Scanning and transmission electron microscopic observation of femoral head feeding vessels in stroke-prone spontaneously hypertensive rats

Abstract

Stroke-prone spontaneously hypertensive rats (SHRSP) are known to show necrosis of the femoral head with a frequency of about 50%. This rat has thus been used as an animal model for necrosis of the femoral head in many studies. In a detailed investigation of feeding vessel disorders that cause femoral head necrosis, we observed changes over time in the feeding vessels using scanning electron microscopy and transmission electron microscopy. In scanning electron microscopy of vascular casts, abnormal findings in feeding vessels of SHRSP with aging from the immature stage included contortion and bending in the lumen with overall narrowing. Under transmission electron microscopy, decreased numbers of smooth muscle cells and increased amounts of collagen fibers were marked, and these changes with hypertrophy of vascular walls might be similar to those of arteriolosclerosis. The structural changes first revealed by transmission electron microscopic observation might cause the friability of the feeding vessels so that contortion and bending occurred, suggesting transient obstruction of blood flow to the femoral head and subsequent induction of femoral head necrosis. These findings should help in understanding the causes of femoral head necrosis in humans, including Perthes' disease.

Abnormalities of Vascular Structure and Function in Children With Perthes Disease

“…32 The stroke prone spontaneously hypertensive rate rat is also a common animal model of arteriosclerosis, hypertension, and cerebrovascular disease and is known to develop spontaneous femoral head ischemia in infancy in ∼50% of cases. 33 Furthermore, abnormal hyperemic responses, such as those observed in the current study, have recently been shown to be associated with cardiovascular disease in adults.…”

DL-3-n-Butylphthalide, an Anti-Oxidant Agent, Prevents Neurological Deficits and Cerebral Injury Following Stroke per Functional Analysis, Magnetic Resonance Imaging and Histological Assessment

“…However, the protective effect of NBP against stroke cannot be explained by hypotension alone because NBP could not change high blood pressure state of SHR [30]. Histopathological changes in the vessel, such as decreased numbers of smooth muscle cells, increased amounts of collagen fibers with hypertrophy of vascular walls and decreased endothelial tight junctions were found in SHR mice [31,32]. These modifications induced chronic mild hypoperfusion in the brain of SHR mice and increased the susceptibility to blood-brain barrier dysfunction and stroke.…”

Proinflammation, profibrosis, and arterial aging

“…94 Furthermore, it has been observed that VSMCs in aortic rings of a normal vessel cultured in a physiologic bath will not proliferate in response to PDGF. 95 However, if the same aortic rings are briefly treated with a combination of collagenase and elastase and then placed in the same bath, the VSMCs in the aortic ring will proliferate in response to exogenously added PDGF. 95 Similar to migration, VSMC proliferation is also dependent on ECM ligand density, but the increase in matrix stiffness is the dominant factor affecting proliferation.…”

“…95 However, if the same aortic rings are briefly treated with a combination of collagenase and elastase and then placed in the same bath, the VSMCs in the aortic ring will proliferate in response to exogenously added PDGF. 95 Similar to migration, VSMC proliferation is also dependent on ECM ligand density, but the increase in matrix stiffness is the dominant factor affecting proliferation. 96 Interestingly, increased matrix stiffness enhances VSMC proliferation induced by PDGF.…”

“…Degraded collagen fragments cause VSMCs to lose their focal adhesion and to round up, and are ready to migrate or proliferate 94 . Furthermore, it has been observed that VSMCs in aortic rings of a normal vessel cultured in a physiologic bath will not proliferate in response to PDGF 95 . However, if the same aortic rings are briefly treated with a combination of collagenase and elastase and then placed in the same bath, the VSMCs in the aortic ring will proliferate in response to exogenously added PDGF 95 .…”