Oxidative Stress After Lung Resection Therapy

Lases, E.C.; Duurkens, Vincent A.M.; Gerritsen, Wim B.; Haas, Fred J. L. M.

doi:10.1378/chest.117.4.999

Cited by 70 publications

(39 citation statements)

References 18 publications

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“…Hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO) are examples of free radicals involved in pulmonary lesions (30,31). NO is a relaxing factor derived from the endothelium, endogenously formed from L-arginine through the action of enzymes called NOS (32).…”

Section: Discussionmentioning

confidence: 99%

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

Samano

Pazetti

Prado

et al. 2009

Braz J Med Biol Res

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Pneumonectomy is associated with high mortality and high rates of complications. Postpneumonectomy pulmonary edema is one of the leading causes of mortality. Little is known about its etiologic factors and its association with the inflammatory process. The purpose of the present study was to evaluate the role of pneumonectomy as a cause of pulmonary edema and its association with gas exchange, inflammation, nitric oxide synthase (NOS) expression and vasoconstriction. Forty-two non-specific pathogen-free Wistar rats were included in the study. Eleven animals died during or after the procedure, 21 were submitted to left pneumonectomy and 10 to sham operation. These animals were sacrificed after 48 or 72 h. Perivascular pulmonary edema was more intense in pneumonectomized rats at 72 h (P = 0.0131). Neutrophil density was lower after pneumonectomy in both groups (P = 0.0168). There was higher immunohistochemical expression of eNOS in the pneumonectomy group (P = 0.0208), but no statistically significant difference in the expression of iNOS. The lumen-wall ratio and pO2/FiO2 ratio did not differ between the operated and sham groups after pneumonectomy. Left pneumonectomy caused perivascular pulmonary edema with no elevation of immunohistochemical expression of iNOS or neutrophil density, suggesting the absence of correlation with the inflammatory process or oxidative stress. The increased expression of eNOS may suggest an intrinsic production of NO without signs of vascular reactivity

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Section: Discussionmentioning

confidence: 99%

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

Samano

Pazetti

Prado

et al. 2009

Braz J Med Biol Res

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“…TE A with lo cal anest he tic can impro ve pul mo nary out co mes by at te nu a ting the physi o lo gic res pon se to sur gery, con trol ling pos tope ra ti ve pa in, per mit ting ear li er ex tu ba ti on, and redu cing length of stay. 14,15,22,23 FI GU RE 7: Effects of general anesthesia and general anesthesia + thoracic epidural analgesia (bupivacaine + fentanyl) on plasma nitric oxide (NO) levels in patients underwent elective lung surgery.…”

Section: Discussionmentioning

confidence: 99%

“…10,11 Sin ce the va li dity and cli ni cal re le van ce of pre emp ti ve anal ge si a has be en qu es tio ned and sta ted that any ef fects of pre emp ti ve analge si a may not trans la te in to cli ni cally re le vant long term im pro ve ments in pa ti ent sa tis fac ti on or out co me, [12][13][14] the ob jec ti ve of the pre sent study was to eva lu a te the con tri bu ti on of pre o pe ra ti vely initi a ted TE A on tho ra cic epi du ral pa in re li ef af ter elec ti ve lung sur gery. Alt ho ugh it has be en sug gested that oxi da ti ve stress may oc cur fol lo wing pulmo nary re sec ti on, 15 chan ges in plas ma and bronc ho al ve o lar li pid pe ro xi da ti on and nit ric oxide (NO) le vels are not stu di ed in pa ti ents un der goning lung sur gery. It can be hypot he si sed that the ti ming of epi du ral anal ge si a might be ex pec ted to al ter plas ma or bronc ho al ve o lar la va ge (BAL) le vels of ma lon di al dehy de (MDA) or NO.…”

Section: Effects Of Preoperatively or Postoperatively Initiated Thoramentioning

confidence: 99%

“…In cre a sed ex ha led H 2 O 2 con cen tra ti ons in bre ath con den sate and MDA le vels in uri ne samp les ha ve be en shown in pa ti ents with lung car ci no ma un der going tho ra co tomy. 15 The se fin dings sug gest that oxi da ti ve stress may oc cur fol lo wing lung sur gery. Chan ges in se ve ral mar kers of oxi da ti ve stress follo wing lung re sec ti on ha ve be en de mons tra ted in anot her study.…”

Section: Anesthesiology and Reanimationmentioning

confidence: 99%

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Effects of Preoperatively or Postoperatively Initiated Thoracic Epidural Analgesia in Patients Undergoing Elective Lung Surgery

Çöçelli¹,

Sarimehmetoğlu²,

Demiryürek³

et al. 2010

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: :The go al of this study was to in ves ti ga te the ef fects of pre o pe ra ti vely and pos tope ra ti vely ini ti a ted tho ra cic epi du ral anal ge si a (TE A) on oxi da ti ve stress, res pi ra tory func ti ons and pos to pe ra ti ve pa in in pa ti ents un der go ing elec ti ve lung sur gery. M Ma a t te e r ri i a al l a an nd d M Me et t h ho od ds s: : A tho ra cic epi du ral cat he ter was in ser ted in to all the pa ti ents be fo re sur gery. In Pre op-TE A Gro up (n= 15), bo lus do se of 0.175% bu pi va ca i ne and 15 µg ml -1 fen tanyl (0.1 ml kg -1 ) were ad mi nis te red pre o pe ra ti vely, fol lo wed by a con ti nu o us in fu si on of 0.125% bu pi va ca i ne and 10 µg ml -1 fen tanyl com bi na ti on (0.1 ml kg -1 h -1 ) in trao pe ra ti vely. In Pos top-TE A Gro up (n= 15), no me di ca ti on was ad mi nis te red vi a the epi du ral cat he ter pre o pe ra ti vely. Pos to pe ra ti ve anal ge si a was ma in ta i ned with pa ti ent-con trol led epi du ral anal ge si a (PCA) in both gro ups for 48 h. We as ses sed pe ro pe ra ti ve IV anal ge sic re qu irt ment and pos to pe ra ti ve pa in and anal ge sic con sump ti on, oxi da ti ve stress, he art ra te, blo od pres su re, res pi ra tory func ti ons and si de ef fects. The pos to pe ra ti ve in ten si ve ca re unit and hos pi tal stay du ra ti ons we re re cor ded. Stu dent's t-test, χ 2 -test, Mann-Whit ney U test, and Wil co xon's sig ned rank test we re used for gro up com pa ri sons and sta tis ti cal conc lu si ons. R Re e s su ul lt ts s: : Vi su al ana lo gu e sco res we re al ways hig her du ring co ug hing and at rest, pe ri o pe rati ve he art ra te was increased in Pos top-TE A Gro up (p< 0.05). To tal pe ro pe ra ti ve fen tanyl re qu i re ment and pos to pe ra ti ve anal ge sic con sump ti on vi a PCA we re lo wer in Pre op-TE A Gro up (p< 0.05). Res pi ra tory func ti on tests we re dec re a sed in both gro ups when com pa red to the pre o pe ra ti ve va lu es (p< 0.05), but the dif fe ren ces we re small in Preop-TEA group (p< 0.05). No mar ked ef fect on oxi da ti ve stress was determined and shor ter length of stay in ICU and hos pi tal shorter in Pre op-TE A Gro up (p< 0.05). C Co on nc c l lu u s si i o on n: : The se re sults sug gest that pre o pe ra ti vely ini ti a ted TE A pro vi des bet ter pos to pe ra ti ve pa in re li ef with impro ving the out co me and shor te ning in ten si ve ca re and hos pi tal stay in pa ti ents un der go ing elec ti ve lung sur gery. Ho we ver, TE A had no mar ked ef fect on oxi da ti ve stress in our study. K Ke ey y W Wo or rd ds s: : Anal ge si a, epi du ral; tho ra co tomy; pa in, pos to pe ra ti ve; oxi da ti ve stress Ö ÖZ ZE ET T A Am ma aç ç: : Bu ça lış ma nın ama cı elek tif ak ci ğer cer ra hi si olan has ta lar da ok si datif stress, so lu num fonksi yon la rı ve pos to pe ra tif ağ rı üze ri ne pre o pe ra tif ve pos to pe ra tif baş la tı lan to ra sik epi du ral anal je zi nin (TE A) et ki le ri ni araş tır mak tı. G Ge er re eç...

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“…The successive hits then damage the already vulnerable alveolar-capillary membrane, leading to overt ARDS. The putative second hit may be a variety of known risk factors for post-operative ARDS such as FFP administration [14], mediastinal lymphatic damage [24], non-protective ventilation strategies [17], and oxygen toxicity [25]. This multiple hit model for perioperative ARDS is supported by a rodent pneumonectomy model, which used intratracheal lipopolysaccharide to mimic sepsis-induced lung injury.…”

Section: Pathophysiologymentioning

confidence: 99%

Volume Management and Resuscitation in Thoracic Surgery

Ashes

Slinger

2014

Curr Anesthesiol Rep

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Lung injury following thoracic surgery is a major cause of morbidity and mortality. A consistent risk factor is excessive perioperative fluid administration, not only following pneumonectomy, but also after lesser lung resections and esophageal surgery. Recent insights into the pathophysiology of lung injury after thoracic surgery include the role of the endothelial glycocalyx, pulmonary endothelium, lung lymphatics, and right ventricular dysfunction. While a restrictive approach to fluid administration may reduce the risk of lung injury, there are concerns regarding the risks of acute kidney injury with this approach. Goal-directed approaches may be applied to the thoracic surgical population, and lung ultrasound appears to be a promising new technique to further guide perioperative fluid therapy. There is a paucity of data to guide the choice of crystalloid or colloid solution. Further research is required regarding prevention, diagnosis, and treatment of lung injury following thoracic surgery.

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Oxidative Stress After Lung Resection Therapy

Cited by 70 publications

References 18 publications

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

Effects of Preoperatively or Postoperatively Initiated Thoracic Epidural Analgesia in Patients Undergoing Elective Lung Surgery

Volume Management and Resuscitation in Thoracic Surgery

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