Animals ; Blood Vessels ; pathology ; ultrastructure ; Cochlea ; blood supply ; Female ; Male ; Rats ; Rats, Inbred SHR ; Rats, Wistar

Elastin is known to occur in the lung parenchyma and pleura as well as in the pulmonary vessels, but no detailed studies of this elastin's linkage between them have been done in three dimensions. For many years we have known that there is abundant elastin in the mammalian lungs, which may be associated with etiology of causing emphysema. We have developed selective casting methods to allow us to determine the location where elastin is found morphologically. The method involves casting either the vasculature via the right ventricle, or the airways via the trachea in the air sacs. Studies of the vasculature were done with the lung inflated to 80% of the vital capacity. The casted lungs were then put in 0.1 N NaOH at 75 degrees C for 48 hours, turning them frequently. THis method removed all non-elastin tissues. The scanning electron microscopy (SEM) was used to reveal the three dimensional pictures of elastin structures from both lung parenchyma and pulmonary vessels. Elastin was seen as fenestrated sheets and some fibers in both the vessels and the airways. Elastin in the two different locations was often interconnected. Studies on 6 dogs, 8 rabbits, and 2 pigs showed no significant species difference at the level of resolution of the SEM, which was used to study the specimens after they had been freeze-dried.
Animal ; Blood Vessels/metabolism/ultrastructure ; Corrosion Casting ; Dogs ; Elastin/*ultrastructure ; Lung/blood supply/*metabolism ; Microscopy, Electron, Scanning ; Pulmonary Alveoli/metabolism/ultrastructure ; Rabbits ; Swine

BACKGROUNDThere have been no detailed reports of the three-dimensional structure and the relationship between the external and internal vascularizations observed successively for a long duration in the rat fetus, although many authors have studied the vascular morphology of the developing brain. This study examined the three-dimensional structure of both the external and internal vascularizations of the prenatal rat telencephalon from embryonic days 12 (E12) to 20 (E20).

METHODA microvascular casting method for scanning electron microscopy (SEM) was used in this study, along with vascular staining using gold-gelatin solution-autometallography (GGS-AMG) after intravascular injection of colloidal gold, as well as hematoxylin-eosin (HE) staining for paraffin embedded specimens.

RESULTSIn GGS-AMG stains, E16 fetuses had a few short perforating cortical blood vessels (SPCVs); E17 fetuses had long perforating cortico-medullary vessels (LPCVs). Older fetuses had specific patterns of vascular networks in the cortex and the deeper subcortical part of the telencephalon. In the cortex, fine longitudinal blood vessels were connected by transverse channels. The deep telencephalon had fine blood vessels running in all directions. Using SEM, the external vascularization was already visible in E12 fetuses as arborizations of arterial branches, forming a mesh of fine vascular networks covering the telencephalon. A coralliform fine venous plexus was observed in the external vascularization of E16 fetuses. There were ring-like anastomoses and bud-like protrusions in the network of small blood vessels, most likely the angiogenesis of fetal vessels. From E12 to E16, an immature and incomplete internal vascularization began to appear. There were short blood vessels with ballooned terminals branching from the external vascularization. They penetrated the brain tissue to form networks in the superficial layer, comparable to SPCVs. In E17 to E20 fetuses, tortuous venous branches, straight arterial blood vessels, and a fine network of small blood vessels formed the external vascularization. There were fewer arterial than venous branches connecting to the fine networks of small blood vessels. LPCVs were noted at E17, at the time the white matter emerged. They branched from the external vascularization, and perpendicularly penetrated the brain surface, traversing the cortical plate, and entering into the deep brain. At E17, arterial and venous blood vessels could be clearly distinguished in the external vascularization. At E20, the cortex and white matter contained specific arrangements of networks of fine blood vessels, as seen by GGS-AMG staining.

CONCLUSIONThese findings show that the development of both the external and internal vascularization follows the development of the telencephalon. In particular, the emergence of the cortical plate and white matter on E16 and E17 influence the development of both the internal and the external vascularization. The laminal arrangement of blood vessels was not observed corresponding to the respective laminal neuronal layers.

Animals ; Blood Vessels ; embryology ; ultrastructure ; Embryo, Mammalian ; Fetus ; Microscopy, Electron, Scanning ; Rats ; Rats, Wistar ; Telencephalon ; blood supply

We have used selective casting methods to separate pulmonary elastin from vascular elastin in the lungs of rabbits, dogs and pigs. The lungs are digested with 0.1 N NaOH at 75 degrees C for 24 approximately 48 hours with frequent turning as the lungs are filled with air to about 80% of the vital capacity prior to the casting which is done at pressure of 20 approximately 50 mmHg. After vascular injections, we saw many small globular bits of casting material well separated from cast vessels and lying in the pulmonary elastin. Surface forces should make the casting material creep along the vessels even if they are not completely filled, so that the spherical shape is the one expected if the case is extruded into the parenchymal space and the air space. We conclude that this suggests that the pulmonary circulation is partially and temporarily 'open' as seen in the spleen and some other organs, rather than a completely 'closed' one as is generally accepted. At least some of these extravasations may be associated with lymphatics, although we have not proved this.
Animal ; Blood Vessels/ultrastructure ; *Capillary Permeability ; Corrosion Casting ; Dogs ; Male ; Microscopy, Electron, Scanning ; *Pulmonary Circulation ; Support, Non-U.S. Gov't ; Swine

OBJECTIVETo investigate the effect of therapeutic ultrasound-induced microbubble destruction on the microcirculation of rat skeletal muscle.

METHODSThirty SD rats were randomized into 5 groups (n=6), namely normal saline, microbubble, ultrasound, high-energy ultrasound microbubble and low-energy ultrasound microbubble groups. Before and after the treatments, the diameter and blood flow velocity in the microvessels in the skeletal muscle were measured, and the structural changes of the injured microvessels observed by electron microscopy.

RESULTSMicrobubble cavitation did not produce significant effect on the mean arterial pressure and diameter of microvessels in rat skeletal muscle (P>0.05), but the blood flow velocity was obviously lowered and blood flow volume reduced in the microvessels. The reduction of the flow velocity and blood flow volume and their subsequent recovery were associated with ultrasound energy, and in the low ultrasound energy group, the flow velocity and blood flow volume in the of venules recovered obviously after about 15 min, which, however, took approximately 1 h for the arterioles. In contrast, recovery of the flow velocity and blood flow volume in the microvessels took more than 2 h in the high ultrasound energy group. Cavitation resulted in endothelium cell rupture, widening of the endothelial interspace and entry of the red blood cells into the extravascular tissues as revealed by electron microscopy, but no rupture of the lining endothelium was observed 2 h after the treatment.

CONCLUSIONSEndothelium cell rupture induced by microbubble cavitation may affect the local microcirculation, and lower ultrasound energy exposure is associated with milder endothelial injury and more rapid recovery.

Animals ; Blood Flow Velocity ; Blood Vessels ; pathology ; physiopathology ; Endothelial Cells ; pathology ; ultrastructure ; Female ; Male ; Microbubbles ; Microcirculation ; Microscopy, Electron ; Microspheres ; Muscle, Skeletal ; blood supply ; Rats ; Rats, Sprague-Dawley ; Ultrasonics

The whole retina, except for the medullary fiber zone in a rabbit eye, is supplied by choroidal circulation. Therefore, the histopathological changes of the sensory retina due to choroidal circulatory disturbance in rabbits may be comparable to that of the human sensory retina in the case of ophthalmic artery occlusion. This study was carried out to evaluate the histopathological changes of the ischemic retina secondary to the occlusion of choroidal circulation. The experimental occlusion of all posterior ciliary arteries and anterior ciliary arteries in the horizontal rectus muscle of rabbit eyes was performed and the subsequent histopathological changes of the sensory retina were observed by transmission electron microscopy. The morphological changes of the sensory retina following the occlusion of the ciliary arterial system are as follows: severe loss of the inner and outer segments of the photoreceptor, mild to moderate degeneration of the ganglion cells, and excellent preservation of the Muller's cell fibers and the extension of the cytoplasmic villous processes to the cytoplasmic vacuolar spaces of other degenerated cells. These findings indicate that the Muller's fibers in the ischemic condition of retina might contribute to the formation of gliosis or scarring of a damaged retina.
Animals ; Arterial Occlusive Diseases/*complications ; Arteries ; Choroid/*blood supply ; Ciliary Body/*blood supply ; Ischemia/*etiology/pathology ; Rabbits ; Retina/*ultrastructure ; *Retinal Vessels

OBJECTIVETo study the effects of enhanced external counterpulsation (EECP) on the vascular morphology, and endothelial function using experimentally induced hypercholesterolemic pigs.

METHODSThirty five male pigs were randomly divided into three groups: 7 normal control animals, 11 hypercholesterolemic animals, and 17 hypercholesterolemic animals receiving EECP. Serum cholesterol was measured. The coronary arteries and aortas were sampled for histopathologic and ultrastructural examination. The NF-kappaB protein expression of porcine coronary arteries was investigated by immunofluorescence.

RESULTSCompared with the normal controls, serum cholesterol levels were significantly higher in the hypercholesterolemic animals with or without EECP. The plaque/intimal area ratio of the aorta decreased significantly in animals receiving EECP [(3.33 +/- 2.40)%, versus (12.03 +/- 7.12)% in those without EECP, P < 0.05]. Lipid deposition, endothelial damage and proliferation of smooth muscle cells were less severe in animals receiving EECP than those not. Moreover, activation and expression of NF-kappaB also decreased significantly (P < 0.05) in animals receiving EECP.

CONCLUSIONSEECP improves the morphology and function of vascular endothelium, and retards the development and progression of atherosclerosis, likely through the inhibition of NF-kappaB signaling pathway.

Animals ; Aorta, Abdominal ; metabolism ; pathology ; ultrastructure ; Atherosclerosis ; blood ; metabolism ; pathology ; Cholesterol ; blood ; Coronary Vessels ; metabolism ; pathology ; ultrastructure ; Counterpulsation ; methods ; Endothelial Cells ; metabolism ; pathology ; Hypercholesterolemia ; blood ; metabolism ; pathology ; Lipoproteins, LDL ; blood ; Male ; Microscopy, Confocal ; Microscopy, Electron, Scanning ; Microscopy, Electron, Transmission ; Muscle, Smooth, Vascular ; metabolism ; pathology ; NF-kappa B ; metabolism ; Random Allocation ; Swine

OBJECTIVE: To investigate the structural characteristics of the cerebral small vessels with an unknown type of pathological lesion (UTPL). METHODS: Contents of beta-amyloid, alpha-actin and collagen IV in cerebral small vessels with UTPL were studied by Congo red staining, immunohistochemical staining and computer image analysis. RESULTS: The low expression levels of alpha-actin and collagen IV (P<0.05) were observed in tunica media of the vessels with UTPL, and no positive expression of beta-amyloid (P>0.05) was observed in these vessel walls. The expressions of proteins mentioned above in UTPL were different from those of cerebral amyloid angiopathy(CAA) and hyaline arteriolosclerosis. CONCLUSION UTPL was different from CAA or hyaline arteriolosclerosis in pathologic feature.
Actins/metabolism* ; Amyloid beta-Peptides/metabolism* ; Autopsy ; Blood Vessels/ultrastructure* ; Brain/pathology* ; Cerebral Amyloid Angiopathy/pathology* ; Collagen Type IV/metabolism* ; Humans ; Image Processing, Computer-Assisted ; Immunohistochemistry ; Staining and Labeling ; Subarachnoid Hemorrhage/pathology*

The integrity of blood vessels controls vascular permeability and extravasation of blood cells, across the endothelium. Thus, the impairment of endothelial integrity leads to hemorrhage, edema, and inflammatory infiltration. However, the molecular mechanism underlying vascular integrity has not been fully understood. Here, we demonstrate an essential role for A-kinase anchoring protein 12 (AKAP12) in the maintenance of endothelial integrity during vascular development. Zebrafish embryos depleted of akap12 (akap12 morphants) exhibited severe hemorrhages. In vivo time-lapse analyses suggested that disorganized interendothelial cell-cell adhesions in akap12 morphants might be the cause of hemorrhage. To clarify the molecular mechanism by which the cell-cell adhesions are impaired, we examined the cell-cell adhesion molecules and their regulators using cultured endothelial cells. The expression of PAK2, an actin cytoskeletal regulator, and AF6, a connector of intercellular adhesion molecules and actin cytoskeleton, was reduced in AKAP12-depleted cells. Depletion of either PAK2 or AF6 phenocopied AKAP12-depleted cells, suggesting the reduction of PAK2 and AF6 results in the loosening of intercellular junctions. Consistent with this, overexpression of PAK2 and AF6 rescued the abnormal hemorrhage in akap12 morphants. We conclude that AKAP12 is essential for integrity of endothelium by maintaining the expression of PAK2 and AF6 during vascular development.
A Kinase Anchor Proteins/*genetics/metabolism ; Animals ; Blood Vessels/abnormalities/*embryology/metabolism ; Cell Cycle Proteins/genetics/metabolism ; Down-Regulation ; Embryo, Nonmammalian/abnormalities/*blood supply/embryology/metabolism ; Gene Deletion ; *Gene Expression Regulation, Developmental ; Hemorrhage/*embryology/genetics/metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Intercellular Junctions/genetics/metabolism/ultrastructure ; Kinesin/genetics/metabolism ; Myosins/genetics/metabolism ; Zebrafish/*embryology/genetics ; p21-Activated Kinases/genetics/metabolism

OBJECTIVETo observe the effects of oral administration of guanxin II decoction (GX II) on cardiovascular function, especially on the dynamics of coronary blood flow in healthy males.

METHODSChanges of heart rate, diastolic pressure, systolic pressure, left ventricular ejection fraction (LVEF), E peak, A peak, E/A value of mitral flow, diastolic peak velocity (Vmax) and diastolic flow velocity time integrals (VTI) of left anterior descending coronary artery (LAD) in 11 healthy male subjects were measured before and after oral administration of GX II, using non-invasive echocardiogram.

RESULTSCompared with those before GX II administration, the changes after administration in heart rate, systolic pressure, diastolic pressure, LVEF, E peak, A peak and E/A value, were insignificantly different (P>0.05), but the Vmax and VTI significantly increased at 30 min, 60 min, 90 min and 120 min after GX II administration (P<0.05).

CONCLUSIONTo increase the coronary blood flow is possibly one of the mechanisms of GX II in treating coronary heart disease and angina pectoris.

Adolescent ; Adult ; Blood Flow Velocity ; drug effects ; Coronary Circulation ; drug effects ; Coronary Disease ; drug therapy ; Coronary Vessels ; drug effects ; ultrastructure ; Diastole ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Echocardiography ; Heart Rate ; drug effects ; Humans ; Male ; Middle Aged ; Systole ; drug effects ; Vasodilator Agents ; pharmacology ; Ventricular Function, Left ; drug effects