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In 1957, Jacobson et al performed bilateral nephrectomies on rats and showed that these animals no longer responsed to phlebotomy or cobalt administration with increased Ep production. Rats that only had their ureters ligated and that developed similar elevations of the blood urea nitrogen still responded to cobalt or phlebotomy in the usual fashion .Similiar results were found in mice , rabbits , baboons , and dogs .In humans , Ep levels were found to be low in the serum of anemic patients with severe uremia , but after successful renal transplantation increases in blood Ep levels and hematocrit were observed. Furthermore , erythropoietic activity was detected in the perfusates from isolated rabbit kidneys and was produced by renal cell cultures in vitro . Although the evidence to support the renal origin of Ep was substantial , Ep had not been extracted from normal kidneys or from various normal kidney fractions until very recently. To explain this difficulty , three different hypotheses have been proposed . Current evidence indicates that the stimulation of Ep production by hypoxia or ischemia may be mediated via increases in renal prostaglandin and cyclic AMP levels . The administration of cyclic AMP to plethoric mice increased Ep production and led to and increased red cell mass in normal mice . prostaglandin raised the renal cyclic AMP concentration in isolated perfused dog kidneys as well as the amount of Ep in the perfusates ;the administration of prostaglandin to polycythemic mice increased both prostaglandin E and Ep blood levels in dogs . The effect on both these parameters as well as on hypoxia-induced Ep production was blocked by indomethacin, a known inhibitor of prostaglandin synthesis .Since prostaglandins are located mainly in the renal medulla , while Ep has been identified by fluorescent antibodies in the renal cortex , these observations are most consistent with the hypothesis that renal hypoxia or ischemia produces a medullary release of prostaglandin which in turn elevates renal corticla cyclic AMP levels. The newly formed cyclic AMP THEN may activate a protein kinase that leads to increased Ep production , possibly through phosphorylation of a precursor renal erythropoietic factor. Although the kidney is the major site controlling Ep formation , after bilateral nephrectomy the production of hormone and erythropoiesis continues in most species , but at a considerably lower level .Anephric mice and rats retain about 10%of their original capacity to increase Ep production in the presence of hypoxia , while anephric patients who become very anemic have Ep in their plasma .The extrarenal Ep of rats appears to be similar to Ep of renal origin since it stimulates heme synthesis by marrow cells and is neutralized by antiserum to urinary Ep . Several lines of study point to the liver as the primary site of extrarenal Ep production. Ep is produced primarily in the liver during fetal life .Hepatectomy abolishes hypoxia-stimulated hormone production in anephric rats , but not in animals with intact kidneys . In partially hepatectomized rats , the extrarenal Ep response to hypoxia correlates directly with liver regeneration and is most increased during the period of greatest proliferation . Administration of colloidal carbon or zymosan, which induces liver reticuloendothelial cell hyperplasia, enhances Ep production in nephrectomized rats exposed to hypoxia .This effect, which is also blocked by hepatectomy , suggests that the liver reticuloendothelial system may be and important factor in extrarenal Ep production . |
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ringzhu(金幣+10): ~~ 2011-03-17 15:20:49
ringzhu(金幣+10): ~~ 2011-03-17 15:20:49
| Current evidence indicates that the stimulation of Ep production by hypoxia or ischemia may be mediated via increases in renal prostaglandin and cyclic AMP levels . 目前已證明缺氧或缺血促進上皮細胞的產生，腎前列腺素和環(huán)磷酸腺苷的增加也可能會導致上皮細胞的產生。The administration of cyclic AMP to plethoric mice increased Ep production and led to and increased red cell mass in normal mice . 環(huán)磷酸腺苷促進多血癥老鼠的上皮細胞數量增加，而對正常鼠則會增加紅細胞的數量。prostaglandin raised the renal cyclic AMP concentration in isolated perfused dog kidneys as well as the amount of Ep in the perfusates 在灌注狗實驗中，前列腺素會提高腎臟中環(huán)磷酸腺苷的濃度，上皮細胞的數量也會增多;the administration of prostaglandin to polycythemic mice increased both prostaglandin E and Ep blood levels in dogs此外，前列腺素會提高多血癥鼠（polycythemic 單詞沒查出來什么意思）的前列腺素E，增加狗血液中的上皮細胞量 . The effect on both these parameters as well as on hypoxia-induced Ep production was blocked by indomethacin, a known inhibitor of prostaglandin synthesis 消炎痛是一種常用的前列腺素產生抑制劑，前列腺素對前列腺素E及血液中上皮細胞和缺氧生成的上皮細胞的作用會受到消炎痛的抑制.Since prostaglandins are located mainly in the renal medulla , while Ep has been identified by fluorescent antibodies in the renal cortex ,有種猜想認為腎臟缺氧或缺血導致腎髓質釋放前列腺素，進而前列腺素促進皮質中環(huán)磷酸腺苷的產生，新生成的環(huán)磷酸腺苷可能通過身形紅細胞生成因子的磷酸化作用，刺激蛋白激酶產生上皮細胞。因為前列腺素主要存在于腎髓質中，腎臟皮層的上皮細胞可以用熒光抗體進行識別，實驗觀測結果與上述猜想相吻合。these observations are most consistent with the hypothesis that renal hypoxia or ischemia produces a medullary release of prostaglandin which in turn elevates renal corticla cyclic AMP levels. The newly formed cyclic AMP THEN may activate a protein kinase that leads to increased Ep production , possibly through phosphorylation of a precursor renal erythropoietic factor. |
7樓2011-03-09 16:40:34
wjmsicuan(金幣+1, 翻譯EPI+1): 很差勁，不過還是慰問下��！ 2011-03-06 19:43:10
 在1957年，Jacobson 等人對大鼠首先進行雙側腎切除，之后放血或用鈷處理，發(fā)現Ep不增高，然而，如果預先只是將大鼠輸尿管結扎，其血液尿素含量增高，之后放血或用鈷處理，其Ep，和正常鼠一樣，增高。在小鼠，家兔，狒狒和狗身上做相同的實驗，獲得的結果相似。在人群中，伴有嚴重尿毒癥的白血病患者的血液Ep水平較低，但在腎移植手術成功后，血液Ep水平升高，且血細胞計數也有所增加。此外，對分離的家兔的腎灌流液，即體外培養(yǎng)的腎細胞的紅血球生成活性進行檢測。雖然支持Ep 來源于腎的證據可靠，但直到現在，人們還沒能從正常的腎或不同的腎fractions提取出 Ep 。為了解釋這個難題，三個不同的假說被提出。最新證據顯示，由組織缺氧和局部缺血誘導的 Ep的產生是通過上調腎臟前列腺素和cAMP水平來介導的。用cAMP處理多血癥小鼠可增加Ep的產生，處理正常小鼠可導致紅細胞塊的增加。前列腺可以上調體外灌流的狗腎臟的cAMP濃度，同時也可以上調灌流液中Ep含量。用前列腺素處理紅細胞增多小鼠，可以增加血液前列腺素E含量，也可以增加狗的血Ep含量。對這2個參數的影響和組織缺氧誘導的Ep增多可以被消炎藥茚甲新阻斷，茚甲新是前列腺素合成的抑制劑。由于前列腺素主要分布于腎髓，而Ep已通過熒光抗體被鑒定存在于腎皮質， 這些觀察結果與假設一致，即腎缺氧或缺血誘導腎髓釋放前列腺素，而前列腺素反過來又上調腎皮質的cAMP濃度。新生成的cAMP，接下來可能可以激活蛋白激酶增加Ep的產生，很可能是通過磷酸化腎紅血球生成因子前體來實現的。 雖然腎是控制Ep生成的主要場所，在大多數物種經歷雙腎切除手術之后，激素和紅血球產生過程仍然繼續(xù)，只是以相當低的速度。無腎小鼠和無腎大鼠在缺氧條件下仍然保留約10%生產Ep的能力,但無腎的病人，常表現為嚴重貧血，在血漿中含有Ep。大鼠腎外的Ep和腎來源的Ep很相似，也可以刺激骨髓細胞生成亞鐵血紅素，可以被抗尿Ep的抗血清中和。一些研究團隊認為肝臟是腎外Ep產生的最初部位。在胎兒期 Ep主要在肝臟中產生。在無腎大鼠中，肝臟切除可以阻斷低氧誘導激素的產生，但在有完整腎的動物中肝臟切除不可阻斷。在部分肝臟切除的大鼠中， 腎外Ep對低氧的反應直接與肝再生相關，且在增殖最旺盛期腎外Ep增加最快。 用膠狀碳或酵母聚糖誘導肝網狀內皮組織增生，可以促進受低氧脅迫的腎切除大鼠的Ep的產生。這個效應同樣可以被肝切除手術阻斷，提示肝網狀內皮系統 可能是腎外Ep產生的重要因素。 第一次翻譯，湊活著看啊 |
2樓2011-03-05 20:56:56
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