Brann B S, Mayfield S R, Goldstein M, Oh W, Stonestreet B S
Department of Pediatrics, Brown University School of Medicine, Women and Infant's Hospital of Rhode Island, Providence 02905.
Crit Care Med. 1994 Sep;22(9):1453-60. doi: 10.1097/00003246-199409000-00016.
To test the hypothesis that, in newborn piglets, the presence of a tension pneumothorax modifies the cardiovascular responses to hypoxia/hypercarbia.
Prospective laboratory study.
Perinatal cardiovascular research laboratory at a university school of medicine.
Seven newborn piglets.
We sequentially exposed the piglets to a baseline (control I) measure, hypoxia/hypercarbia, tension pneumothorax with normoxia/normocarbia, and tension pneumothorax with hypoxia/hypercarbia added.
Brain and systemic blood pressures and blood flow (radionuclide-microspheres) were measured. Hypoxia/hypercarbia resulted in increased brain perfusion (207 +/- 61% of control, mean +/- SEM, p < .05) and heart perfusion (176 +/- 58% of control, p < .05) and decreased gastrointestinal perfusion (-37 +/- 9% of control, p < .05). Tension pneumothorax with normoxia/normocarbia reduced the cardiac output (-70 +/- 8% of control, p < .05), which was redistributed toward the brain (p < .05) at the expense of the gastrointestinal tract (p < .05). Although this redistribution in cardiac output persisted during tension pneumothorax with hypoxia/hypercarbia added, sustained reductions in cardiac output (-57 +/- 11%, of control, p < .01) were associated with smaller increases in perfusion to brain (55 +/- 54 vs. 207 +/- 61% of control, tension pneumothorax with hypoxia/hypercarbia added, and hypoxia/hypercarbia time periods, respectively, p < .05) and heart (65 +/- 49 vs. 176 +/- 58% of control, tension pneumothorax with hypoxia/hypercarbia added, and hypoxia/hypercarbia time periods, respectively, p < .05) and larger decreases in blood flow to gastrointestinal tract, pancreas, and kidneys (p < .05) than with hypoxia/hypercarbia alone.
Tension pneumothorax-induced reductions in cardiac output limit the hypoxia/hypercarbia-mediated increases in perfusion to brain and heart and accentuate the hypoxia/hypercarbia-related decreases in perfusion to kidneys and splanchnic organs.
验证在新生仔猪中,张力性气胸的存在会改变心血管系统对缺氧/高碳酸血症反应的这一假设。
前瞻性实验室研究。
一所大学医学院的围产期心血管研究实验室。
7只新生仔猪。
我们依次让仔猪接受基线(对照I)测量、缺氧/高碳酸血症、常氧/常碳酸血症下的张力性气胸,以及添加缺氧/高碳酸血症的张力性气胸。
测量脑和全身血压以及血流量(放射性核素微球法)。缺氧/高碳酸血症导致脑灌注增加(为对照值的207±61%,均值±标准误,p<0.05)和心脏灌注增加(为对照值的176±58%,p<0.05),而胃肠道灌注减少(为对照值的-37±9%,p<0.05)。常氧/常碳酸血症下的张力性气胸使心输出量降低(为对照值的-70±8%,p<0.05),心输出量重新分配至脑部(p<0.05),代价是胃肠道灌注减少(p<0.05)。尽管在添加缺氧/高碳酸血症的张力性气胸期间心输出量的这种重新分配持续存在,但心输出量持续降低(为对照值的-57±11%,p<0.01)与脑灌注增加幅度较小(分别为对照值的55±54%与207±61%,添加缺氧/高碳酸血症的张力性气胸期和缺氧/高碳酸血症期,p<0.05)以及心脏灌注增加幅度较小(分别为对照值的65±49%与176±58%,添加缺氧/高碳酸血症的张力性气胸期和缺氧/高碳酸血症期,p<0.05)相关,且与单独缺氧/高碳酸血症相比,胃肠道、胰腺和肾脏的血流量减少幅度更大(p<0.05)。
张力性气胸引起的心输出量降低限制了缺氧/高碳酸血症介导的脑和心脏灌注增加,并加剧了缺氧/高碳酸血症相关的肾脏和内脏器官灌注减少。