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"Latar Belakang : Striktur uretra adalah kelainan berupa penyempitan lumen uretra akibat terbentuknya jaringan parut yang melibatkan epitel dan jaringan erektil korpus spongiosum. Patofisiologi kelainan ini belum sepenuhnya diketahui. Degradasi matriks ekstraselular diduga berperan penting dalam terjadinya striktur uretra. Matriks metaloproteinase (MMP-1), Tissue inhibitor of metalloproteinase (TIMP-1) dan Transforming growth factor (TGF-β) berperan pada degradasi matriks ekstraselular. Tujuan penelitian ini adalah untuk mengetahui peran MMP-1, TIMP-1, rasio TIMP- 1/MMP-1 dan TGF-β pada fase remodeling striktur uretra dan hubungannya dengan kolagen total dan kolagen tipe-I. Metode : Penelitian eksperimental ini dilakukan pada kelinci New Zealand jantan dewasa yang dibagi menjadi dua kelompok, yaitu kelompok kelinci yang dilakukan insisi mukosa dan elektrokoagulasi untuk menimbulkan striktur uretra (Kelompok kelinci striktur uretra) dan kelompok kelinci kontrol. Dilakukan pengamatan dan eutanasia pada empat kelinci pada masing-masing kelompok pada hari ke-7, 14, 21, 28, dan 56. Dilakukan pemeriksaan adanya hambatan pada uretra dengan kateter no 8F selanjutnya dilakukan pemeriksaan hematoksilin-eosin untuk melihat gambaran histopatologi, pemeriksaan Trichrome-Masson untuk melihat kolagen total, pemeriksaan imunohistokimia untuk melihat kolagen tipe-I. Pemeriksaan ELISA untuk mengukur kadar MMP-1, TIMP-1dan TGF-β. Rasio MMP-1/TIMP-1 dihitung dengan membagi kadar MMP-1 dengan kadar TIMP-1. Persentase kolagen total dan persentase kolagen tipe-1 dihitung dengan menggunakan program image J 1,46q. Uji statistik dengan General Linear Model. Hasil: Pada kelompok striktur uretra didapatkan kadar MMP-1 yang lebih rendah, TIMP-1 yang lebih tinggi, rasio MMP-1/TIMP-1 yang lebih rendah, dan TGF-β yang lebih tinggi bila dibandingkan dengan kelompok kontrol. Terdapat korelasi positif kuat antara kadar TGF-β dengan persentase kolagen total (r = 0,617, p: 0,004) dan korelasi lemah antara kadar MMP-1 dengan persentase kolagen total (r = 0,561, p: 0,010). Simpulan: Striktur uretra tidak hanya disebabkan oleh dekomposisi kolagen tetapi juga oleh ketidakseimbangan degradasi matriks ekstraselular yang ditandai oleh menurunnya MMP-1, meningkatnya TIMP-1 dan menurunnya rasio MMP-1/TIMP-1.

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Background: Urethral stricture is a narrowing of urethral lumen due to scar formation involving epithelium and corpus spongiosum. The pathophysiology process of this abnormality is not fully understood. Extracellular matrix degradation supposed to play an important role as the etiology of urethral stricture. Matrix metalloprotein (MMP-1), Tissue inhibitor of metalloprotein (TIMP-1) and Transforming growth factor-β (TGF-β) are involved in matrix extraselular degradation. The purpose of this study was to investigate the role of MMP-1, TIMP-1, MMP-1/TIMP-1 rasio and TGF-β at remodeling phase of urethral stricture and their correlations to total collagen and collagen type I.

Metode: This study was an experimental study in adult male New Zealand rabbits, divided into two groups, namely the urethral stricture group and the control group. Euthanasia was performed in four rabbits of each group on days 7, 14, 21, 28, and 56. Urethral stricture was confirmed by urethral catether no 8F. Several laboratory examination were done, including haematoxylin-eosin, trichrome-masson, immune- histochemistry and ELISA to determine levels of MMP-1, TIMP-1, TGF-β, MMP- 1/TIMP-1 rasio, total collagen and collagen type-1. Percentage of total collagen and collagen type I were counted with image J 1.46q programme. General linear model was used for statistical analysis

Results : This study found level of MMP-1 was lower, TIMP-1 was higher, MMP-1/ TIMP-1 rasio was lower, and TGF-β was higher in the urethral stricture group compared with control. There was a strong positif correlation between TGF-β level and total collagen percentage (r = 0.617; p = 0.004) and weak positive correlation between MMP-1 level with total collagen percentage (r = 0.561; p = 0.010).

Conclusions : Urethral stricture is not only caused by collagen decomposition but also by imbalance of extracellular matrix degradation which is marked by decreased MMP-1 level and MMP-1/TIMP-1 rasio, increased TIMP-1 level."

"ABSTRAKLatar belakangHipoperfusi splanknik tetap terjadi pada pasca-resusitasi renjatan perdarahan. Hipoperfusi splanknik dapat menimbulkan kerusakan mukosa usus, translokasi bakteri usus ke sistemik, dan kemungkinan gagal organ multipel. Tujuan penelitian ini adalah mempelajari pengaruh anestesi epidural torasik (AEV) Iidokain terhadap perubahan perfusi splanknik pasca-resusitasi renjatan perdarahan.Metode dan Bahan Penelitian Suatu penelitian acak tersamar ganda dilakukan pada 16 ekor Macaca nemestrina, terdiri atas kelompok kontrol (n = 8) dan AET (n = 8). Kedua kelompok mendapat ketamin pada tahap persiapan, dan dilakukan pemasangan kateter epidural pada 17-8, selanjutnya diberikan anestesia-umum. Renjatan perdarahan dicapai dengan cara darah dialirkan secara pasif keluar tubuh secara bertahap sehingga tekanan arteri rerata (TAR) 40 mm Hg dan dipertahankan selama 60 menit. Resusitasi dilakukan dengan cara darah dikembalikan disertai pemberian kristaloid. Pasca-resusitasi, kelompok AET mendapatkan lidokain 2% dan kontrol salin melalui kateter epidurai. Pemantauan tekanan parsial CO2 gaster (PQCOQ), selisih tekanan CO2 gaster - arteri [P(g-a)CO2], pH mukosa gaster (pHi), parameter hemodinamik, asam basa dan Iaktat darah dilakukan secara berkala. Kadar norepinefrin dan kortisol diukur pada menit 90, kultur darah, dilakukan pada saat prarenjatan dan menit 180, biopsi usus, hati dan ginjal dilakukan saat prarenjatan, menit 60, 90, dan 270 selama penelitian.HasilNilai PgCO; lebih rendah secara bermakna pada kelompok TEA pada menit ke- 90 (11,0 (SD 8,0) vs. 19,0 (8,0) kPa; p=0,038), 150 (9,9 (8,-4) vs. (19,5 (8,6) kPa; p=0,023), dan pada akhir penelitian (270 menit) (10,1 (8,3) vs. 20,7 (10,0) kPa; p=0,041); di mana P(g-a) CO2 lebih rendah pada kelompok TEA pada menit ke-150 dan 270; and pHi lebih rendah pada kelompok TEA pada menit ke-90 and 150. Parameter Iain tidak menunjukkan perbedaan yang bermakna. Translokasi bakteri ditemukan Iebih sedikit pada kelompok AET dari pada kontrol. Histopatologi duodenum kelompok AEI' lebih sedikit mengalami perburukan dari pada kontrol (p = 0,0456).KesimpulanPerfusi splanknik kelompok AEl'|id0kBir1 pascz-rresusitasi renjatan perdarahan lebih baik dari pada kontrol.

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ABSTRACT

Background

Splanchnic hypoperfusion still exists despite of successful resuscitation of hemorrhagic shock. Studies have shown that splanchnic hypoperfusion may lead to increased permeability of gastrointestinal mucosa, bacterial translocation, and increased risk of developing multiple organ failure. The aim of this study was to assess the effect of lidocaine thoracic epidural anesthesia (TEA) on splanchnic perfusion in post-resuscitation of hemorrhagic shock.

Methods

This is a double blind randomized controlled study. Sixteen Macaca nemescrinas were randomly selected into two groups, i.e TEA group (n=8) and control (n=8). Both groups were anesthetized with ketamine during preparation, an epidural catheter was inserted at 17-8, then were given the same anesthesia procedure. Hemorrhagic shock was induced by drawing blood gradually to a mean arterial pressure (MAP) of 40 mm Hg, and maintained for 60 minutes. Animals were then resuscitated by their own blood and crystalloid solution. Post resuscitation, the control group were given salin epidurally and the TEA group Iidocaine 2%. During this study PgCO2, P(g-a)CO2, pHi, hemodynamic parameters, acid-base balance and lactate acid were monitored. Blood norepinephrine and cortisol concentrations were measured at 90 minute, blood sample at preshock and 180 minute were cultured and intestinal, liver, and kidney biopsies were done at preshock, 60 minute, 90 minute, and 270 minute during timeof study.

Results

Means of PgCO2 were consistently significantly lower in the TEA group compared to control at 90 minute (11.0 (SD 8.0) vs. 19.0 (8.0) kPa; p=0.038), 150 minute (9.9 (8.4) vs. (19.5 (8.6) kPa; p=0.023, and at the end of this study (270 minute) (10.1 (8.3) vs. 20] (10.0) kPa; p=.041); whereas P(g~a)CO, were lower in TEA group at 150 and 270 minute and pHi were lower in TEA group at 90 and 150 minute. Other parameters did not show significant difference between groups. Bacterial translocations were less in TEA group than in control group. Duodenum histopathology deterioration was less in the TEA group than in control (p = 0,0456).

Conclusion

Splanchnic perfusion in hemorrhagic shock post resuscitation in TEA Iidocaine group as better than in control group."

"ABSTRAKLatar belakangHipoperfusi splanknik tetap terjadi pada pasca-resusitasi renjatan perdarahan. Hipoperfusi splanknik dapat menimbulkan kerusakan mukosa usus, translokasi bakteri usus ke sistemik, dan kemungkinan gagal organ multipel. Tujuan penelitian ini adalah mempelajari pengaruh anestesi epidural torasik (AEV) Iidokain terhadap perubahan perfusi splanknik pasca-resusitasi renjatan perdarahan.Metode dan Bahan Penelitian Suatu penelitian acak tersamar ganda dilakukan pada 16 ekor Macaca nemestrina, terdiri atas kelompok kontrol (n = 8) dan AET (n = 8). Kedua kelompok mendapat ketamin pada tahap persiapan, dan dilakukan pemasangan kateter epidural pada 17-8, selanjutnya diberikan anestesia-umum. Renjatan perdarahan dicapai dengan cara darah dialirkan secara pasif keluar tubuh secara bertahap sehingga tekanan arteri rerata (TAR) 40 mm Hg dan dipertahankan selama 60 menit. Resusitasi dilakukan dengan cara darah dikembalikan disertai pemberian kristaloid. Pasca-resusitasi, kelompok AET mendapatkan lidokain 2% dan kontrol salin melalui kateter epidurai. Pemantauan tekanan parsial CO2 gaster (PQCOQ), selisih tekanan CO2 gaster - arteri [P(g-a)CO2], pH mukosa gaster (pHi), parameter hemodinamik, asam basa dan Iaktat darah dilakukan secara berkala. Kadar norepinefrin dan kortisol diukur pada menit 90, kultur darah, dilakukan pada saat prarenjatan dan menit 180, biopsi usus, hati dan ginjal dilakukan saat prarenjatan, menit 60, 90, dan 270 selama penelitian.HasilNilai PgCO; lebih rendah secara bermakna pada kelompok TEA pada menit ke- 90 (11,0 (SD 8,0) vs. 19,0 (8,0) kPa; p=0,038), 150 (9,9 (8,-4) vs. (19,5 (8,6) kPa; p=0,023), dan pada akhir penelitian (270 menit) (10,1 (8,3) vs. 20,7 (10,0) kPa; p=0,041); di mana P(g-a) CO2 lebih rendah pada kelompok TEA pada menit ke-150 dan 270; and pHi lebih rendah pada kelompok TEA pada menit ke-90 and 150. Parameter Iain tidak menunjukkan perbedaan yang bermakna. Translokasi bakteri ditemukan Iebih sedikit pada kelompok AET dari pada kontrol. Histopatologi duodenum kelompok AEI' lebih sedikit mengalami perburukan dari pada kontrol (p = 0,0456).KesimpulanPerfusi splanknik kelompok AEl'|id0kBir1 pascz-rresusitasi renjatan perdarahan lebih baik dari pada kontrol.

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ABSTRACT

Background

Splanchnic hypoperfusion still exists despite of successful resuscitation of hemorrhagic shock. Studies have shown that splanchnic hypoperfusion may lead to increased permeability of gastrointestinal mucosa, bacterial translocation, and increased risk of developing multiple organ failure. The aim of this study was to assess the effect of lidocaine thoracic epidural anesthesia (TEA) on splanchnic perfusion in post-resuscitation of hemorrhagic shock.

Methods

This is a double blind randomized controlled study. Sixteen Macaca nemescrinas were randomly selected into two groups, i.e TEA group (n=8) and control (n=8). Both groups were anesthetized with ketamine during preparation, an epidural catheter was inserted at 17-8, then were given the same anesthesia procedure. Hemorrhagic shock was induced by drawing blood gradually to a mean arterial pressure (MAP) of 40 mm Hg, and maintained for 60 minutes. Animals were then resuscitated by their own blood and crystalloid solution. Post resuscitation, the control group were given salin epidurally and the TEA group Iidocaine 2%. During this study PgCO2, P(g-a)CO2, pHi, hemodynamic parameters, acid-base balance and lactate acid were monitored. Blood norepinephrine and cortisol concentrations were measured at 90 minute, blood sample at preshock and 180 minute were cultured and intestinal, liver, and kidney biopsies were done at preshock, 60 minute, 90 minute, and 270 minute during timeof study.

Results

Means of PgCO2 were consistently significantly lower in the TEA group compared to control at 90 minute (11.0 (SD 8.0) vs. 19.0 (8.0) kPa; p=0.038), 150 minute (9.9 (8.4) vs. (19.5 (8.6) kPa; p=0.023, and at the end of this study (270 minute) (10.1 (8.3) vs. 20] (10.0) kPa; p=.041); whereas P(g~a)CO, were lower in TEA group at 150 and 270 minute and pHi were lower in TEA group at 90 and 150 minute. Other parameters did not show significant difference between groups. Bacterial translocations were less in TEA group than in control group. Duodenum histopathology deterioration was less in the TEA group than in control (p = 0,0456).

Conclusion

Splanchnic perfusion in hemorrhagic shock post resuscitation in TEA Iidocaine group as better than in control group."