Pathophysiological basis of smoke inhalation injury

被引：65

作者：

Murakami, K ^{[1
]}

Traber, DL ^{[1
]}

机构：

[1] Univ Texas, Med Branch, Dept Anesthesiol, Galveston, TX 77555 USA

来源：

NEWS IN PHYSIOLOGICAL SCIENCES | 2003年 / 18卷

关键词：

D O I：

10.1152/nips.01427.2002

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Smoke inhalation injury results in serious respiratory failure. When smoke inhalation injury is combined with burn injury or pneumonia, the physiological responses are different and more severe than those of smoke inhalation injury alone. Treatment strategies should be planned based on these pathophysiological aspects.

引用

页码：125 / 129

页数：5

共 15 条

[1] LUNG EDEMA FORMATION FOLLOWING INHALATION INJURY - ROLE OF THE BRONCHIAL BLOOD-FLOW [J].

ABDI, S ;

HERNDON, DN ;

TRABER, LD ;

ASHLEY, KD ;

STOTHERT, JC ;

MAGUIRE, J ;

BUTLER, R ;

TRABER, DL .

JOURNAL OF APPLIED PHYSIOLOGY, 1991, 71 (02) :727-734

[2] EFFECTS OF ALLOPURINOL ON SMOKE-INHALATION IN THE OVINE MODEL [J].

AHN, SY ;

SUGI, K ;

TALKE, P ;

THEISSEN, JL ;

LINARES, HA ;

TRABER, LD ;

HERNDON, DN ;

TRABER, DL .

JOURNAL OF APPLIED PHYSIOLOGY, 1990, 68 (01) :228-234

[3]

BASADRE JO, 1988, SURGERY, V104, P208

[4] Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. [J].

Brower, RG ;

Matthay, MA ;

Morris, A ;

Schoenfeld, D ;

Thompson, BT ;

Wheeler, A ;

Wiedemann, HP ;

Arroliga, AC ;

Fisher, CJ ;

Komara, JJ ;

Perez-Trepichio, P ;

Parsons, PE ;

Wolkin, R ;

Welsh, C ;

Fulkerson, WJ ;

MacIntyre, N ;

Mallatratt, L ;

Sebastian, M ;

McConnell, R ;

Wilcox, C ;

Govert, J ;

Thompson, D ;

Clemmer, T ;

Davis, R ;

Orme, J ;

Weaver, L ;

Grissom, C ;

Eskelson, M ;

Young, M ;

Gooder, V ;

McBride, K ;

Lawton, C ;

d'Hulst, J ;

Peerless, JR ;

Smith, C ;

Brownlee, J ;

Pluss, W ;

Kallet, R ;

Luce, JM ;

Gottlieb, J ;

Elmer, M ;

Girod, A ;

Park, P ;

Daniel, B ;

Gropper, M ;

Abraham, E ;

Piedalue, F ;

Glodowski, J ;

Lockrem, J ;

McIntyre, R .

NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (18) :1301-1308

[5] Ligation of the bronchial artery in sheep attenuates early pulmonary changes following exposure to smoke [J].

Efimova, O ;

Volokhov, AB ;

Iliaifar, S ;

Hales, CA .

JOURNAL OF APPLIED PHYSIOLOGY, 2000, 88 (03) :888-893

[6] Nitric oxide synthase inhibition restores hypoxic pulmonary vasoconstriction in sepsis. [J].

Fischer, SR ;

Deyo, DJ ;

Bone, HG ;

McGuire, R ;

Traber, LD ;

Traber, DL .

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1997, 156 (03) :833-839

[7] Human and rat neutrophils constitutively express neural nitric oxide synthase mRNA [J].

Greenberg, SS ;

Ouyang, J ;

Zhao, XF ;

Giles, TD .

NITRIC OXIDE-BIOLOGY AND CHEMISTRY, 1998, 2 (03) :203-212

[8] THE MORPHOLOGY OF SMOKE-INHALATION INJURY IN SHEEP [J].

HUBBARD, GB ;

LANGLINAIS, PC ;

SHIMAZU, T ;

OKERBERG, CV ;

MASON, AD ;

PRUITT, BA .

JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1991, 31 (11) :1477-1486

[9] Activation of poly(ADP-ribose) polymerase-1 is a central mechanism of lipopolysaccharide-induced acute lung inflammation [J].

Liaudet, L ;

Pacher, P ;

Mabley, JG ;

Virág, L ;

Soriano, FG ;

Haskó, G ;

Szabó, C .

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2002, 165 (03) :372-377

[10] Gabexate mesilate, a synthetic protease inhibitor, attenuates endotoxin-induced pulmonary vascular injury by inhibiting tumor necrosis factor production by monocytes [J].

Murakami, K ;

Okajima, K ;

Uchiba, M ;

Okabe, H ;

Takatsuki, K .

CRITICAL CARE MEDICINE, 1996, 24 (06) :1047-1053

← 1 2 →