Tang C, Hsu H K, Chen X Y, Liu M S
Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, MO 63104.
Circ Shock. 1993 Sep;41(1):19-25.
Changes in the distribution of (Na+ + K+)-ATPase in two subcellular fractions, the sarcolemma and the light vesicle, of rat heart during sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). The alpha-subunit of (Na+ + K+)-ATPase was photoaffinity labeled with [alpha-32P]8-N3ATP. The results show that septic rat heart exhibits hyperdynamic (hypermetabolic) phase during early (9 hr post-CLP), followed by hypodynamic (hypometabolic) phase during late (18 hr post-CLP) sepsis. Marker enzyme and beta-adrenergic receptor assays depict that the light vesicle fraction is the intracellular site of surface receptor. The incorporation of the photolabel into the alpha-subunit (M(r) = 98,000) of the (Na+ + K+)-ATPase in sarcolemmal fraction was increased by 60% (P < 0.01) during early sepsis, but was decreased by 63% (P < 0.01) during late sepsis. In contrast, the binding of 98,000-M(r) peptide in light vesicles was decreased by 40% (P < 0.01) in early sepsis, but was increased by 102% (P < 0.01) during late sepsis. The ouabain-sensitive (Na+ + K+)-ATPase activity was increased by 31% (P < 0.05) during the early sepsis, but was decreased by 32% (P < 0.01) during late sepsis in the sarcolemmal fraction; while in the light vesicle fraction, the (Na+ + K+)-ATPase activity was decreased by 21% (P < 0.01) during early sepsis, but was increased by 47% (P < 0.01) during the late phase of sepsis. The yield of membrane proteins for each specific fraction remained unchanged for control, early sepsis, and late sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了败血症期间大鼠心脏肌膜和轻囊泡这两个亚细胞组分中（Na⁺ + K⁺）-ATP酶分布的变化。通过盲肠结扎和穿刺（CLP）诱导败血症。用[α-³²P]8-N₃ATP对（Na⁺ + K⁺）-ATP酶的α亚基进行光亲和标记。结果显示，败血症大鼠心脏在早期（CLP后9小时）表现为高动力（高代谢）阶段，随后在晚期（CLP后18小时）败血症期间表现为低动力（低代谢）阶段。标记酶和β-肾上腺素能受体分析表明，轻囊泡组分是表面受体的细胞内位点。在早期败血症期间，肌膜组分中光标记掺入（Na⁺ + K⁺）-ATP酶的α亚基（M(r)=98,000）增加了60%（P<0.01），但在晚期败血症期间减少了63%（P<0.01）。相反，早期败血症期间轻囊泡中98,000-M(r)肽的结合减少了40%（P<0.01），但在晚期败血症期间增加了102%（P<0.01）。哇巴因敏感的（Na⁺ + K⁺）-ATP酶活性在早期败血症期间在肌膜组分中增加了31%（P<0.05），但在晚期败血症期间减少了32%（P<0.01）；而在轻囊泡组分中，（Na⁺ + K⁺）-ATP酶活性在早期败血症期间减少了21%（P<0.01），但在败血症晚期增加了47%（P<0.01）。对照、早期败血症和晚期败血症各特定组分的膜蛋白产量保持不变。（摘要截断于250字）
