中国小儿急救医学
中國小兒急救醫學
중국소인급구의학
CHINESE PEDIATRIC EMERGENCY MEDICINE
2008年
6期
534-536
,共3页
赵宁%夏红卫%刘绍基%文伟%陶莉%陈秀英
趙寧%夏紅衛%劉紹基%文偉%陶莉%陳秀英
조저%하홍위%류소기%문위%도리%진수영
妊娠期高血压疾病%新生儿肺出血%内皮素-1%一氧化氮
妊娠期高血壓疾病%新生兒肺齣血%內皮素-1%一氧化氮
임신기고혈압질병%신생인폐출혈%내피소-1%일양화담
Hypertension,pregnancy-induced%Pulmonary hemorrhage%ET-1%NO
目的 了解妊娠期高血压疾病与新生儿肺出血之间的关系.方法 在2005年6月至2007年6月对四家医院收治的正常孕妇(孕A组)、妊娠期高血压孕妇(孕B组)及其所产新生儿(婴A组、婴B组)进行血内皮素(ET)-1和NO水平测定,并比较正常孕妇与妊娠期高血压孕妇所产新生儿肺出血的发生率.结果 孕B组及婴B组分别较孕A组及婴A组血ET-1水平增高[(6.66±2.73)ng/L vs (3.24±1.74)ng/L,(6.42±3.17)ng/L vs (3.91±2.02)?ng/L],NO水平降低[(85.80±46.15)μmol/L vs (110.85±76.56)μmol/L,(82.73±48.51)μmol/L vs(122.23±75.08)μmol/L],差异有非常显著性(P<0.002,P<0.001).婴B组新生儿肺出血发生率为13.3%(20/155例),明显高于婴A组3.9%(5/128例),差异有显著性(χ2=5.9,P=0.01).结论 妊娠期高血压孕妇NO生成减少及ET-1异常升高,导致胎盘血管强烈收缩,胎儿发生缺血缺氧,可最终引起新生儿肺出血.及早防治妊娠期高血压,可降低新生儿肺出血发生率.
目的 瞭解妊娠期高血壓疾病與新生兒肺齣血之間的關繫.方法 在2005年6月至2007年6月對四傢醫院收治的正常孕婦(孕A組)、妊娠期高血壓孕婦(孕B組)及其所產新生兒(嬰A組、嬰B組)進行血內皮素(ET)-1和NO水平測定,併比較正常孕婦與妊娠期高血壓孕婦所產新生兒肺齣血的髮生率.結果 孕B組及嬰B組分彆較孕A組及嬰A組血ET-1水平增高[(6.66±2.73)ng/L vs (3.24±1.74)ng/L,(6.42±3.17)ng/L vs (3.91±2.02)?ng/L],NO水平降低[(85.80±46.15)μmol/L vs (110.85±76.56)μmol/L,(82.73±48.51)μmol/L vs(122.23±75.08)μmol/L],差異有非常顯著性(P<0.002,P<0.001).嬰B組新生兒肺齣血髮生率為13.3%(20/155例),明顯高于嬰A組3.9%(5/128例),差異有顯著性(χ2=5.9,P=0.01).結論 妊娠期高血壓孕婦NO生成減少及ET-1異常升高,導緻胎盤血管彊烈收縮,胎兒髮生缺血缺氧,可最終引起新生兒肺齣血.及早防治妊娠期高血壓,可降低新生兒肺齣血髮生率.
목적 료해임신기고혈압질병여신생인폐출혈지간적관계.방법 재2005년6월지2007년6월대사가의원수치적정상잉부(잉A조)、임신기고혈압잉부(잉B조)급기소산신생인(영A조、영B조)진행혈내피소(ET)-1화NO수평측정,병비교정상잉부여임신기고혈압잉부소산신생인폐출혈적발생솔.결과 잉B조급영B조분별교잉A조급영A조혈ET-1수평증고[(6.66±2.73)ng/L vs (3.24±1.74)ng/L,(6.42±3.17)ng/L vs (3.91±2.02)?ng/L],NO수평강저[(85.80±46.15)μmol/L vs (110.85±76.56)μmol/L,(82.73±48.51)μmol/L vs(122.23±75.08)μmol/L],차이유비상현저성(P<0.002,P<0.001).영B조신생인폐출혈발생솔위13.3%(20/155례),명현고우영A조3.9%(5/128례),차이유현저성(χ2=5.9,P=0.01).결론 임신기고혈압잉부NO생성감소급ET-1이상승고,도치태반혈관강렬수축,태인발생결혈결양,가최종인기신생인폐출혈.급조방치임신기고혈압,가강저신생인폐출혈발생솔.
Objective To study the relationship between pregnancy-induced hypertension(PIH) and neonatal pulmonary hemorrhage(PH).Methods Normal gravida,gravida with PIH and their neonates hospitalized from June 2005 to June 2007 were served as study objects.The concentration of serum ET-1 and NO were detected in gravidas and their neonates.The PH prevalence of neonates whose mother were normal or with PIH were compared.Results Compared with the normal gravidas and their neonates,the level of serum ET-1 was higher [(6.66±2.73)ng/L vs (3.24±1.74)ng/L,(6.42±3.17)ng/L vs (3.91±2.02)ng/L] and the level of NO was lower [(85.80±46.15)μmol/L vs (110.85±76.56)μmol/L,(82.73±48.51)μmol/L vs (122.23±75.08)μmol/L] in gravidas with PIH and their infants (P<0.002,P<0.001).In the neonates whose mothers with PIH,the prevalence of PH was much higher than those whose mothers were normal.Conclusion Production of NO decreases and ET-1 increases abnormally in gravidas with PIH,which leads to strong contraction of placental vessels,fetal hypoxic-ischemic change,and finally fetal or neonatal PH.Prophylaxis and treatment of PIH can decrease prevalence of neonatal PH.
