PDF(Pubmed)
Abstract：
UNASSIGNED: Geometrical alterations in the coronary resistance artery network and the potential involvement of Tenascin C (TNC) extracellular matrix protein were investigated in diabetic and control mice.
UNASSIGNED: Diabetes was induced by streptozotocin (STZ) injections (n = 7-11 animals in each group) in Tenascin C KO (TNC KO) mice and their Wild type (A/J) littermates. After 16-18 weeks the heart was removed and the whole subsurface network of the left coronary artery was prepared (down to branches of 40 μ m outer diameter), in situ pressure-perfused and studied using video-microscopy. Outer and inner diameters, wall thicknesses and bifurcation angles were measured on whole network pictures reconstructed into collages at 1.7 μ m pixel resolutions.
UNASSIGNED: Diabetes induced abnormal morphological alterations including trifurcations, sharp bends of larger branches, and branches directed retrogradely (p < 0.001 by the χ 2 test). Networks of TNC KO mice tended to form early divisions producing parallelly running larger branches (p < 0.001 by the χ 2 probe). Networks of coronary resistance arteries were substantially more abundant in 100-180 μ m components, appearing in 2-5 mm flow distance from orifice in diabetes. This was accompanied by thickening of the wall of larger arterioles ( > 220 μ m) and thinning of the wall of smaller (100-140 μ m) arterioles (p < 0.001). Blood flow should cover larger distances in diabetic networks, but interestingly STZ-induced diabetes did not generate further geometrical changes in TNC KO mice.
UNASSIGNED: Diabetes promotes hypertrophic and hypotrophic vascular remodeling and induces vasculogenesis at well defined, specific positions of the coronary vasculature. TNC plays a pivotal role in the formation of coronary network geometry, and TNC deletion causes parallel fragmentation preventing diabetes-induced abnormal vascular morphologies.
UNASSIGNED: Diabetes was induced by streptozotocin (STZ) injections (n = 7-11 animals in each group) in Tenascin C KO (TNC KO) mice and their Wild type (A/J) littermates. After 16-18 weeks the heart was removed and the whole subsurface network of the left coronary artery was prepared (down to branches of 40 μ m outer diameter), in situ pressure-perfused and studied using video-microscopy. Outer and inner diameters, wall thicknesses and bifurcation angles were measured on whole network pictures reconstructed into collages at 1.7 μ m pixel resolutions.
UNASSIGNED: Diabetes induced abnormal morphological alterations including trifurcations, sharp bends of larger branches, and branches directed retrogradely (p < 0.001 by the χ 2 test). Networks of TNC KO mice tended to form early divisions producing parallelly running larger branches (p < 0.001 by the χ 2 probe). Networks of coronary resistance arteries were substantially more abundant in 100-180 μ m components, appearing in 2-5 mm flow distance from orifice in diabetes. This was accompanied by thickening of the wall of larger arterioles ( > 220 μ m) and thinning of the wall of smaller (100-140 μ m) arterioles (p < 0.001). Blood flow should cover larger distances in diabetic networks, but interestingly STZ-induced diabetes did not generate further geometrical changes in TNC KO mice.
UNASSIGNED: Diabetes promotes hypertrophic and hypotrophic vascular remodeling and induces vasculogenesis at well defined, specific positions of the coronary vasculature. TNC plays a pivotal role in the formation of coronary network geometry, and TNC deletion causes parallel fragmentation preventing diabetes-induced abnormal vascular morphologies.
摘要：
■在糖尿病和对照小鼠中研究了冠状动脉阻力动脉网络的几何改变以及TenascinC（TNC）细胞外基质蛋白的潜在参与。
在生腱蛋白CKO（TNCKO）小鼠及其野生型（A/J）同窝猫中通过链脲佐菌素（STZ）注射（每组n=7-11只动物）诱导糖尿病。16-18周后，取出心脏，制备左冠状动脉的整个地下网络（直到外径为40μm的分支），原位压力灌注和使用视频显微镜研究。外径和内径，在以1.7μm像素分辨率重建成拼贴的整个网络图片上测量壁厚和分叉角。
■糖尿病引起的异常形态学改变，包括三叉根，较大树枝的急弯，和分支逆行(χ2检验p<0.001)。TNCKO小鼠的网络倾向于形成早期分裂，产生平行运行的较大分支（χ2探针p<0.001）。冠状动脉阻力动脉网络在100-180μm成分中基本上更丰富，出现在2-5毫米的流量距离从孔口在糖尿病。这伴随着较大小动脉壁的增厚（>220μm）和较小（100-140μm）小动脉壁的变薄（p<0.001）。在糖尿病网络中，血流应该覆盖更大的距离，但有趣的是，STZ诱导的糖尿病在TNCKO小鼠中没有产生进一步的几何学变化。
■糖尿病促进肥厚性和低肥厚性血管重塑，并在明确定义的情况下诱导血管生成，冠状动脉血管的特定位置。TNC在冠状动脉网络几何形状的形成中起着关键作用，和TNC缺失导致平行片段化,防止糖尿病诱导的异常血管形态。
在生腱蛋白CKO（TNCKO）小鼠及其野生型（A/J）同窝猫中通过链脲佐菌素（STZ）注射（每组n=7-11只动物）诱导糖尿病。16-18周后，取出心脏，制备左冠状动脉的整个地下网络（直到外径为40μm的分支），原位压力灌注和使用视频显微镜研究。外径和内径，在以1.7μm像素分辨率重建成拼贴的整个网络图片上测量壁厚和分叉角。
■糖尿病引起的异常形态学改变，包括三叉根，较大树枝的急弯，和分支逆行(χ2检验p<0.001)。TNCKO小鼠的网络倾向于形成早期分裂，产生平行运行的较大分支（χ2探针p<0.001）。冠状动脉阻力动脉网络在100-180μm成分中基本上更丰富，出现在2-5毫米的流量距离从孔口在糖尿病。这伴随着较大小动脉壁的增厚（>220μm）和较小（100-140μm）小动脉壁的变薄（p<0.001）。在糖尿病网络中，血流应该覆盖更大的距离，但有趣的是，STZ诱导的糖尿病在TNCKO小鼠中没有产生进一步的几何学变化。
■糖尿病促进肥厚性和低肥厚性血管重塑，并在明确定义的情况下诱导血管生成，冠状动脉血管的特定位置。TNC在冠状动脉网络几何形状的形成中起着关键作用，和TNC缺失导致平行片段化,防止糖尿病诱导的异常血管形态。
