Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat

Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat. Intravascular coagulation in the rat kidney was induced by intravenous infusion of thrombin for 1hr. The proximal tubular free-flow (Pt) and stop-flow (Psf) pres...

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Veröffentlicht in:Kidney international 1983-09, Vol.24 (3), p.323-329
Hauptverfasser: Ståhl, Erik, Boberg, Ulf, Larsson, Lars, Rammer, Lennart, Persson, A. Erik G., Rammer, L
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container_start_page 323
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Boberg, Ulf
Larsson, Lars
Rammer, Lennart
Persson, A. Erik G.
Rammer, L
description Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat. Intravascular coagulation in the rat kidney was induced by intravenous infusion of thrombin for 1hr. The proximal tubular free-flow (Pt) and stop-flow (Psf) pressures were measured by micropuncture. Some proximal tubules were obstructed with solid paraffin before infusion of thrombin. In certain rats saralasin or indomethacin was administered for 1hr starting 30min after the thrombin infusion, and the effect on the tubular pressures was studied. The deposition of fibrin in the glomeruli was examined by light and electron microscopy. Pt fell from 15±1 (SE) to 7±2mm Hg (P < 0.05) during the infusion of thrombin. After a brief period of increased pressure the Psf fell rapidly from 37±1 to 17±1mm Hg (P < 0.05). In the previously obstructed nephrons the pressure (Po) increased parallel to the increase in Psf but remained elevated after the infusion of thrombin, 54±2mm Hg. The arterial blood pressure (Pa) increased from 119±2 to 138±3mm Hg (P < 0.05). Saralasin raised the Psf from 15±1 to 19±1mm Hg (P < 0.05) but had no effect on Pt, Po, or Pa. Indomethacin did not influence the pressures. Morphological examination revealed fibrin in all glomeruli of normal nephrons. In the previously obstructed nephrons the deposition of fibrin was almost totally prevented. The results suggest that glomerular filtration is important for deposition of fibrin in the kidney. Effets de l'obstruction tubulaire rénale sur la pression de stop-flow et le dépôt glomérulaire de fibrine pendant la coagulation intravasculaire chez le rat. Une coagulation intravasculaire dans le rein de rat a été induite par la perfusion intraveineuse de thrombine pendant 1hr. Les pressions tubulaires proximales en flux libre (Pt) et en stop-flow (Psf) ont été mesurées par microponction. Certains tubules proximaux étaient obstrués avec de la paraffine solide avant la perfusion de thrombine. Chez certains rats, de la saralasine ou de l'indométhacine ont été administrées pendant 1hr, en commençant 30min après la perfusion de thrombine, et leur effect sur les pressions tubulaires a été étudié. Le dépôt de fibrine dans les glomérules a été examiné en microscopie optique et électronique. Pt a chuté de 15 ± 1 (SE) à 7 ± 2mm Hg (P < 0.05) pendant la perfusion de thrombine. Après une brève période d'élévation de la pression, Psf a chuté rapidement de 37 ± 1 à 17 ± 1mm Hg (P < 0.
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After a brief period of increased pressure the Psf fell rapidly from 37±1 to 17±1mm Hg (P < 0.05). In the previously obstructed nephrons the pressure (Po) increased parallel to the increase in Psf but remained elevated after the infusion of thrombin, 54±2mm Hg. The arterial blood pressure (Pa) increased from 119±2 to 138±3mm Hg (P < 0.05). Saralasin raised the Psf from 15±1 to 19±1mm Hg (P < 0.05) but had no effect on Pt, Po, or Pa. Indomethacin did not influence the pressures. Morphological examination revealed fibrin in all glomeruli of normal nephrons. In the previously obstructed nephrons the deposition of fibrin was almost totally prevented. The results suggest that glomerular filtration is important for deposition of fibrin in the kidney. Effets de l'obstruction tubulaire rénale sur la pression de stop-flow et le dépôt glomérulaire de fibrine pendant la coagulation intravasculaire chez le rat. 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Erik G.</creatorcontrib><creatorcontrib>Rammer, L</creatorcontrib><title>Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description><![CDATA[Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat. Intravascular coagulation in the rat kidney was induced by intravenous infusion of thrombin for 1hr. The proximal tubular free-flow (Pt) and stop-flow (Psf) pressures were measured by micropuncture. Some proximal tubules were obstructed with solid paraffin before infusion of thrombin. In certain rats saralasin or indomethacin was administered for 1hr starting 30min after the thrombin infusion, and the effect on the tubular pressures was studied. The deposition of fibrin in the glomeruli was examined by light and electron microscopy. Pt fell from 15±1 (SE) to 7±2mm Hg (P < 0.05) during the infusion of thrombin. After a brief period of increased pressure the Psf fell rapidly from 37±1 to 17±1mm Hg (P < 0.05). In the previously obstructed nephrons the pressure (Po) increased parallel to the increase in Psf but remained elevated after the infusion of thrombin, 54±2mm Hg. The arterial blood pressure (Pa) increased from 119±2 to 138±3mm Hg (P < 0.05). Saralasin raised the Psf from 15±1 to 19±1mm Hg (P < 0.05) but had no effect on Pt, Po, or Pa. Indomethacin did not influence the pressures. Morphological examination revealed fibrin in all glomeruli of normal nephrons. In the previously obstructed nephrons the deposition of fibrin was almost totally prevented. The results suggest that glomerular filtration is important for deposition of fibrin in the kidney. Effets de l'obstruction tubulaire rénale sur la pression de stop-flow et le dépôt glomérulaire de fibrine pendant la coagulation intravasculaire chez le rat. Une coagulation intravasculaire dans le rein de rat a été induite par la perfusion intraveineuse de thrombine pendant 1hr. Les pressions tubulaires proximales en flux libre (Pt) et en stop-flow (Psf) ont été mesurées par microponction. Certains tubules proximaux étaient obstrués avec de la paraffine solide avant la perfusion de thrombine. Chez certains rats, de la saralasine ou de l'indométhacine ont été administrées pendant 1hr, en commençant 30min après la perfusion de thrombine, et leur effect sur les pressions tubulaires a été étudié. Le dépôt de fibrine dans les glomérules a été examiné en microscopie optique et électronique. Pt a chuté de 15 ± 1 (SE) à 7 ± 2mm Hg (P < 0.05) pendant la perfusion de thrombine. Après une brève période d'élévation de la pression, Psf a chuté rapidement de 37 ± 1 à 17 ± 1mm Hg (P < 0.05). Dans les néphrons préalablement obstrués, la pression (P0) s'est élevée parallèlement à l'augmentation de Psf mais est restée élevée après la perfusion de thrombine, 54 ± 2mm Hg. La pression artérielle (Pa) s'est élevée de 119 ± 2 à 138 ± 3mm Hg (P < 0.05). La saralasine a augmenté la Psf de 15 ± 1 à 19 ± 1mm Hg (P < 0.05), mais n'a pas eu d'effet sur Pt, Po ou Pa. L'indométhacine n'a pas influencé ces pressions. L'examen morphologique a révélé de la fibrine dans tous les glomérules des néphrons normaux. Dans les néphrons préalablement obstrués, le dépôt de fibrine était pratiquement complètement prévenu. Ces résultats suggèrent que la filtration glomérulaire est importante pour le dépôt de fibrine dans le rein.]]></description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Coagulation</subject><subject>Constriction, Pathologic</subject><subject>Fibrin - metabolism</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Indomethacin - pharmacology</subject><subject>Kidney - blood supply</subject><subject>Kidney - pathology</subject><subject>Kidney Glomerulus - metabolism</subject><subject>Kidney Tubules - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Platelet diseases and coagulopathies</subject><subject>Pressure</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Saralasin - pharmacology</subject><subject>Thrombin</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1983</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkc-P1CAUgInRrLOrJ89GDsaL6QiltPRoNutqsokXPRMK7404nVKBrvFP8L-WmU7mZEL49b73Hvkg5BVnW86E-rD3W94rseUtf0I2XNai4p2UT8mGMSWrWgr1nFyn9JOVcy_YFblq20bWTG7I3ztEsJkGpBEmM9K8DMtoIg1DynGx2YeJlpFymCscw286R0hpiUDN5OhuDAeIpwQHc0h-5ZGiH6KfqFvKvKN-ytE8mmRPpA1mVzYntDD5B9Bo8gvyDM2Y4OV5vSHfP919u_1cPXy9_3L78aGyTc1yZQ2iZNIohA4c8la0rjN9p2Q_ICIHwYaaOzO0otzWDrEWDe_6RllANjBxQ96tdecYfi2Qsj74ZGEczQRhSVqxTtW8FwV8v4I2hpQioJ6jP5j4R3Omj-L13uujeF3EF_r1uewyHMBd2LPpEn97jhcNZsRoJuvTBeubmit5bPpmxSaTi-RLfO-PndZGciWgSHr0EHWyHiYLzsfyk9oF_98H_gNI3Kua</recordid><startdate>198309</startdate><enddate>198309</enddate><creator>Ståhl, Erik</creator><creator>Boberg, Ulf</creator><creator>Larsson, Lars</creator><creator>Rammer, Lennart</creator><creator>Persson, A. 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Erik G.</creatorcontrib><creatorcontrib>Rammer, L</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ståhl, Erik</au><au>Boberg, Ulf</au><au>Larsson, Lars</au><au>Rammer, Lennart</au><au>Persson, A. Erik G.</au><au>Rammer, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>1983-09</date><risdate>1983</risdate><volume>24</volume><issue>3</issue><spage>323</spage><epage>329</epage><pages>323-329</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract><![CDATA[Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat. Intravascular coagulation in the rat kidney was induced by intravenous infusion of thrombin for 1hr. The proximal tubular free-flow (Pt) and stop-flow (Psf) pressures were measured by micropuncture. Some proximal tubules were obstructed with solid paraffin before infusion of thrombin. In certain rats saralasin or indomethacin was administered for 1hr starting 30min after the thrombin infusion, and the effect on the tubular pressures was studied. The deposition of fibrin in the glomeruli was examined by light and electron microscopy. Pt fell from 15±1 (SE) to 7±2mm Hg (P < 0.05) during the infusion of thrombin. After a brief period of increased pressure the Psf fell rapidly from 37±1 to 17±1mm Hg (P < 0.05). In the previously obstructed nephrons the pressure (Po) increased parallel to the increase in Psf but remained elevated after the infusion of thrombin, 54±2mm Hg. The arterial blood pressure (Pa) increased from 119±2 to 138±3mm Hg (P < 0.05). Saralasin raised the Psf from 15±1 to 19±1mm Hg (P < 0.05) but had no effect on Pt, Po, or Pa. Indomethacin did not influence the pressures. Morphological examination revealed fibrin in all glomeruli of normal nephrons. In the previously obstructed nephrons the deposition of fibrin was almost totally prevented. The results suggest that glomerular filtration is important for deposition of fibrin in the kidney. Effets de l'obstruction tubulaire rénale sur la pression de stop-flow et le dépôt glomérulaire de fibrine pendant la coagulation intravasculaire chez le rat. Une coagulation intravasculaire dans le rein de rat a été induite par la perfusion intraveineuse de thrombine pendant 1hr. Les pressions tubulaires proximales en flux libre (Pt) et en stop-flow (Psf) ont été mesurées par microponction. Certains tubules proximaux étaient obstrués avec de la paraffine solide avant la perfusion de thrombine. Chez certains rats, de la saralasine ou de l'indométhacine ont été administrées pendant 1hr, en commençant 30min après la perfusion de thrombine, et leur effect sur les pressions tubulaires a été étudié. Le dépôt de fibrine dans les glomérules a été examiné en microscopie optique et électronique. Pt a chuté de 15 ± 1 (SE) à 7 ± 2mm Hg (P < 0.05) pendant la perfusion de thrombine. Après une brève période d'élévation de la pression, Psf a chuté rapidement de 37 ± 1 à 17 ± 1mm Hg (P < 0.05). Dans les néphrons préalablement obstrués, la pression (P0) s'est élevée parallèlement à l'augmentation de Psf mais est restée élevée après la perfusion de thrombine, 54 ± 2mm Hg. La pression artérielle (Pa) s'est élevée de 119 ± 2 à 138 ± 3mm Hg (P < 0.05). La saralasine a augmenté la Psf de 15 ± 1 à 19 ± 1mm Hg (P < 0.05), mais n'a pas eu d'effet sur Pt, Po ou Pa. L'indométhacine n'a pas influencé ces pressions. L'examen morphologique a révélé de la fibrine dans tous les glomérules des néphrons normaux. Dans les néphrons préalablement obstrués, le dépôt de fibrine était pratiquement complètement prévenu. Ces résultats suggèrent que la filtration glomérulaire est importante pour le dépôt de fibrine dans le rein.]]></abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>6645205</pmid><doi>10.1038/ki.1983.161</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Animals
Biological and medical sciences
Blood Coagulation
Constriction, Pathologic
Fibrin - metabolism
Hematologic and hematopoietic diseases
Indomethacin - pharmacology
Kidney - blood supply
Kidney - pathology
Kidney Glomerulus - metabolism
Kidney Tubules - physiopathology
Male
Medical sciences
Platelet diseases and coagulopathies
Pressure
Rats
Rats, Inbred Strains
Saralasin - pharmacology
Thrombin
title Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat
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