Telestroke significantly reduced OTD and hospital stay durations in stroke patients without increasing the risk of mortality or sICH. Therefore, telemedicine can improve stroke care in regional areas with minor experience in thrombolysis. Further randomized controlled trials are needed to assess the benefits of telestroke systems, especially in terms of cost-effectiveness and quality of life outcomes.

Abstract-Preeclampsia is a leading cause of maternal and fetal morbidity/mortality; however, the pathophysiological mechanisms are unclear. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs; particularly MMP-2), cleave the inactive precursor big ET-1 (bET-1) to active ET-1. Notably, expression levels of MMP-2 have been shown to be on the increase in women who subsequently develop preeclampsia. We hypothesized that the increased MMP-2 expression leads to increased bET-1 conversion, thereby increasing vasoconstriction in preeclampsia. A reduced uteroplacental perfusion pressure (RUPP) model of preeclampsia in the rat was used to assess mesenteric artery vascular function. Responses to bET-1 (3-310 nmol/L) and ET-1 (1-200 nmol/L) were studied in the presence or absence of inhibitors of enzymes known to cleave bET-1. Vascular contractility in response to bET-1 was greater in RUPP than Sham (P<0.001), whereas neither responses to ET-1 nor maximal contractility to high potassium salt solution (123.70 mmol/L) were different. MMP inhibition with GM6001 (30 μmol/L) significantly decreased responses to bET-1 in RUPP (P<0.001) but not Sham-operated rats. Interestingly, combined treatment with GM6001 and L-NG-nitroarginine methyl ester (100 μmol/L) revealed a NO modulation of MMPs that was reduced in RUPP. In summary, we found increased vascular contractility to bET-1 in the RUPP model of preeclampsia that was likely attributable to upstream enzymatic pathways. These data are consistent with a greater contribution of MMP to cleavage of bET-1 to ET-1 ex vivo in RUPP, suggesting that this enzyme may be partially responsible for increased bET-1-induced contractility.

Abstract-Preeclampsia is a major cause of maternal and fetal morbidity and mortality that has been associated with endothelial dysfunction attributed, in part, to dyslipidemia, an imbalance in angiogenic factors and oxidative stress. One of the many factors that have been shown to be elevated in women with preeclampsia is low-density lipoprotein (LDL) and the more oxidizable, small dense LDL, which can lead to increased vascular oxidative stress and decreased bioavailability of NO. Lectin-like oxidized LDL-1 receptor (LOX-1) is a specific receptor for oxidized LDL. We hypothesized that a reduction of placental perfusion using a rat model of reduced uteroplacental perfusion pressure would result in enhanced LOX-1 expression in the maternal vasculature causing impaired vascular endothelial function through the actions of increased superoxide production and decreased NO-mediated vasodilation. We demonstrated a significant increase in the expression of the LOX-1 receptor (4.3-fold; Pϭ0.002), endothelial NO synthase (2.7-fold; Pϭ0.001), and superoxide (Pϭ0.02) in thoracic aorta of the reduced uteroplacental perfusion pressure model, whereas maximal vasodilator function was modestly decreased (PϽ0.05). Endothelial-dependent vasodilator function was unaffected by either oxidized LDL or an LOX-1 receptor inhibitor in controls but was modestly increased in the presence of both oxidized LDL and the LOX-1 receptor inhibitor in reduced uteroplacental perfusion pressure (Pϭ0.03). In summary, we have shown that, in a rat model of preeclampsia, there is a dramatic increase in the expression levels of both the LOX-1 receptor and the endothelial NO synthase enzyme, along with evidence of increased superoxide production and subsequent modestly decreased endothelial function. (Hypertension. 2012;59:1014-1020.)Key Words: preeclampsia Ⅲ vascular function Ⅲ LOX-1 receptor Ⅲ oxidized LDL Ⅲ RUPP P reeclampsia is one of the most enduring and inadequately understood pathologies of pregnancy, which affects 5% to 8% of pregnancies and is a major cause of maternal and fetal morbidity and mortality.1,2 This almost uniquely human disorder is characterized by de novo hypertension Ͼ140/90 mm Hg after the 20th week of gestation accompanied by proteinuria more than ϩ2. Although the diagnosis is reasonably clear, the underlying causes remain obscure, likely because of the extreme complexity of this disorder. Interestingly, the only currently known cure for preeclampsia is removal of the placenta and, hence, delivery of the baby, suggesting a central role for this organ. It is thought that an underperfused placenta is responsible for the release of placental debris and multiple factors, which, in turn, causes the maternal syndrome.3,4 Indeed, preeclampsia has been associated with both increased systemic vascular resistance and endothelial dysfunction.One of the many factors that have been shown to be elevated in women with preeclampsia is low-density lipoprotein (LDL) and the more oxidizable, small dense LDL. 5-10Combined with a significant volume ...