解放军医学院学报
解放軍醫學院學報
해방군의학원학보
Academic Journal of Chinese Pla Medical School
2013年
8期
873-875,902
,共4页
肿瘤坏死因子α%肾血管%收缩敏感性
腫瘤壞死因子α%腎血管%收縮敏感性
종류배사인자α%신혈관%수축민감성
tumor necrosis factor-α%renal vessel%constriction sensitivity
目的观察肿瘤坏死因子-α(tumor necrosis factor-α，TNF-α)对肾血管收缩敏感性的影响。方法28只大鼠制备离体灌注肾模型，随机分为4组(n=7)。A1组：无钙Kreb's液灌流组；A2组：无钙Kreb's液+TNF-α(100μg/L)灌流组；B1组：无钙Kreb's液+2-APB(30μmol/L)灌流组；B2组：无钙Kreb's液+TNF-α(100μg/L)+2-APB(30μmol/L)灌流组，4组在刺激期均加内皮素(endothelin，ET)(1 nmol/L)刺激。灌流结束后，计算肾脏水肿率，HE染色观察肾小球及肾小管形态、结构。结果平衡期过后，各组基础灌注压比较无统计学差异(P＞0.05)。A1、A2组ET刺激后，肾灌注压较基础压均明显升高(P＜0.05)；A2组灌注压升高值显著高于A1组(P＜0.01)。B1、B2组ET刺激后，肾灌注压均略升高，但与基础灌注压比较无统计学差异(P＞0.05)；两组灌注压升高值比较无统计学差异(P＞0.05)。4组肾脏的水肿率均低于30%，灌流后肾脏标本切片均未发现明显的器质性损伤，与灌流前相符。结论 TNF-α可能通过上调1，4，5-三磷酸肌醇受体(IP3R)进而增强ET引起的肾血管收缩。
目的觀察腫瘤壞死因子-α(tumor necrosis factor-α，TNF-α)對腎血管收縮敏感性的影響。方法28隻大鼠製備離體灌註腎模型，隨機分為4組(n=7)。A1組：無鈣Kreb's液灌流組；A2組：無鈣Kreb's液+TNF-α(100μg/L)灌流組；B1組：無鈣Kreb's液+2-APB(30μmol/L)灌流組；B2組：無鈣Kreb's液+TNF-α(100μg/L)+2-APB(30μmol/L)灌流組，4組在刺激期均加內皮素(endothelin，ET)(1 nmol/L)刺激。灌流結束後，計算腎髒水腫率，HE染色觀察腎小毬及腎小管形態、結構。結果平衡期過後，各組基礎灌註壓比較無統計學差異(P＞0.05)。A1、A2組ET刺激後，腎灌註壓較基礎壓均明顯升高(P＜0.05)；A2組灌註壓升高值顯著高于A1組(P＜0.01)。B1、B2組ET刺激後，腎灌註壓均略升高，但與基礎灌註壓比較無統計學差異(P＞0.05)；兩組灌註壓升高值比較無統計學差異(P＞0.05)。4組腎髒的水腫率均低于30%，灌流後腎髒標本切片均未髮現明顯的器質性損傷，與灌流前相符。結論 TNF-α可能通過上調1，4，5-三燐痠肌醇受體(IP3R)進而增彊ET引起的腎血管收縮。
목적관찰종류배사인자-α(tumor necrosis factor-α，TNF-α)대신혈관수축민감성적영향。방법28지대서제비리체관주신모형，수궤분위4조(n=7)。A1조：무개Kreb's액관류조；A2조：무개Kreb's액+TNF-α(100μg/L)관류조；B1조：무개Kreb's액+2-APB(30μmol/L)관류조；B2조：무개Kreb's액+TNF-α(100μg/L)+2-APB(30μmol/L)관류조，4조재자격기균가내피소(endothelin，ET)(1 nmol/L)자격。관류결속후，계산신장수종솔，HE염색관찰신소구급신소관형태、결구。결과평형기과후，각조기출관주압비교무통계학차이(P＞0.05)。A1、A2조ET자격후，신관주압교기출압균명현승고(P＜0.05)；A2조관주압승고치현저고우A1조(P＜0.01)。B1、B2조ET자격후，신관주압균략승고，단여기출관주압비교무통계학차이(P＞0.05)；량조관주압승고치비교무통계학차이(P＞0.05)。4조신장적수종솔균저우30%，관류후신장표본절편균미발현명현적기질성손상，여관류전상부。결론 TNF-α가능통과상조1，4，5-삼린산기순수체(IP3R)진이증강ET인기적신혈관수축。
Objective To study the effect of TNF-αon renal vasoconstriction sensitivity. Methods A rat in vitro perfusion kidney model was established. Twenty eight male SD rats were randomly divided into A1 group, A2 group, B1 group and B2 group (7 in each group). Rats in the 4 groups underwent perfusion with Ca2+-free Kreb's solution, TNF-αand Ca2+-free Kreb's solution (100μg/L), Ca2+-free Kreb's solution and 2-APB (30 μmol/L), TNF-α (100 μg/L) and Ca2+ -free Kreb's solution and 2-APB (30 μmol/L) respectively, and stimulated with 1nmol/L endothelin (ET). Then, kidney edema rate was calculated. Morphology and structure of glomeruli and renal tubules were observed. Results No significant difference was found in the basic perfusion pressure among the 4 groups (P > 0.05). Although the renal perfusion pressure was significantly higher than the basic perfusion pressure in A1 and A2 groups (P<0.05), it was significantly higher in A2 group than in A1 group after ET stimulation (P<0.05). Although the renal perfusion pressure was slightly higher in B1 and B2 groups, no significantly difference was found in the perfusion pressure and basic perfusion pressure between the two groups (P>0.05). The kidney edema rate was lower than 30%in the 4 groups. No significant organic injury was observed in renal tissue sections after perfusion. Conclusion TNF-αcan stimulate ET–induced renal vasoconstriction by up-regulating the IP3R.
