Abluminal plasma induces vasoconstriction meditated by serotonin and counterbalanced by endothelial nitric oxide synthase in healthy and malarial mouse arteries

Table 1 and 2. Raw data for vascular function of middle cerebral arteries (MCAs) from ECM and control animals evaluated ex vivo using pressure myographyThis table contains raw internal and external diameter measurements of MCAs from experimental cerebral malaria (ECM) and uninfected control mice during stimulation with serotonin (5-HT), methacholine (MCh), and sodium nitroprusside (SNP). Diameter data are presented as percentage change from basal diameter values. Data include concentration–response values and individual biological replicates. Also, this table contains raw internal and external diameter measurements of MCAs from ECM and uninfected mice stimulated with MCh or SNP in the presence or absence of the NOS inhibitor L-NAME. Diameter data are presented as percentage change from basal diameter values. Data include concentration–response values and individual vessel replicates.Table 3. Raw data for plasma-induced vascular reactivity of aortic ringsThis table contains raw vascular tension measurements from aortic rings exposed to increasing concentrations (0.1%, 0.3%, 1%, and 3%) of plasma from ECM or uninfected control mice. Tension data are presented as variation from basal tension values. Data include individual replicate measurements obtained during concentration–response experiments.Table 4. Raw data for NOS-dependent modulation of plasma-induced vasoconstrictionThis table contains raw vascular tension measurements from aortic rings stimulated with plasma from ECM or uninfected mice in the presence or absence of the NOS inhibitor L-NAME. Tension data are presented as variation from basal tension values. Data include measurements obtained under KH buffer conditions and during plasma concentration–response experiments.Table 5. Raw data for calcium channel-dependent plasma-induced vasoconstrictionThis table contains raw vascular tension measurements from aortic rings stimulated with plasma from ECM or control mice during pharmacological inhibition of calcium signaling using nifedipine and EGTA. Tension data are presented as variation from basal tension values. Data include sequential measurements from individual experimental replicates.Table 6. Raw data for sex-independent 5-HT₂A-mediated plasma-induced vasoconstrictionThis table contains raw vascular tension measurements from male and female aortic rings stimulated with plasma from ECM or uninfected mice in the presence or absence of the 5-HT₂A receptor antagonist ketanserin following NOS inhibition with L-NAME. Tension data are presented as variation from basal tension values. Data include concentration–response values and individual biological replicates.Table 7. Raw data for vascular reactivity of aortic rings from ECM mice stimulated with plasmaThis table contains raw vascular tension measurements from aortic rings obtained from ECM and uninfected mice stimulated with serotonin (5-HT), acetylcholine (ACh), plasma from ECM or control animals, and L-NAME. Tension data are presented as variation from basal tension values. Data include concentration–response values and individual biological replicates.Table 8. Raw data for polarized vasoconstrictive responses to plasma and serotoninThis table contains raw internal diameter measurements of isolated 3rd order mesenteric arterioles following luminal or abluminal application of plasma or serotonin (5-HT). Diameter data are presented as percentage change from basal diameter values. Data include individual vessel responses and measurements obtained after acetylcholine (ACh) stimulation.表1与表2 实验性脑型疟（experimental cerebral malaria, ECM）与对照动物的大脑中动脉（middle cerebral arteries, MCAs）离体压力肌动描记法检测的原始血管功能数据 本数据集包含经5-羟色胺（serotonin, 5-HT）、乙酰甲胆碱（methacholine, MCh）及硝普钠（sodium nitroprusside, SNP）刺激时，实验性脑型疟小鼠与未感染对照小鼠的大脑中动脉内径与外径原始测量数据。数据以相对于基础内径的百分比变化形式呈现，涵盖浓度-反应关系数据及独立生物学重复样本结果。此外，本数据集还包含在一氧化氮合酶（nitric oxide synthase, NOS）抑制剂L-NAME存在或不存在的条件下，经乙酰甲胆碱或硝普钠刺激的实验性脑型疟小鼠与未感染小鼠的大脑中动脉内径与外径原始测量数据，同样以相对于基础内径的百分比变化形式呈现，涵盖浓度-反应关系数据及独立血管样本重复结果。 表3 血浆诱导的主动脉环血管反应性原始数据 本数据集包含暴露于实验性脑型疟小鼠与未感染对照小鼠血浆（浓度梯度为0.1%、0.3%、1%及3%）的主动脉环的原始血管张力测量数据。张力数据以相对于基础张力的变化值形式呈现，涵盖浓度-反应实验中获得的独立重复测量结果。 表4 NOS依赖性调控血浆诱导血管收缩的原始数据 本数据集包含在一氧化氮合酶抑制剂L-NAME存在或不存在的条件下，经实验性脑型疟或未感染小鼠血浆刺激的主动脉环的原始血管张力测量数据。张力数据以相对于基础张力的变化值形式呈现，涵盖Krebs-Henseleit缓冲液（KH缓冲液）条件下及血浆浓度-反应实验中获得的测量结果。 表5 钙通道依赖性血浆诱导血管收缩的原始数据 本数据集包含使用硝苯地平（nifedipine）与乙二醇双(β-氨基乙基醚)四乙酸（EGTA）进行钙信号药理学抑制后，经实验性脑型疟或对照小鼠血浆刺激的主动脉环的原始血管张力测量数据。张力数据以相对于基础张力的变化值形式呈现，涵盖独立实验重复的序列测量结果。 表6 不依赖性别的5-HT₂A受体介导血浆诱导血管收缩的原始数据 本数据集包含经L-NAME抑制一氧化氮合酶后，在5-HT₂A受体拮抗剂酮色林（ketanserin）存在或不存在的条件下，经实验性脑型疟或未感染小鼠血浆刺激的雌雄小鼠主动脉环的原始血管张力测量数据。张力数据以相对于基础张力的变化值形式呈现，涵盖浓度-反应关系数据及独立生物学重复样本结果。 表7 实验性脑型疟小鼠主动脉环经血浆刺激后的血管反应性原始数据 本数据集包含从实验性脑型疟小鼠与未感染小鼠中分离的主动脉环，经5-羟色胺、乙酰胆碱（acetylcholine, ACh）、实验性脑型疟或对照动物血浆及L-NAME刺激后的原始血管张力测量数据。张力数据以相对于基础张力的变化值形式呈现，涵盖浓度-反应关系数据及独立生物学重复样本结果。 表8 血浆与5-羟色胺诱导的极性血管收缩反应原始数据 本数据集包含对分离的三级肠系膜小动脉分别向管腔侧或腔外侧施加血浆或5-羟色胺刺激后的原始内径测量数据。内径数据以相对于基础内径的百分比变化形式呈现，涵盖独立血管样本的反应数据及乙酰胆碱刺激后获得的测量结果。