cytiotrophoblast Sync

Normal implantation is characterized by extensive remodeling of the spiral arterioles within the decidua
basalis as shown schematically inFigure 40-2(Chap. 5, p. 93). Endovascular trophoblasts replace the
vascular endothelial and muscular linings to enlarge the vessel diameter. The veins are invaded only
superficially. In some cases ofpreeclampsia, however, there may be incomplete trophoblastic invasion.
With this,decidual vessels, but not myometrial vessels, become lined with endovascular trophoblasts. The
deeper myometrialarterioles do not lose their endothelial liningand musculoelastic tissue, and their mean
external diameter is only half that of corresponding vessels in normalplacentas (Fisher, 2014). In general,
the magnitude of defective trophoblastic invasion is thought to correlate with severity of the hypertensive
disorder (Madazli, 2000). Usingelectron microscopy, De Wolfandcoworkers (1980) examined arteries
taken from the implantation site. They reported that early preeclamptic changes included endothelial
damage, insudation ofplasma constituents into vesselwalls, proliferation of myointimal cells, and medial
necrosis. Lipid accumulated first in myointimal cells and then within macrophages. These lipid-laden
cellchanges, shown inFigure 40-3,were referredto asatherosisby s Hertig(1945). Nelson and colleagues
(2014) completed placental examination in more than 1200 women with preeclampsia. These
investigators reportedthat vascular lesions includingspiralarteriole narrowing, atherosis, and infarcts were
more common in placentas from women diagnosed with preeclampsia before 34 weeks. Thus, the
abnormally narrow spiralarteriolar lumen likely impairs placental blood flow. McMahon and colleagues
(2014) have provided evidence that decreased soluble antiangiogenic growth factors may be involvedin
faulty endovascular remodeling. Diminished perfusion and a hypoxic environment eventually lead to
release of placental debrisor s microparticlesthat incite a systemic inflammatory response s (Lee, 2012;
Redman, 2012). Fisher and Roberts (2014) have provided an elegant review of the molecular mechanisms
involvedin these interactions. Defective placentation is posited to further cause the susceptible (pregnant)
woman to develop gestational hypertension, the preeclampsia syndrome, preterm delivery, a growth-
restricted fetus, and/or placental abruption (Brosens, 2011; Kovo, 2010; McElrath, 2008; Nelson, 2014).
In addition, Staff and coworkers (2013) have hypothesizedthat acute atherosis identifies a group of
women at increased risk for later atherosclerosis and cardiovascular disease
Implantasi normal ditandai dengan renovasi luas arteriol spiral dalam desidua basalis seperti yang ditunjukkan
secara skematis inFigure 40-2 (Bab. 5, hal. 93). Trofoblas endovascular mengganti lapisan endotel vaskular dan otot
untuk memperbesar diameter pembuluh. Vena diserang hanya dangkal. Dalam beberapa kasus ofpreeclampsia,
bagaimanapun, mungkin ada invasi trofoblas tidak lengkap. Dengan ini, pembuluh desidua, tetapi tidak pembuluh
miometrium, menjadi berjajar dengan trofoblas endovascular. Semakin dalam arteriol miometrium tidak kehilangan
endotel mereka liningand jaringan musculoelastic, dan diameter eksternal berarti mereka hanya setengah dari kapal
yang sesuai di normalplacentas (Fisher, 2014). Secara umum, besarnya invasi trofoblas rusak diduga berkorelasi
dengan keparahan gangguan hipertensi (Madazli, 2000). Usingelectron mikroskop, De Wolfandcoworkers (1980)
meneliti arteri diambil dari situs implantasi. Mereka melaporkan bahwa perubahan preeklampsia awal termasuk
kerusakan endotel, insudation ofplasma konstituen dalam vesselwalls, proliferasi sel myointimal, dan nekrosis
medial. Lipid akumulasi pertama dalam sel myointimal dan kemudian dalam makrofag. Cellchanges ini sarat-lipid,
ditampilkan inFigure 40-3, yang referredto asatherosisby s Hertig (1945). Nelson dan rekan (2014) telah
menyelesaikan pemeriksaan plasenta di lebih dari 1200 wanita dengan preeklamsia. Peneliti ini reportedthat lesi
vaskular termasuk spiral arteri menyempit, atherosis, dan infark lebih umum pada plasenta dari wanita yang
didiagnosis dengan preeklamsia sebelum 34 minggu. Dengan demikian, lumen spiralarteriolar normal sempit
cenderung merusak aliran darah plasenta. McMahon dan rekan (2014) telah memberikan bukti bahwa penurunan
faktor pertumbuhan antiangiogenic larut dapat involvedin renovasi endovascular rusak. Berkurang perfusi dan
lingkungan hipoksia akhirnya menyebabkan pelepasan plasenta debrisor s microparticlesthat menghasut respon
inflamasi sistemik s (Lee, 2012; Redman, 2012). Fisher dan Roberts (2014) telah memberikan review elegan
mekanisme molekuler involvedin interaksi ini. Plasentasi yang rusak mengemukakan untuk lebih menyebabkan
rentan wanita (hamil) untuk mengembangkan hipertensi gestasional, sindrom preeklamsia, kelahiran prematur,
sebuah hambatan pertumbuhan janin, dan / atau solusio plasenta (Brosens, 2011; Kovo, 2010; McElrath, 2008;
Nelson 2014). Selain itu, staf dan rekan kerja (2013) memiliki atherosis akut hypothesizedthat mengidentifikasi
sekelompok perempuan pada peningkatan risiko untuk aterosklerosis kemudian dan penyakit kardiovaskular

The WorldHealthOrganization (WHO) systematically

reviews maternal mortality worldwide, and in developed countries, 16 percent of maternal deaths were
reported to be due to
hypertensive disorders (Khan, 2006). The WorldHealthOrganization ( WHO ) secara sistematis
ulasan kematian ibu di seluruh dunia , dan di negara-negara maju , 16 persen kematian ibu dilaporkan disebabkan
gangguan hipertensi ( Khan , 2006) .