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Acid-base Balance and Imbalance,酸碱平衡紊乱及其分析,阎春玲 Department of Pathophysiology,Acid-base balance,The basic meaning of acid-base balance is the stable H+ in the body fluid. pH: 7.357.45 Compatible with life 6.8 - 8.0,因酸碱负荷过度、不足或 调节机制障碍导致体液酸碱度 稳定性失衡的病理过程。,Acid-base disturbance:,In disease, because of overload, loss or deficiency and disorder in regulation of acid and base, the homeostasis can be destroyed.,Normal acid-base balance,Section 1,1. Acid- H+ donor,volatile acid (挥发酸 ) Nonvolatile acid/fixed acid (固定酸 ),daily production :300-400L/d,volatile acid H2CO3,CO2,H2O,H2CO3,CA,H+ + HCO3-,Reabsorption in kidney,RBC、kidney tubules-epithelium 、alveolar epithelial cell 、gastric mucosa,Source of acid,volatile acid,Pco2 is most important factor in pH of body tissues,Fixed acid (nonvolatile acid ),(50-100mmol/d),Base- H+ acceptor,碱性氨基酸分解 Endogenous: deaminationNH3 Less than acid production 有机酸盐转变 Exogenous input: vegetables, and fruits,Regulation of acid-base balance,Buffer systems (体液缓冲) Respiratory regulation (肺) Renal regulation (肾) Cellular regulation (细胞调节),1. Buffer systems in body fluid,弱酸及其共轭碱构成的具有缓冲酸或碱能力的缓冲对,HCO3-/H2CO3 is the most important buffer pair,the most important buffer pair (50%)。 fixed acid and base buffer system PH is dermatied by HCO3-/H2CO3,特点:Open Buffer System 反应快;但被消耗,不持久; 不彻底,直接受肾、肺调节。,2. Respiratory regulation,PaCO2 (N:40mmHg) pH of CSF to stimulate central chemoreceptor the respiratory centerPulmonary ventilation volume PaCO2 60mmHg (8kPa) Pulmonary ventilation volume 10 times PaCO2 80mmHg (10.7kPa) inhibit respiratory center,named as carbon dioxide narcosis,特点: 作用较快 (数分钟内开始发挥作用,30分钟达到高峰); 代偿能力大; 只对挥发性酸有效。,3. Renal regulation,“排酸保碱” 起效慢,1224h 作用强大持久,NaHCO3重吸收 (bicarbonate conservation),磷酸盐酸化 (phosphate acidification),氨的排泄 (ammonia excretion),Renal regulation,Bicarbonate conservation (NaHCO3重吸收),Phosphate acidification (磷酸盐酸化),K+,K+,Cl-,Ammonia excretion (氨的排泄),4.Cellular regulation,红细胞 肌细胞,HHb,特点: 缓冲强于细胞外液; 24h起效; 引起血钾改变。,组织细胞,血液,H,K,Na,肝脏细胞,NH3,H,OH-,NH4,NH3,尿素,骨骼,Ca3(PO4)2,H,Ca2,PO43-,Ca2,PO43-,H,H2PO4-,Parameters of acid-base balance,Section 2,1. pH,pH: acidosis pH: alkalosis,7.357.45,kassier,pH正常,No disturbsnce Complete compensation Acidosis + Alklosis,2. PaCO2 -“respiratory factor”. (Partial pressure of carbon dioxide),正常值: 40mmHg (3346mmHg) H2CO3: 40 X 0.03=1.2mmol/L,Higher PaCO2 is due to the inhibition of respiration. Lower PaCO2 is due to overventilation.,PaCO2 是物理溶解在动脉血中的CO2产生的张力。,PaCO246mmHg Primary increase: respiratory acidosis Secondary increase: metabolic alkalosis (compensated by lung) PaCO233mmHg Primary decrease: respiratory alkalosis Secondary decrease: metabolic acidosis (compensated by lung),Significance,3. AB (actual bicarbonate),正常值: 2227 mmol/L,AB is measured under “actual condition” in which both respiratory factor and metabolic factor affected the HCO3 . CO2 +H2O=H2CO3=H+HCO3 ,(24mmol/L),4. SB (Standard bicarbonate),意义: 原发性代碱;原发性代酸 反映代谢因素的指标,PCO2不影响其大小,正常值: 2227 mmol/L,only affected by metabolic factor,(24mmol/L),AB 和 SB关系:,Normally : ABSB: metabolic acidosis ABSB: metabolic alkalosis ABSB (CO2 retention) respiratory acidosis ABSB (CO2 depletion) respiratory alkalosis,5. BB (buffer base),意义:反映代谢因素的指标。 原发性BB 代酸 原发性BB 代碱,正常值: 4552mmol/L(48mmol/L),Sum of all buffer bases in blood 血液中一切具有缓冲作用的阴离子总量。 (标准条件下测定) HCO3-, HPO42-, Hb-, HbO2-, Pr-,6.BE (base excess),正常值: 03 mmol/L,标准条件下,将1升全血或血浆滴定到 pH 7.4所需的酸或碱的量。 用酸滴定称碱剩余(+BE), 用碱滴定称碱缺失(-BE),Normal BE= -3.0+3.0 Only metabolic factor determines BE In metabolic alkalosis the positive BE increases. In metabolic acidosis the negative BE increases.,Significance,7. AG (anion gap) (阴离子间隙),血浆中未测定阴离子(UA) 与未测定阳离子(UC)的差值。,AG = UA - UC,AG = Na+ - Cl- - HCO3- = 140-104-24 = 12 (mmol/L),正常范围1014mmol/L,意义:反映代谢因素,区别不同类型代谢性酸中毒和混合型酸碱平衡紊乱。,Na+ + UC = HCO3- + Cl- + UA,常用指标小结,1. 区分酸碱中毒:pH 2. 反映呼吸因素指标:PaCO2 3. 反映代谢因素指标:SB,AB ,BB,BE,AG,Simple acid-base disturbance,Section 3,41,H2CO3 (1),pH ,metabolic,respiratory,Metabolic acidosis,Respiratory alkalosis,Respiratory acidosis,Metabolic alkalosis,1. Metabolic acidosis,Metabolic acidosis is defined as a decrease of pH induced by primary decrease in plasma bicarbonate ( HCO-3)concentration.,案例4-1:,患者女性,46岁,患糖尿病10余年,因昏迷状态入院。体检血压90/40mmHg,脉搏101次/min,呼吸深大,28次/min。生化检验:血糖10.1mmol/L,-羟丁酸1.0mmol/L,, K+5.6mmol/L,Na+160mmol/L,Cl-104mmol/L; pH7.13,PaCO230mmHg, AB9.9mmol/L,SB10.9mmol/L,BE-18.0mmol/L;尿:酮体(+),糖(+),酸性;心电图出现传导阻滞。 思考题:该病人是否发生了酸碱紊乱?哪些指标说明发生了酸碱紊乱?,主要原因: HCO3- 丢失; 固定酸过多,(1) Etiology,H增多或 HCO3 -减少,Excessive production of fixed acids 1)Lactic acidosis: shock, heart failure, respiratory failure, severe anemia,carbon monoxide poisoning etc. 2) ketoacidosis: diabetes, starvation, alcohol poisoning,(2) Disorders in the excretion of acidic metabolites Renal failure:,GFR -fixed acids,2) Type I renal tubular acidosis (RTA-I):,(3) Excessive loss of HCO3- 1) Loss from intestinal juice:,diarrhea; intestinal suction intestinal fistula biliary fistula,型远端肾小管性酸中毒(Distal RTA)。 是远端小管排H障碍引起的,2) Kidney loss of HCO-3 : Type II renal tubular acidosis(RTA-II): 型-近端肾小管性酸中毒(Proximal RTA). 是近端小管重吸收HCO3-障碍引起的。 Depressant of C.A,(4) Excessive intake of exogenous acids,水杨酸中毒 含氯药物摄入过多,(5) Blood dilution 大量输入生理盐水,引起HCO3- 稀释 (6) Hyperkalemia,H,Na +,肾小管,H,K,K,H,H,K,Na +,K,高钾血症和反常性碱性尿,反常性 碱性尿,肾小管性酸中毒,酸中毒患者排碱性尿称为反常性碱性尿。,Acid-Base Disturbance,(2)Classification,Normal AG metabolic acidosis High AG metabolic acidosis,AG增大型代酸,特点: 血浆HCO3减少 AG增大(固定酸增加) 血Cl含量正常,1)缺氧、严重肝病乳酸生成,转化处理障碍乳酸; 糖尿病、饥饿等脂肪动员酮体生成。,2)严重肾衰竭 GFR 固定酸排出,3)固定酸摄入过多(水杨酸中毒),Acid-Base Disturbance,AG正常型代酸,特点: AG正常 血浆HCO3减少 血Cl含量增加,1)腹泻:大量碱性肠液丢失,3)肾保碱功能障碍:近端肾小管泌H+障碍导致HCO3-丢失;远端肾小管泌H+障碍使HCO3-生成,同时尿铵及可滴定酸排出;大量应用CA抑制剂。,2)大量输入生理盐水稀释体内HCO3-,4)含氯的酸性盐(NH4Cl)输入过多,在体内代谢生成HCl。,Acid-Base Disturbance,缓冲作用即刻发生,HCO3-被不断消耗,特点,(3) Compensation,Buffer System:,Respiratory regulation:,特点,H,颈动脉体 主动脉体的 化学感受器,反射,呼吸 中枢 兴奋,增加呼吸 频率 幅度,排出CO2,数分钟后启动,30分钟见效,12-24小时达高峰,HCO3-,PaCO2,pH,加强泌H 、泌NH4,回吸收HCO3-,H ,HCO3-,pH,HCO3-,PaCO2,特点,起效慢,3-5天达高峰, 有一定的局限性, 如对肾脏疾病引起的代酸代偿作用差,renal regulation,Compensation by cells and bone,慢性骨损伤-Chronic metabolic acidosis,(佝偻病),(骨质疏松症) (骨营养不良),(4) Changes of parameters and electrolytes,原发性 SB AB BB BE 继发性: PaCO2 血K,负值,PH 失代偿型代谢性酸中毒,pH正常,代偿型代谢性酸中毒,案例4-1:,K+5.6mmol/L,Na+160mmol/L,Cl-104mmol/L; pH7.13,PaCO230mmHg, AB9.9mmol/L,SB10.9mmol/L,BE-18.0mmol/L;,pH, SB, AB , PaCO2, BE-, K+, AG, Cl-正常 高AG型代酸(酮症酸中毒),(5)Alterations of metabolism and function,抑制心肌收缩力 Negative inotropic action,心律失常 Arrhthmias,Cardiovascular system,抑制心肌兴奋收缩偶联,K+,抑制钙内流; 抑制肌浆网释放钙,2019/8/24,Ca2+与肌钙蛋白结合障碍,troponin,shock?,Vasodilatation: Acidosis blunt the vasomotor response to catecholamines。 血管对儿茶酚胺的反应性降低-血管扩张,血压,CNS-“抑制”,Depression of mental activity,slowness, tired, confused, coma,gamma-aminobutyric acid -氨基丁酸,Respiratory system,Deep and rapid respiration 深大呼吸,Osseous system (Chronic) rickets、 osteodystrophy,案例4-1:,患者女性,46岁,患糖尿病10余年,因昏迷状态入院。体检血压90/40mmHg,脉搏101次/min,呼吸深大,28次/min。生化检验:血糖10.1mmol/L,-羟丁酸1.0mmol/L,, K+5.6mmol/L,Na+160mmol/L,Cl-104mmol/L; pH7.13,PaCO230mmHg, AB9.9mmol/L,SB10.9mmol/L,BE-18.0mmol/L;尿:酮体(+),糖(+),酸性;心电图出现传导阻滞。 思考题:该病人是否发生了酸碱紊乱?哪些指标说明发生了酸碱紊乱?,治疗原发病 (treatment of primary disease),应用碱性药物 (Administration of NaHCO3),(6) Principles of prevention and treatment,K+ Ca2+ ?,乳酸钠、 三羟甲基氨基甲烷(THAM),16mM,2. Respiratory acidosis,Respiratory acidosis is defined as a decease of pH induced by primary increase in plasma carbonic acid(H2CO3) concentration.,案例4-2:,患者:男,15岁,因溺水窒息。查血气:PH 7.15,PaCO2 80mmHg,HCO3- 27mmol/L。 问题:该患者发生何种了酸碱平衡紊乱?,(1) Etiology,Decreased elimination of CO2 Excessive inspiration of CO2,Trauma, infection of brain, excessive sedatives, narcotics, alcohol, etc.,poliomyelitis,Hypokalemia Amyosthenia gravis .,Trauma , Pneumothorax, Chest deformity .,Drowning, foreign bodies, edema ,COPD,Pulmonary disease,(2)Classification,Acute respiratory acidosis (24小时以内) Chronic respiratory acidosis (持续24h以上的CO2潴留),(3) Compensation,Acute respiratory acidosis: cells,RBC,plasma,CO2+H2OH2CO3,CO2 ,chronic respiratory acidosis Renal regulation,泌H+ 泌氨 HCO3-重吸收 尿pH,Acute: pH PaCO2 AB SB PaCO2 10mmHg HCO3代偿性 1 mmol/L,Chronic: pH PaCO2 AB SB PaCO2 10mmHg HCO3代偿性 3.5 mmol/L,(4)Changes of parameters and electrolytes,案例4-2:患者:男,15岁,因溺水窒息。查血气:PH 7.15,PaCO2 80mmHg,HCO3- 27mmol/L。 分析?,与代酸相同,但CNS症状更明显,?,Why ?,(5)Alterations of metabolism and function,CO2 直接弥散进入脑组织,Carbon dioxide narcosis: PaCO2 80 mmHg,Celebral vascular dilation cerebral blood flow increase,Hypoxia,肺性脑病,(Pulmonary encephalopathy),intracranial hypertension and brain edema.,增加肺泡通气量 (Increase alveolar ventilation),应用碱性药物 (supplement of base),(6) Principles of prevention and treatment,Be careful to alkaline drug(NaHCO3) THAM,85,案例4-3:,一男性患者,60岁,因进食即呕吐10天而入院。近20天明显消瘦,卧床不起。精神恍惚,嗜睡,皮肤干燥松弛,眼窝深陷,呈重度脱水征。呼吸17次/min,血压120/70mmHg,诊断为幽门梗阻。血液生化检验:K+3.4mmol/L, Na+158mmol/L,Cl-90mmol/L;血气:pH7.50,PaO262mmHg,PaCO249mmHg,BE8.0mmol/L,HCO3-45mmol/L。 思考题: 该患者属于何种类型的酸碱平衡紊乱? 原因和机制如何? 该患者有无水电紊乱?,3. Metabolic alkalosis,Metabolic alkalosis is defined as an increase of pH induced by primary increase in plasma bicarbonate ( HCO-3).,(1) Etiology,1) H loss,vomiting ( HCl ),Loss from stomach:,Loss from kidney:,长期应用袢利尿剂(抑制髓袢升支对Cl-、Na+和H2O的重吸收)远端肾小管 H+-Na+交换排H+ 、排Cl- ,HCO3-重吸收 血HCO3-、Cl- Diuretics- furosemide 低氯性碱中毒 醛固酮增多或糖皮质激素使用过多 肾排H+、K+ -重吸收NaHCO3 ,Primary hyperaldosteronism Secondary hyperaldosteronism caused by: hypovolemia Cushings syndrome,低氯性碱中毒,利尿剂,2) Excessive intake of alkaline substances,3) Hypokalemia / hypochloremia 低钾/低氯性碱中毒 paradoxical acidic urine,Excessive intake of NaHCO3 or stored blood,4)Misuse of mechanical ventilation in chronic respiratory acidosis,原因呕吐丢失HCl;脱水造成浓缩性HCO3;低钾碱中毒,案例4-3: 一男性患者,60岁,因进食即呕吐10天而入院。近20天明显消瘦,卧床不起。精神恍惚,嗜睡,皮肤干燥松弛,眼窝深陷,呈重度脱水征。呼吸17次/min,血压120/70mmHg,诊断为幽门梗阻。血液生化检验:K+3.4mmol/L, Na+158mmol/L,Cl-90mmol/L;血气:pH7.50,PaO262mmHg,PaCO249mmHg,BE8.0mmol/L,HCO3-45mmol/L。,(2) Clasification,Chloride-responsive alkalosis 盐水反应性碱中毒 Chloride-resistant alkalosis 盐水抵抗性碱中毒,(3) Compensation,4) Renal regulation,Secrete H+ Secrete NH3 Reabsorb HCO3- Urine pH ,细胞外液H,肾小管腔,碱中毒低血钾,3) Intracellular regulation,原发性: pH SB AB BB BE 继发性: PaCO2 血K,正值,(4) Changes of parameters and electrolytes,案例4-3,血气:pH7.50,PaO262mmHg,PaCO249mmHg,BE8.0mmol/L,HCO3-45mmol/L 分析:患者幽门梗阻呕吐丢失HCl等而导致HCO3-pH,BE正值,继发性PaCO2,PaO2,属于失代偿型代谢性碱中毒。 患者低Cl-、脱水应属于盐水反应性碱中毒,(1) Central Nervous System,-氨基丁酸(GABA),(5)Alterations of metabolism and function,restlessness,mental derangement,delirium,2) Neuromuscular excitability (神经肌肉应激性升高),机制: pH, 血中游离Ca2+,手足搐搦 (Carpopedal Spasm),3) Hypoxia (left-shift of oxygen-Hb dissociation curve),4) Hypokalemia,治疗原发病 (treatment of primary disease),saline-responsive alkalosis KCl saline-resistant alkalosis,(6) Principles of prevention and treatment,Replenish 0.9% NaCl Na+ Cl-( mmol/L) - 0.9%NaCl 154 154 Plasma 140 104 - a) Dilute the HCO3- b) Increase the blood volume, reduce the reabsorption of HCO3-. c) increased Cl- in distal tubule leads to increased excretion of HCO3- in collecting duct.,103,案例4-4,4. Respiratory alkalosis,Respiratory alkalosis is defined as an increase of pH induced by Primary decrease in plasm H2CO3 Concentration.,(1) Etiology,CO2排出过多,Psychogenic factors: Nervousness, anxiety, hysteria, etc. (2) Brain diseases: Encephalitis, meningitis, etc. (3) Reflective stimulation: Hypoxemia, fever, pain, NH3, salicylate etc. (4) Misuse of mechanical ventilation,案例4-4 原因发热、肺炎、肺水肿、低氧血症等刺激呼吸频率CO2呼出过多,(2) Classification and Compensation,Acute respiaratory alkalosis 24h,血H2CO3,血K,1)Acute respiaratory alkalosis,RBC,plasma,2)Chronic respiaratory alkalosis,泌H+ 泌氨 HCO3-重吸收 尿pH ,急性: pH PaCO2 AB SB PaCO2 10 mmHg HCO3代偿性 2 mmol/L,慢性: pH PaCO2 AB SB PaCO2 10mmHg HCO3代偿性 4 mmol/L,(4) Changes of parameters and electrolytes,案例4-4 血气:pH7.52, PaCO230mmHg,PaO257mmHg,BE-1.2mmol/L,HCO3-23.3mmol/L,K+、Na+、Cl-正常。 分析:患者发热、肺炎、肺水肿并缺氧,引起呼吸急促,使PaCO2原发性pH,继发性HCO3-,属于失代偿型呼吸性碱中毒。,眩晕、四肢感觉异常、意识障碍、抽搐等碱中毒症状,(5)Alterations of metabolism and function,CNS dysfunction:GABA,cerebral blood flow ,(6) Principles of prevention and treatment,Treatment of primary disease Prevent mis-operation of mechanical ventilator 5CO2 mixtrue gas inhalation or mask,115,各型酸碱平衡紊乱指标的变化,代酸,呼酸,代碱,呼碱,小结,117,单纯型ABD小结 1、概念: 根据原发变化因素及方向命名。 2、代偿变化规律: 代偿变化与原发变化方向一致。 3 、血气特点: 呼吸性ABD,血液pH与其它指标变化方向相反; 代谢性ABD,血液pH与其它指标变化方向相同。 4、原因和机制: 代酸:固定酸生成及HCO3-丢失HCO3-降低。 呼酸:CO2排出减少吸入过多,使血浆H2CO3升高。 代碱:丢失,过量负荷,血增多。 呼碱:通气过度CO2呼出过多,使血中H2CO3降低。,118,5、对机体的影响: CNS 离子改变 其它 酸中毒 抑制性紊乱 血钾增高 血管麻痹,心律失常 收缩力降低 碱中毒 兴奋性紊乱 血钾降低 肌肉痉挛 6、代偿调节 (1) 代谢性ABD,各调节机制都起作用,尤其是肺和肾; 呼吸性ABD,细胞内外离子交换是急性紊乱的主要机制(两对离子交换),肾调节是慢性紊乱的主要机制。 (2)代偿是有限度的。 (3)pH值取决于代偿能否维持HCO3-/H2CO3比值为20/1。,例一、患者腰痛3月入院,诊断为肾盂肾炎,血液生化测定 pH = 7.32, PaCO2 = 20 mmHg, BE=-15.3mmol/L, SB= 19.2mmol/L。 该病人发生何种酸碱平衡紊乱?,代酸,例二、糖尿病患者,血液生化测定 pH = 7.30, PaCO2 = 34 mmHg, SB= 16mmol/L, Na+= 140 mmol/L, K+=4.5 mmol/L CL- =104 mmol/L , HCO3- = 21mmol/L 该病人发生何种酸碱平衡紊乱?,AG增高性代酸,综合举例,例三某溃疡病患者,因反复呕吐入院,血气分析为 pH 7.49,PaCO2 48mmHg,HCO- 36mmol/L。 该病人酸碱失衡类型为: A 代酸 B 代碱 C 呼碱 D 呼碱 例四某肝性脑病患者, 血气分析为pH 7.47, PaCO2 26.6mmHg,HCO- .3mmol/L。 应诊断为: A 代碱 B 呼碱 C 呼酸 D 代酸,Mixed acid-base Disturbance,Section 4,A mixed acid-base disturbance is defined as the simultaneous existance of two or more simple acid-base disturbance in the same patient.,Concept,酸碱一致型(相加型) 酸碱混合型(相消型),Double acid-base disturbance (二重性),呼吸心跳骤停 肺疾患并心衰或休克,pH PaCO2 HCO3-,Respiratory acidosis + metabolic acidosis,Causes,Characteristics,通气障碍(CO2潴留)伴有产酸(固定酸潴留)。,高热合并呕吐 肝硬化应用利尿剂,pH PaCO2 HCO3-,Respiratory alkalosis + metabolic alkalosis,Causes,Characteristics,慢性肺疾患应用利尿剂或合并呕吐,pH PaCO2 HCO3-,Respiratory acidosis plus metabolic alkalosis,Causes,Characteristics,(-)、,水杨酸中毒或肾衰合并通气过度,Metabolic acidosis + respiratory alkalosis,Causes,Characteristics,pH PaCO2 HCO3-,(-)、,肾衰伴呕吐 酮症酸中毒伴呕吐 呕吐伴有腹泻,Metabolic acidosis + metabolic alkalosis,Causes,Characteristic,pH 、PaCO2 、HCO3- 不定,呼酸+代酸(AG)+代碱 呼碱+代酸(AG)+代碱,Triple acid-base disturbance (三重性),Section 5,Judgment of acid-base disorders,“一划五看”简易判断法,一划:将多种指标简化成三项,并用箭头表示其升降,SB AB BB,BE(-),HCO3-,H2CO3,PaCO2,pH ,H+,五看:一看pH定酸碱,1. pH升高:失偿型碱中毒 p

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