and 30 min and at 1, 2, 4, 8, 16, 24, and 48 hr following ischemia. The patterns of epithelial injury and repair in proximal tubule (PT) segments S1, S2, and S3 were followed, and associated changes in renal function were determined. We found that S1 and S2 cells alike are only reversibly injured and recover completely to normalcy within 4 hr, whereas S3 cells selectively undergo progressive cell injury and death and are exfoliated into tubular lumina. The necrotic S3 cells are replaced by mitotic division of survivor cells 24 to 48 hr following the ischemic insult. In addition, there was selective damage within tubular cells. Within 5 min of blood reflow following ischemia, the majority of brush border microvilli (MV) in all three PT segments underwent coalescence by membrane fusion and thus were interiorized into the cytoplasm of PT cells. A minority of MV fragmented and were shed into PT lumina, but nephron obstruction by shed membranes was only mild and transient, unlike in the 1-hr ischemia model. Loss of MV reached a maximum at 15 min. By 30 min, MV began to reappear; by 2 hr, large numbers of MV had been regenerated; and by 4 hr, S1 and S2 cells appeared normal. The regenerative process included the luminal repositioning of previously interiorized MV membrane. MV regeneration occurred in S3 segments also, but before the process was complete, the cells developed features of irreversible cellular injury. Glomerular nitration rate (GFR) was 22% of control at 30 min of reflow, rose progressively to 55% of normal by 7 to 8 hr, and was normal at 24 hr. Single nephron filtration rate (SNGFR) was not significantly different from normal throughout. Proximal tubular sodium reabsorption was depressed and urinary sodium excretion increased at 30 min and at 2 to 3 hr, i.e., at times when MV alterations were prominent, but both were normal by 7 to 8 hr when MV in S1 and S2 cells had been fully reconstituted. Our major conclusions are: 1) There is differential susceptibility by cell type to ischemic injury in rat PT. 2) A rapid brush border loss/ regeneration cycle occurs after ischemic injury. 3) Intact brush border may be required for normal sodium reabsorption by PT. Reasons for the GFR/SNGFR discrepancy are unclear, but tubular malfunction may partly explain the phenomenon.
Lésions ischémiques et réparation dans le tube proximal du rat: Différences entre les segments S1, S2, et S3. Des rats ont été soumis à une occlusion unilatérale de l'artère rénale de 25 min puis étudiés 5, 15, 30 min, 1, 2, 4, 8, 16, 24, et 48 hr après l'ischémie. Les modalités des lésions épithéliales et de leur réparation dans les segments S1, S2, et S3 du tube proximal (PT) ont été suivies et les modifications associées du fonctionnement rénal ont été évaluées. Nous avons constaté que les cellules S1 et S2 ne sont lésées que de façon réversible et paraissent à nouveau normales après 4 hr, alors que les cellules S3 subissent un processus progressif de destruction qui aboutit à la mort suivie d'exfoliation dans la lumière tubulaire. Les cellules S3 nécrotiques sont remplacées par des divisions mitotiques des cellules survivantes 24 à 48 hr après l'ischémie. De surcroît il existe une lésion sélective des cellules tubulaires. Dans les 5 min qui suivent le rétablissement de la circulation, la majorité des microvillosités (MV) de la bordure en brosse des trois segments de PT subissent une coalescence par fusion des membranes et sont incluses è l'intérieur du cytoplasme des cellules du PT. Une minorité des MV se fragmentent et sont déversées dans la lumière tubulaire, mais l'obstruction néphronique qu'elles réalisent est modérée et transitoire, à la différence de ce qui se produit dans l'ischémie d'une durée d'une heure. La perte des MV atteint un maximum à 15 min. A 30 min, les MV commencent à réapparaître; à 2 hr un grand nombre de MV ont été régénérées et à 4 hr les cellules S1 et S2 paraissent normales. Le processus de régénération inclue la reposition luminale des MV antérieurement en position intra-cellulaire. La régénération des MV se produit aussi dans les segments S3 mais avant que ce processus ne soit achevé les dextructions cellulaires irréversibles apparaissent. La filtration glomérulaire (GFR) est 22% des contrôles 30 min après le rétablissement de la circulation et augmente progressivement jusqu'a 55% des valeurs normales è 7–8 hr, et redevient normale è 24 hr. Les nitrations glomérulaires individuelles (SNGFR) ne sont pas significativement différentes de la normale tout au long de cette évolution. La réabsorption proximale du sodium est diminuée et 1'excrétion urinaire du sodium augmente à 30 min et à 2–3 hr, c'est-à-dire quand les lésions de MV sont importantes, mais réabsorption proximale et excrétion urinaire redeviennent normales à 7–8 hr, c'est-à-dire quand les MV des cellules S1 et S2 sont complètement reconstituées. Nos conclusions sont: 1) il existe une différence de sensibilité à l'ischémie selon le type cellulaire du tube proximal du rat. 2) Un cycle rapide de destruction et régénération de la bordure en brosse survient après l'ischémie 3) L'intégrité de la bordure en brosse est nécessaire pour une réabsorption normale du sodium par PT. Les raisons de l'absence de correspondance entre GFR et SNGFR ne sont pas claires, un dysfonctionnement tubulaire, cependant, pourrait expliquer en partie ce phénomène.</description><subject>Animals</subject><subject>Cytoplasm - ultrastructure</subject><subject>Glomerular Filtration Rate</subject><subject>Ischemia - etiology</subject><subject>Kidney - blood supply</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidney Tubules, Proximal - pathology</subject><subject>Kidney Tubules, Proximal - physiopathology</subject><subject>Kidney Tubules, Proximal - ultrastructure</subject><subject>Male</subject><subject>Microscopy, Electron</subject><subject>Microvilli - ultrastructure</subject><subject>Rats</subject><subject>Renal Artery Obstruction - physiopathology</subject><subject>Sodium - metabolism</subject><subject>Time Factors</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1978</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkDtPwzAURi3EqzwWZgZPDKgpdhw7Dhsqr0pIDIXZcuzrYppHsRME_56UVkxMV1ff0ad7D0JnlEwoYfJq6Se0yOVE5jtoRHnKEppzvotGhEiepJzJQ3QU4zsZ9oKRA7QvZJqlbITsLJo3qL3BVtd6AVg3FgdYaR-wb3D3BjjoDq9C--VrXeGuL_sKrvGtdw4CNAYi1nXbLH7ROR3jeTr-LZkzHGFRQ9PFE7TndBXhdDuP0ev93cv0MXl6fphNb54Sk4miS2yhbQaCu5Q6nRbaCF1mUtOCc8GoIBmU2mhHSUGA5SkXopQut0aU1BgqHDtGF5ve4dyPHmKnah8NVJVuoO2jyjNKMknyAbzcgCa0MQZwahWG98K3okStjaqlV2ujSq7h821rX9Zg_9CNwiHONjEMn316CCoavxZjfQDTKdv6_1p_AIjsgfo</recordid><startdate>197807</startdate><enddate>197807</enddate><creator>Venkatachalam, Manjeri A.</creator><creator>Bernard, David B.</creator><creator>Donohoe, John F.</creator><creator>Levinsky, Norman G.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>197807</creationdate><title>Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments</title><author>Venkatachalam, Manjeri A. ; Bernard, David B. ; Donohoe, John F. ; Levinsky, Norman G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-d9ad4e65f21fa29ac6ab48a1955631604ebacaf1090e372566b8f7dc6b1cc16f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1978</creationdate><topic>Animals</topic><topic>Cytoplasm - ultrastructure</topic><topic>Glomerular Filtration Rate</topic><topic>Ischemia - etiology</topic><topic>Kidney - blood supply</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidney Tubules, Proximal - pathology</topic><topic>Kidney Tubules, Proximal - physiopathology</topic><topic>Kidney Tubules, Proximal - ultrastructure</topic><topic>Male</topic><topic>Microscopy, Electron</topic><topic>Microvilli - ultrastructure</topic><topic>Rats</topic><topic>Renal Artery Obstruction - physiopathology</topic><topic>Sodium - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Venkatachalam, Manjeri A.</creatorcontrib><creatorcontrib>Bernard, David B.</creatorcontrib><creatorcontrib>Donohoe, John F.</creatorcontrib><creatorcontrib>Levinsky, Norman G.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Venkatachalam, Manjeri A.</au><au>Bernard, David B.</au><au>Donohoe, John F.</au><au>Levinsky, Norman G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>1978-07</date><risdate>1978</risdate><volume>14</volume><issue>1</issue><spage>31</spage><epage>49</epage><pages>31-49</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><abstract>Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments. Rats were subjected to 25 min of unilateral renal artery occlusion and were studied at 5, 15, and 30 min and at 1, 2, 4, 8, 16, 24, and 48 hr following ischemia. The patterns of epithelial injury and repair in proximal tubule (PT) segments S1, S2, and S3 were followed, and associated changes in renal function were determined. We found that S1 and S2 cells alike are only reversibly injured and recover completely to normalcy within 4 hr, whereas S3 cells selectively undergo progressive cell injury and death and are exfoliated into tubular lumina. The necrotic S3 cells are replaced by mitotic division of survivor cells 24 to 48 hr following the ischemic insult. In addition, there was selective damage within tubular cells. Within 5 min of blood reflow following ischemia, the majority of brush border microvilli (MV) in all three PT segments underwent coalescence by membrane fusion and thus were interiorized into the cytoplasm of PT cells. A minority of MV fragmented and were shed into PT lumina, but nephron obstruction by shed membranes was only mild and transient, unlike in the 1-hr ischemia model. Loss of MV reached a maximum at 15 min. By 30 min, MV began to reappear; by 2 hr, large numbers of MV had been regenerated; and by 4 hr, S1 and S2 cells appeared normal. The regenerative process included the luminal repositioning of previously interiorized MV membrane. MV regeneration occurred in S3 segments also, but before the process was complete, the cells developed features of irreversible cellular injury. Glomerular nitration rate (GFR) was 22% of control at 30 min of reflow, rose progressively to 55% of normal by 7 to 8 hr, and was normal at 24 hr. Single nephron filtration rate (SNGFR) was not significantly different from normal throughout. Proximal tubular sodium reabsorption was depressed and urinary sodium excretion increased at 30 min and at 2 to 3 hr, i.e., at times when MV alterations were prominent, but both were normal by 7 to 8 hr when MV in S1 and S2 cells had been fully reconstituted. Our major conclusions are: 1) There is differential susceptibility by cell type to ischemic injury in rat PT. 2) A rapid brush border loss/ regeneration cycle occurs after ischemic injury. 3) Intact brush border may be required for normal sodium reabsorption by PT. Reasons for the GFR/SNGFR discrepancy are unclear, but tubular malfunction may partly explain the phenomenon.
Lésions ischémiques et réparation dans le tube proximal du rat: Différences entre les segments S1, S2, et S3. Des rats ont été soumis à une occlusion unilatérale de l'artère rénale de 25 min puis étudiés 5, 15, 30 min, 1, 2, 4, 8, 16, 24, et 48 hr après l'ischémie. Les modalités des lésions épithéliales et de leur réparation dans les segments S1, S2, et S3 du tube proximal (PT) ont été suivies et les modifications associées du fonctionnement rénal ont été évaluées. Nous avons constaté que les cellules S1 et S2 ne sont lésées que de façon réversible et paraissent à nouveau normales après 4 hr, alors que les cellules S3 subissent un processus progressif de destruction qui aboutit à la mort suivie d'exfoliation dans la lumière tubulaire. Les cellules S3 nécrotiques sont remplacées par des divisions mitotiques des cellules survivantes 24 à 48 hr après l'ischémie. De surcroît il existe une lésion sélective des cellules tubulaires. Dans les 5 min qui suivent le rétablissement de la circulation, la majorité des microvillosités (MV) de la bordure en brosse des trois segments de PT subissent une coalescence par fusion des membranes et sont incluses è l'intérieur du cytoplasme des cellules du PT. Une minorité des MV se fragmentent et sont déversées dans la lumière tubulaire, mais l'obstruction néphronique qu'elles réalisent est modérée et transitoire, à la différence de ce qui se produit dans l'ischémie d'une durée d'une heure. La perte des MV atteint un maximum à 15 min. A 30 min, les MV commencent à réapparaître; à 2 hr un grand nombre de MV ont été régénérées et à 4 hr les cellules S1 et S2 paraissent normales. Le processus de régénération inclue la reposition luminale des MV antérieurement en position intra-cellulaire. La régénération des MV se produit aussi dans les segments S3 mais avant que ce processus ne soit achevé les dextructions cellulaires irréversibles apparaissent. La filtration glomérulaire (GFR) est 22% des contrôles 30 min après le rétablissement de la circulation et augmente progressivement jusqu'a 55% des valeurs normales è 7–8 hr, et redevient normale è 24 hr. Les nitrations glomérulaires individuelles (SNGFR) ne sont pas significativement différentes de la normale tout au long de cette évolution. La réabsorption proximale du sodium est diminuée et 1'excrétion urinaire du sodium augmente à 30 min et à 2–3 hr, c'est-à-dire quand les lésions de MV sont importantes, mais réabsorption proximale et excrétion urinaire redeviennent normales à 7–8 hr, c'est-à-dire quand les MV des cellules S1 et S2 sont complètement reconstituées. Nos conclusions sont: 1) il existe une différence de sensibilité à l'ischémie selon le type cellulaire du tube proximal du rat. 2) Un cycle rapide de destruction et régénération de la bordure en brosse survient après l'ischémie 3) L'intégrité de la bordure en brosse est nécessaire pour une réabsorption normale du sodium par PT. Les raisons de l'absence de correspondance entre GFR et SNGFR ne sont pas claires, un dysfonctionnement tubulaire, cependant, pourrait expliquer en partie ce phénomène.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>682423</pmid><doi>10.1038/ki.1978.87</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0085-2538 |
| ispartof | Kidney international, 1978-07, Vol.14 (1), p.31-49 |
| issn | 0085-2538 1523-1755 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_74104807 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Cytoplasm - ultrastructure Glomerular Filtration Rate Ischemia - etiology Kidney - blood supply Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - pathology Kidney Tubules, Proximal - physiopathology Kidney Tubules, Proximal - ultrastructure Male Microscopy, Electron Microvilli - ultrastructure Rats Renal Artery Obstruction - physiopathology Sodium - metabolism Time Factors |
| title | Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T00%3A04%3A16IST&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=Ischemic%20damage%20and%20repair%20in%20the%20rat%20proximal%20tubule:%20Differences%20among%20the%20S1,%20S2,%20and%20S3%20segments&rft.jtitle=Kidney%20international&rft.au=Venkatachalam,%20Manjeri%20A.&rft.date=1978-07&rft.volume=14&rft.issue=1&rft.spage=31&rft.epage=49&rft.pages=31-49&rft.issn=0085-2538&rft.eissn=1523-1755&rft_id=info:doi/10.1038/ki.1978.87&rft_dat=%3Cproquest_cross%3E74104807%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=74104807&rft_id=info:pmid/682423&rft_els_id=S0085253815319244&rfr_iscdi=true |