title: Effect of donor pre-mortem hypoxia and hypotension on graft function and start of warm ischemia in donation after cardiac death lung transplantation.
abstract: BACKGROUND
  The start of warm ischemic time (WIT) of donor lungs in donation after cardiac death (DCD) is not clearly defined. We investigated the effect of donor pre-mortem hypotension and hypoxia to determine which physiologic factor is the determinant of WIT onset in controlled DCD lung transplantation.
  
  
  METHODS
  Twenty mechanically-ventilated donor pigs were placed in 4 groups (n = 5 each) and exposed to each of the pseudo-agonal conditions for 60 minutes: (1) control group, no intervention and optimum ventilation, followed by cardiac arrest; (2) hypotension (HT) group, controlled cardiac tamponade reducing systolic blood pressure to <50 mm Hg, followed by cardiac arrest; (3) hypoventilation (HV) group, ventilation with room air at 5 breaths/min, followed by cardiac arrest; (4) non-circulation (NC) group, initial cardiac arrest, followed by a 60-minute standoff time. The lung graft was retrieved and the left lung was transplanted to the recipient. Graft function was evaluated for 4 hours after contralateral pulmonary artery ligation. The reperfusion injury was evaluated based on tissue cytokine expression, wet weight-to-dry weight ratio, and histology at the end of the reperfusion period.
  
  
  RESULTS
  Impaired post-transplant graft function was seen in the HV group, which had significantly poorer oxygenation during the reperfusion period than the other groups (p < 0.001). The HV group also had higher tissue levels of interleukin-8 (p < 0.05), a higher wet weight-to-dry weight ratio (p < 0.05), and histologic findings of graft tissue injury than the control group. The difference in these parameters among the control, HT, and NC groups was not significant.
  
  
  CONCLUSIONS
  Only pre-mortem hypoxia provoked by hypoventilation significantly impaired lung graft function in DCD lung transplantation. Ventilatory rather than circulatory deterioration can trigger the onset of warm ischemia.
authors.affiliation: Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama, Japan.
authors.forename: Kentaroh
authors.initials: K
authors.lastname: Miyoshi
authors.forename: Takahiro
authors.initials: T
authors.lastname: Oto
authors.forename: Shinji
authors.initials: S
authors.lastname: Otani
authors.forename: Shin
authors.initials: S
authors.lastname: Tanaka
authors.forename: Masaaki
authors.initials: M
authors.lastname: Harada
authors.forename: Tomokazu
authors.initials: T
authors.lastname: Kakishita
authors.forename: Shiro
authors.initials: S
authors.lastname: Hori
authors.forename: Naohisa
authors.initials: N
authors.lastname: Waki
authors.forename: Masaomi
authors.initials: M
authors.lastname: Yamane
authors.forename: Shinichiro
authors.initials: S
authors.lastname: Miyoshi
mesh_terms: D000818:Animals; D003643:Death; D007022:Hypotension / Q000150:complications*; D000860:Hypoxia / Q000150:complications*; D008168:Lung / Q000503:physiopathology*; D016040:Lung Transplantation; D013552:Swine; D052096:Warm Ischemia