Vreman H J, Wong R J, Kim E C, Nabseth D C, Marks G S, Stevenson D K
Department of Pediatrics, Division of Neonatal and Developmental Medicine, Stanford University School of Medicine, Stanford, CA, 94305-5119, USA.
Placenta. 2000 May;21(4):337-44. doi: 10.1053/plac.1999.0495.
Carbon monoxide (CO) has been shown to affect vascular tone in smooth muscle cells and thus, may regulate regional or systemic blood pressure as well as fetoplacental vascular tone and fetal blood delivery. To assess the potential of vascular tissue to produce CO, we determined haem oxygenase (HO) activity through in vitro quantitation of CO production with gas chromatography and its inhibition by 33-66 microm of chromium mesoporphyrin (CrMP) in homogenate preparations of rat aorta and vena cava and human umbilical cord tissues. We compared these results to HO activity in rat heart and liver. We also discuss normalization of HO activity on a per mg protein as well as per g fresh weight (FW) tissue basis. We found that both rat vascular tissue HO activities (per g FW) were equal, but greater than that of heart (x3) and less than that of liver (x0.2). For human cord tissues, HO activities of artery and vein were equal, but greater than that of Wharton's jelly. Also, HO activity in rat vascular tissues was 3x greater than that of the human cord tissues. HO activity was completely inhibited by CrMP in rat heart (90 per cent) and liver (96 per cent), but incompletely (50-66 per cent) in both rat and human vascular tissues. We established that it is unlikely that other non-haem CO-generating processes account for this unique insensitivity of HO to CrMP inhibition. In fact, high concentrations of other potent metalloporphyrin inhibitors affected vascular tissue HO even less. We found that the degree of in vitro HO inhibition appeared to be related to the concentration of haem in the reaction medium. We conclude that the presence of HO activity in cord tissues supports the possibility that CO plays a role in fetoplacental blood flow regulation.
一氧化碳（CO）已被证明会影响平滑肌细胞的血管张力，因此，可能调节局部或全身血压以及胎儿-胎盘血管张力和胎儿血液供应。为了评估血管组织产生CO的潜力，我们通过气相色谱法体外定量CO生成以及在大鼠主动脉、腔静脉和人脐带组织的匀浆制剂中用33 - 66微摩尔的中卟啉铬（CrMP）抑制CO生成，来测定血红素加氧酶（HO）活性。我们将这些结果与大鼠心脏和肝脏中的HO活性进行了比较。我们还讨论了以每毫克蛋白质以及每克新鲜组织重量（FW）为基础的HO活性归一化。我们发现，大鼠血管组织的HO活性（每克FW）是相等的，但高于心脏（3倍）且低于肝脏（0.2倍）。对于人脐带组织，动脉和静脉的HO活性相等，但高于华通胶的活性。此外，大鼠血管组织中的HO活性比人脐带组织高3倍。HO活性在大鼠心脏（90%）和肝脏（96%）中被CrMP完全抑制，但在大鼠和人血管组织中均被不完全抑制（50 - 66%）。我们确定，不太可能是其他非血红素CO生成过程导致了HO对CrMP抑制的这种独特不敏感性。事实上，高浓度的其他强效金属卟啉抑制剂对血管组织HO的影响更小。我们发现，体外HO抑制程度似乎与反应介质中血红素的浓度有关。我们得出结论，脐带组织中存在HO活性支持了CO在胎儿-胎盘血流调节中起作用的可能性。
