Ischemic postconditioning alleviates lung injury and maintains a better expression of aquaporin-1 during cardiopulmonary bypass

Background It has found that ischemic postconditioning （IPO） might decrease pulmonary ischemia/reperfusion （I/ R） injury,which is one of the main reasons of lung injury caused by cardiopulmonary bypass （CPB）.It was found that aquaporins （AQPs） play a role in the maintenance of fluid homeostasis.But it is still unclear whether IPO influences the expression of aquaporin-1 （AQP1）.This study was designed to investigate whether IPO can reduce CPB-related lung injury and affect the expression of AQP1 of lungs.Methods Twelve healthy dogs were divided into control group （C group） and ischemia postconditioning group （IPO group）.CPB procedures were implemented.Ten minutes later,the left pulmonary artery was separated and blocked.Postconditioning consisted of two cycles of 5-minute pulmonary artery reperfusion/5-minute reocclusion starting at the beginning of reperfusion.The 2×4 cm tissues of both sides of pulmonary apex,superior,middle and inferior lobe were taken before CPB （T1）,before occlusion and reopening of left pulmonary artery （T2,T3）,and 2 hours after CPB （T4）.Samples were used to evaluate lung injury degrees and to detect the expression of AQP1.At T1 and T4,blood was collected from femoral artery to calculate pulmonary function.Results At T4,each pulmonary function showed significant deterioration compared with T1.Lung injury could be found at the onset of CPB.However,the expression of AQP1 decreased and wet to dry weight ratio （W/D） increased after T2.In the left lung of C group,the worst pulmonary function and structures were detected.The slightest changes were discovered in the right lung of C group.A close relationship between W/D and lung injury score was found.The lung injury score was negatively related with the expression of AQP1.It was found that the expression of AQP1 was negatively connected with W/D.Conclusions In dog CPB models,lung injury induced by CPB was related with down regulated expression of AQP1.AQP1 is believed to be involved in the mechanisms of     

A correlative study between AQP4 expression and the manifestation of DWI after the acute ischemic brain edema in rats

Objective To investigate the rule of the aquaporin-4 (AQP4) expression in acute ischemic brain edema, and to study the correlation between AQP4 expression and diffusion-weighted imaging (DWI).Methods Thirty-six Wistar rats were divided into 2 groups randomly, control group (n=12) and operation group (n=24) in which right middle cerebral artery of each animal had been occluded unilaterally (MCAO) at interval times of: 15 minutes, 30 minutes, 1 hours, 3 hours, 6 hours and 24 hours, respectively. The operation process of the control group was the same as the operation group except for the MCAO. All groups were examined using DWI. The apparent diffusion coefficient (ADC), relative density (rd) and relative area (rs) of the biggest hyperintensity signal layer on DWI were measured. After that the animals were sacrificed and perfused with the mixture solution consisting of TTC. The biggest layers of the ischemic cerebral tissues in each rat corresponding to the DWI were stained with TTC and examined with immunochemistry (△S) , in situ hybridization (α) and histology.Results There was no significant change in the control group. In the operation group, a hyperintensity signal was found in the DWI of the right MAC territory at 15 minutes after MCAO. The ADC value decreased quickly within one hour after MCAO, while the AQP4 expression, rd-DWI and rs-DWI increased rapidly during this stage. As time progressed, the ADC value decreased further to （2.1±0.6）×10(-4) mm2/s at 3 hours, and then began to increase slowly till 24 hours. But the AQP4 expression (△S and α) and rd as well as the rs continuously increased slowly between 1 hour and 6 hours after MCAO, followed a peak after 6 hours. The AQP4 expression (α) showed a positive relationship with the rs-DWI, they all presented two peaks and a plateau. The corresponding sequential pathologic changes were a gradual increase of intracellular edema (within one hour), then an emergence of vasogenic edema (1-6 hours), and final necrosis and liquefaction (6-24 hours). Conclusions Upregulated expression of AQP4 may play a significant role in acute ischemic brain edema, especially during the stages of intracellular edema and necrosis, but it has no correlation to vasogenic edema. Certainly, the high expression of AQP4 is perhaps one of the most important reasons of the decrease of ADC and hyperintensity on the DWI in the intracellular edema.     

Alveolar stability under different combinations of positive end-expiratory pressure and tidal volume: alveolar microscopy in isolated injured rat lungs

Background High positive end-expiratory pressure （PEEP） and low tidal volume （VT） ventilation is thought to be a protective ventilation strategy. It is hypothesized that the stabilization of collapsible alveoli during expiration contributes to lung protection. However, this hypothesis came from analysis of indirect indices like the analysis of the pressure-volume curve of the lung. The purpose of this study was to investigate isolated healthy and injured rat lungs by means of alveolar microscopy, in which combination of PEEP and VT is beneficial with respect to alveolar stability （I-E%）. Methods Alveolar stability was investigated in isolated, non-perfused mechanically ventilated rat lungs. Injured lungs were compared with normal lungs. For both groups three PEEP settings （5, 10, 20 cmH20） were combined with three VT settings （6, 10, 15 ml/kg） resulting in nine PEEP-VT combinations per group. Analysis was performed by alveolar microscopy. Results In normal lungs alveolar stability persisted in all PEEP-VT combinations （I-E% （3.2±11.0）%）. There was no significant difference using different settings （P 〉0.01）. In contrast, alveoli in injured lungs were extremely instable at PEEP levels of 5 cmH20 （mean I-E% 100%） and 10 cmH2O （mean I-E% （30.7±16.8）%）; only at a PEEP of 20 cmH20 were alveoli stabilized （mean I-E% of （0.2±9.3）%）. Conclusions In isolated healthy lungs alveolar stability is almost unaffected by different settings of PEEP and VT. In isolated injured lungs only a high PEEP level of 20 cmH2O resulted in stabilized alveoli whereas lower PEEP levels are associated with alveolar instability.     

Role of Nuclear Transcription Factor-κB in Endotoxin-induced Shock in Rats

To investigate the role of NF-κB in endotoxic shock in rats. the model of endotoxinshock rats was induced by intravenous infusion of lipopolysaccharidc (LPS). 1 h. 2 h. 4 h and 6 h after LPS injection, the activation of NF-κB in blood mononuclear cells and the content of TNF-α and IL-6 in plasma was detected by enzyme-linked immunoadsordent assay (ELISA). The level of mean arterial pressure (MAP) and the histopathological changes of lung and liver were also observed. The activation of NF-κB in mononuclear cells increased 1 h after LPS injection and reached its peak 2 h after the injection, and its level was higher than that of normal group. The level of TNF-α was increased 1 h after the infusion and peaked 2 h after the injection, and its level was higher than that of normal group after LPS infusion. The content of IL-6 increased gradually with time. the IL-6 level was higher than that of normal group after LPS injection. MAP was decreased gradually with time and its level was lower than that of normal group after LPS injection. Pathological examination showed that endotoxic shock could cause pulmonary alveolar hemorrhage, edema and infiltration of inflammatory cell in lung tissue and congestion, edema, capillary dilation and inflammatory cell infiltration in liver tissue. It is concluded that NF-κB can up-regulate the expression of TNF-α and IL-6 in plasma and play an important role in endotoxin induced shock in rats.     

Downregulation of Aquaporin 4 Expression through Extracellular Signal-regulated Kinases1/2 Activation in Cultured Astrocytes Following Scratch-injury

ObjectiveTo investigate the role of extracellular signal-regulated kinase1/2 (ERK1/2) pathway in the regulation of aquaporin 4 (AQP4) expression inculturedastrocytes after scratch-injury. MethodsThe scratch-injury model was produced in cultured astrocytes of rat by a 10-μL plastic pipette tip. The morphological changes of astrocytes and lactate dehydrogenase (LDH) leakages were observed to assess the degree of scratch-injury. AQP4 expressionwas detected by immunofluorescence staining and Western blot, and phosphorylated-ERK1/2 (p-ERK1/2) expression was determined by Western blot. To explore the effect of ERK1/2 pathway on AQP4 expression in scratch-injured astrocytes, 10 μmol/L U0126 (ERK1/2inhibitor) was incubated in the medium at 30 min before the scratch-injury in some groups. ResultsIncreases in LDH leakage were observed at 1, 12, and 24 h after scratch-injury, and AQP4 expression was reduced simultaneously. Decrease in AQP4 expressionwas associated with a significant increase in ERK1/2 activation. Furthermore, pretreatment with U0126 blocked both ERK1/2 activation and decrease in AQP4 expression induced by scratch-injury. ConclusionThese results indicate that ERK1/2 pathway down-regulates AQP4 expression in scratch-injured astrocytes, and ERK1/2 pathway might be a novel therapeutic target in reversing the effects of astrocytes that contribute to traumatic brain edema.     

Expression and role of AQP1 in cervical squamous carcinoma and its precancerous lesions

Objective： To investigate the expression of aquaporin 1 in cervical squamous carcinomas （CSC） and cervical precancerous lesions, and the relationship between the tumor clinicopathological parameters, prognosis and the expression of AQP1. Methods： Immunohistochemical method （EliVision） was used to detect the expression of AQP1 in samples from 106 patients [20 with normal cervical tissue, 30 with cervical intraepithelial neoplasia （stage Ⅰ and Ⅱ） and 56 with CSC]. Survival analysis was performed by Kaplan-Meier method. Results： AQP1 protein was expressed in vascular endothelia of all samples. It showed upregulation of AQP1 expression in CSC. There was a significant difference between CSC and normal cervical tissues （P〈0.05）. AQP1 was expressed in some tumor cells and unexpressed in normal squamous epithelial cells. And APQl-expressing tumor cells were positively related to lymph node metastasis. Patients with APQl-expressing tumor cells had the lower survival rate than the ones without. Conclusion： Abnormal expression of AQP1 plays an important role in the development of CSC. Positive expression of AQP1 in tumor cells maybe enhances tumor metastasis and could be used as a marker for tumor prognosis.     

Effects of tetrandrine on phenotypic modulation of vascular smooth muscle cells and expression of p38 MAPK as well as MKP-1 after intimal injury of rabbit carotid arteries

Objective： To study the effects of tetrandrine （Tet） on phenotypic modulation of vascular smooth muscle cells （VSMCs） and expression of p38 mitogen-activated protein kinase （p38MAPK） as well as mitogen-activated protein kinase phosphatase-1 （MKP-1） after vascular intimal injury. Methods： HE staining was used to analyze vascular morphology of sham-injured group, injured group and Tet-treated group at day 28. lmmunohistochemistry, Western blot and RT-PCR were respectively used to detect the expression change of smooth muscle a-actin （SMa-actin）, proliferation cell nuclear antigen （PCNA）, p38MAPK and MKP-1 of injured group and Tet group at days 7, 14 and 28 after balloon injury. Results： ① All layers of vascular wall in sham-injured group were intact at day 28. The neointimal area was significantly increased and the lumen area notably decreased in injured group at day 28. The neointimal proliferation in Tet treated group was less than that in injured group, and the lumen area of Tet group was significantly increased than that of injured group at day 28. ②Compared with the injured group, the expression of SMa-actin, PCNA, p38MAPK and MKP-1 of vascular wall in Tet group was no difference, and the neointimal proliferation condition was also basically as same as injured group at day 7 after injury. The expression of PCNA and p38MAKP in Tet group was obviously lower than that in injured group, and the expression of MKP-1 in Tet group was obviously higher than that in injured group at days 14 and 28 after injury. The expression of SMa-actin in Tet group was slightly higher than that in injured group at days 14 and 28 after injury. Conclusions： Tet could reduce neointimal proliferation by inhibiting VSMCs phenotypic modulation and p38MAPK signaling transduction pathway as well as its down regulation.     

Relationship between AQP4 expression and structural damage to the blood-brain barrier at early stages of traumatic brain injury in rats

Background Although some studies have reported that aquaporin-4 （AQP4） plays an important role in the brain edema after traumatic brain injury （TBI）, little is known about the AQP4 expression in the early stage of TBI, or about the correlation between the structural damage to the blood-brain barrier （BBB） and angioedema. The aim of this project was to investigate the relationship between AQP4 expression and damage to the BBB at early stages of TBI. Methods One hundred and twenty healthy adult Wistar rats were randomly divided into two groups： sham operation group （SO） and TBI group. The TBI group was divided into five sub-groups according to the different time intervals： 1, 3, 6, 12, and 24 hours. The brains of the animals were taken out at different time points after TBI to measure brain water content. The cerebral edema and BBB changes in structure were examined with an optical microscopy （OM） and transmission electron microscopy （TEM）, and the IgG content and AQP4 protein expression in traumatic brain tissue were determined by means of immunohistochemistry and Western blotting. The data were analyzed with SPSS 13.0 statistical software. Results In the SO group, tissue was negative for IgG, and there were no abnormalities in brain water content or AQP4 expression. In the TBI group, brain water content significantly increased at 6 hours and peaked at 24 hours following injury. IgG expression significantly increased from 1 to 6 hours following injury, and remained at a high level at 24 hours. Pathological observation revealed BBB damage at 1 hour following injury. Angioedema appeared at 1 hour, was gradually aggravated, and became obvious at 6 hours. Intracellular edema occurred at 3 hours, with the presence of large glial cell bodies and mitochondrial swelling. These phenomena were aggravated with time and became obvious at 12 hours. In addition, microglial proliferation was visible at 24 hours. AQP4 protein expression were reduced at 1 hour, lowest at 6 hours, and began to increase at 12 hours, showing a V-shaped curve. Conclusions The angioedema characterized by BBB damage was the primary type of early traumatic brain edema. It was followed by mixed cerebral edema that consisted of angioedema and cellular edema and was aggravated with time. AQP4 expression was down-regulated during the angioedema attack, but AQP4 expression was upregulated during intracellular edema.     

急性肺损伤大鼠呼吸膜AQP1和AQP5的表达

目的确定水通道蛋白AQP1及AQP5是否在大鼠肺泡毛细血管膜(呼吸膜)表达,进而研究急性肺损伤(ALI)大鼠AQP1和AQP5的表达调节及激素干预的作用。方法采用亲和的抗人AQP1和AQP5抗体,应用免疫组化及免疫电镜的方法研究AQP1及AQP5在呼吸膜的分布。选用肺泡内灌注脂多糖(LPS)制作大鼠ALI动物模型,研究ALI时呼吸膜AQP1及AQP5的变化。结果免疫染色显示AQP1主要表达于正常肺组织的微血管内皮,而AQP5主要表达于肺泡I型上皮细胞。免疫组化分析进一步表明LPS灌注后4h~48h AQP1及AQP5在呼吸膜的表达均下降;AQP1蛋白于LPS灌注后24h及激素干预后有部分恢复(P0.05),而AQP5无这种恢复现象。结论 ALI时AQP1及AQP5在呼吸膜的表达减少,提示ALI时AQP1和AQP5的下降表达可能与其液体转运的异常有关。     

AQP1、AQP2及AQP3在人腺性膀胱炎组织中的表达

目的：研究水通道蛋白（aquaporin,AQP）1、2、3在人腺性膀胱炎组织中的分布及表达情况。方法：取经尿道腺性膀胱炎电切手术切取的腺性膀胱炎组织及周围正常膀胱组织各30例,应用免疫组织化学S-P法检测AQP1、AQP2及AQP3的分布及表达，并通过计算机对染色结果进行灰度值测定。结果：在腺性膀胱炎组织中AQP1主要表达在微血管内皮细胞，免疫组化阳性指数35.947；AQP2主要表达在炎性膀胱黏膜上皮细胞的胞膜及胞质内，免疫组化阳性指数34.644；AQP3则呈阴性表达。AQP1在正常膀胱组织中主要表达于膀胱黏膜下微血管和小动脉的内皮细胞, AQP2和AQP3表达于膀胱黏膜上皮细胞的细胞膜及胞质中。AQP1、AQP2及AQP3在正常膀胱组织的免疫组化阳性指数分别为57.038、61.425及60.468，与在腺性膀胱炎组织中的表达比较差异有显著性（P<0.01）。结论：腺性膀胱炎时AQPs的表达量明显减低，炎症病变影响AQPs在膀胱组织中的的表达。     

脂多糖对大鼠肺损伤及肺组织中AQP1和AQP5表达的影响

目的: 探讨大鼠经静脉注射脂多糖(LPS)对急性肺损伤(ALI)及肺组织中水通道蛋白1(AQP1)和水通道蛋白5(AQP5)表达的影响,阐明其作用机制。方法: SPF级2月龄雄性Wistar大鼠48只随机分为对照组和LPS组(n=24),分别经尾静脉注射生理盐水和LPS,每组分别于注射后2、6、12和24 h时间点采集标本,每个时间点6只。HE染色观察肺组织病理学变化;测定大鼠肺湿/干质量(W/D)比、肺渗透指数;ELISA法检测血清肿瘤坏死因子α(TNF-α)和巨噬细胞炎性蛋白1α(MIP-1α)水平;采用Western blotting、免疫组织化学和Real-Time PCR方法检测大鼠肺组织中AQP1和AQP5蛋白及mRNA表达水平。结果: 与对照组比较,LPS组大鼠血清TNF-α和MIP-1α水平在注射LPS后2、6和12h时间点均明显升高(P<0.05),至24h时逐渐恢复正常。HE染色,注射LPS后2h大鼠肺组织出现水肿和炎性细胞浸润,以12h时间点最明显;LPS组各时间点大鼠肺W/D比、肺渗透指数均较对照组明显升高(P<0.05),12h时间点最明显。与对照组比较,LPS组各时间点大鼠肺组织中AQP1和AQP5 mRNA及蛋白表达水平均明显下降(P<0.01),以12h时间点下降最明显。结论: LPS可导致大鼠ALI和肺组织中AQP1及AQP5表达水平下调,并参与了肺水肿的形成。     

脑疏宁对脑外伤大鼠脑水肿及脑组织AQP4表达的影响

目的 观察脑疏宁对脑外伤大鼠脑组织含水量及水通道蛋白4(AQP4)表达的影响,探讨其治疗创伤性脑水肿的机制.方法 SD大鼠264只,随机分为假手术组(88只)、模型组(88只)和脑疏宁组(88只),建立大鼠创伤性脑损伤模型.分别在6 h,1、3、5 d 4个时间点测定脑组织含水量、伊文思蓝(EB)含量,并采用免疫组化方法检测脑组织AQP4蛋白的表达,电镜观察血脑屏障超微结构改变.结果 模型组大鼠伤后各时间点伤侧脑组织含水量、EB含量及伤灶周围AQP4蛋白表达水平明显高于假手术组(均P<0.001);电镜下内皮细胞紧密连接开放、星形胶质细胞足突肿胀.中药治疗组各时间点脑组织含水量、EB含量及AQP4表达水平均较模型组降低(P<0.05);血脑屏障紧密连接的破坏减少、星形胶质细胞足突肿胀减轻.结论 脑疏宁可改善血脑屏障损伤,减轻创伤后脑水肿.其作用可能与抑制AQP4在损伤脑组织中的表达、减轻星形胶质细胞损害有关.     

水通道蛋白1、3在膀胱尿路上皮癌中的表达及临床意义

目的探讨膀胱尿路上皮癌中水通道蛋白1、3(AQP1、AQP3)的表达与分布,及其与组织学分级和病理分期之间的关系及临床意义。方法采用免疫组化S-P法、蛋白免疫印迹(Western-blot)法对60例膀胱尿路上皮癌组织及30例正常膀胱组织中AQP1及AQP3的表达进行检测,并分析与其不同组织学分级、不同病理分期和有无淋巴结转移的关系。结果 AQP1在膀胱尿路上皮癌组织及正常膀胱组织中主要表达在微血管的内皮细胞的细胞膜及细胞质中,AQP3主要表达在膀胱尿路上皮癌的癌细胞的胞膜及胞质中。免疫组织化学S-P法和Western blot法检测的结果基本一致。正常膀胱组织与不同分级的膀胱尿路上皮癌组织中AQP1及AQP3的蛋白表达量分别比较,差异均有统计学意义(P<0.01);正常膀胱组织与不同病理分期的膀胱尿路上皮癌组织中AQP1及AQP3的蛋白表达量比较,差异均有统计学意义(P<0.01);AQP1及AQP3在有淋巴结转移的膀胱癌组织中的表达量分别与无淋巴结转移的膀胱癌组织比较,差异均有统计学意义(P<0.01)。结论 AQP1和AQP3的表达与膀胱癌的组织学分级及病理分期有关,在膀胱癌形成及发展过程中起重要作用,对预测膀胱癌的侵袭性、分期及临床诊疗有指导意义。     

水通道蛋白在大鼠氧化性白内障晶状体上的表达

目的 观察Ⅰ型水通道蛋白（AQP1）在正常及氧化性白内障模型大鼠晶状体上的表达，探讨其在氧化性白内障发生过程中的作用。方法 将健康清洁级Wistar大鼠60只离体透明晶状体随机分为2组，实验组加2mmol／L H2O2，空白组不加H2O2，其余处理相同。分别于12、24及48h观察两组大鼠晶状体的混浊情况；运用免疫组织化学方法及计算机图像分析技术检测AQP1的表达。结果 加入培养液后48h，空白组晶状体透明，而实验组的晶状体有不同程度的混浊；实验组晶状体的AQP1表达较空白组少，差异有显著性意义（P〈0．05）。结论 AQP1的减少在氧化性白内障的发生中有一定作用，氧化损伤可能通过减少AQP1在晶状体上皮细胞膜上的表达，影响晶状体囊膜水代谢，以诱发白内障。     

人参二醇组皂苷对内毒素休克大鼠心肌AQP1表达水平的影响

目的：探讨人参二醇组皂苷(PDS)对内毒素休克大鼠心肌的保护作用,并揭示其保护作用与水通道蛋白1（AQP1）表达的关系。方法：40只Wistar大鼠分为空白对照组（CTR）、模型组(LPS)、地塞米松组(DEX)及PDS组。LPS（5 mg·kg-1）舌下静脉注射复制内毒素休克模型,监测大鼠平均动脉压（MAP）及动脉压下降的百分数,测量休克240 min大鼠血清天冬氨酸氨基转移酶(AST)、肌酸激酶(CK)和乳酸脱氢酶(LDH)含量及心肌组织匀浆超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的变化,Western blotting方法检测心肌组织AQP1表达情况。结果：以血压下降至基础血压(0 min)的2/3判定为休克状态,注射LPS5 min　后各组动物均进入休克状态,20 min后平均动脉压（MAP）代偿性回升,于休克第60 min时,LPS组MAP进行性下降,而PDS和DEX组MAP维持稳定而持久的代偿变化;休克240 min时,PDS和DEX组血清AST、CK和LDH含量显著低于LPS组（P<0.05）,心肌组织匀浆SOD活性高于LPS组（P<0.05）,MDA含量低于LPS组（P<0.05）。Western blotting结果显示：与CTR组比较,LPS组AQP1表达显著降低(P<0.05),PDS组和DEX组AQP1表达水平明显高于LPS组（P<0.05）。结论：PDS对内毒素休克大鼠心肌具有保护作用,其机制可能是通过增强内毒素血症时心肌毛细血管内皮细胞AQP1蛋白表达,抑制心肌间质水肿而发挥作用。     

大鼠溺死时肺组织水通道蛋白1的变化

目的 观察溺死大鼠肺组织中水通道蛋白1(aquaporin AQF1)的变化。方法 取对照组、实验组大鼠肺组织，用免疫组织化学法和免疫电镜胶体金法，观察及定位肺组织中水通道蛋白1。结果 免疫组化显示溺死时肺间质的毛细血管内皮、支气管上皮及肺泡上皮AQP1的阳性表达，积分光密度值差别有统计学意义。免疫电镜显示肺泡(型上皮细胞AQP1的胶体金数的差别有统计学意义。结论 AQP1在大鼠溺死时肺组织中表达有阳性意义且定位在Ⅰ型上皮细胞膜上。     

水通道蛋白-1及其在心脏中作用的研究进展

水通道蛋白-1(AQP1)是水通道蛋白(AQPs)家族中发现最早且分布最广泛的成员,具有特殊的分子结构,受多种因素的调节。除转运水分子外,AQP1还能转运多种气体分子并参与细胞游走过程。心脏组织中AQP1主要在红细胞、毛细血管内皮细胞以及心肌细胞中表达。心肌细胞内AQP1定位于细胞质膜,可能参加兴奋—收缩偶联过程以及水分子的转运,调节心脏的各种生理和病理过程的水代谢。体外循环心脏手术可以影响AQPs的表达及活性,导致术后心肌水肿。心脏中AQPs的研究对临床工作有重要的指导意义。     

水通道蛋白-1及其在心脏中作用的研究进展

水通道蛋白-1（AQP1）是水通道蛋白（AQPs）家族中发现最早且分布最广泛的成员,具有特殊的分子结构,受多种因素的调节。除转运水分子外,AQP1还能转运多种气体分子并参与细胞游走过程。心脏组织中AQP1主要在红细胞、毛细血管内皮细胞以及心肌细胞中表达。心肌细胞内AQP1定位于细胞质膜,可能参加兴奋—收缩偶联过程以及水分子的转运,调节心脏的各种生理和病理过程的水代谢。体外循环心脏手术可以影响AQPs的表达及活性,导致术后心肌水肿。心脏中AQPs的研究对临床工作有重要的指导意义。