A prospective study of cerebrovascular disease in Japanese rural communities, Akabane and Asahi. Part 1: evaluation of risk factors in the occurrence of cerebral hemorrhage and thrombosis. (1/14)

An epidemiological study of cerebrovascular disease in Akabane and Asahi, Japan, was made. (These cities are located near Nagoy, Japan.) The study population included 4,737 men and women aged 40 to 79 at the time of entry into the study. There were 4,186 persons who were examined and, of these, 264 cases of cerebrovascular attacks were observed between 1964 and 1970. The incidence rate of stroke in those persons not responding to the survey was 15.9 times higher than in those persons examined according to person-year observation in Akabane. The risk factors for cerebral hemorrhage and thrombosis were evaluated by age-adjusted and sex-adjusted relative risks. The predisposing factors to cerebral hemorrhage appeared to be high blood pressure, high left R wave, ST depression, T abnormality, capillary fragility counts, previous medical history of stroke and albuminuria. For cerebral thrombosis, the predisposing factors appeared to be high blood pressure, ST depression and funduscopic sclerotic findings, and those factors assumed to be significant were glycosuria and smoking habits. Ocular funduscopic abnormality was the most prominent risk factor for cerebral thrombosis, while high blood pressure and ECG abnormalities were highly related to cerebral hemorrhage. It was suggested that those subjects with a relatively higher blood pressure may have a higher relative risk of cerebral hemorrhage than those with a lower (normal range) blood pressure. A previous or family history of stroke also appeared significantly related to cerebral hemorrhage.  (+info)

Polycystin 1 is required for the structural integrity of blood vessels. (2/14)

Autosomal dominant polycystic kidney disease (ADPKD), often caused by mutations in the PKD1 gene, is associated with life-threatening vascular abnormalities that are commonly attributed to the frequent occurrence of hypertension. A previously reported targeted mutation of the mouse homologue of PKD1 was not associated with vascular fragility, leading to the suggestion that the vascular lesion may be of a secondary nature. Here we demonstrate a primary role of PKD1 mutations in vascular fragility. Mouse embryos homozygous for the mutant allele (Pkd1(L)) exhibit s.c. edema, vascular leaks, and rupture of blood vessels, culminating in embryonic lethality at embryonic day 15.5. Kidney and pancreatic ductal cysts are present. The Pkd1-encoded protein, mouse polycystin 1, was detected in normal endothelium and the surrounding vascular smooth muscle cells. These data reveal a requisite role for polycystin 1 in maintaining the structural integrity of the vasculature as well as epithelium and suggest that the nature of the PKD1 mutation contributes to the phenotypic variance in ADPKD.  (+info)

Rapid thawing increases the fragility of the cryopreserved arterial wall. (3/14)

OBJECTIVE: To extend present knowledge of the biomechanical and structural changes which occur in the cryopreserved, rapidly thawed arterial wall. MATERIALS AND METHODS: Minipig iliac arterial segments were cryopreserved at -196 degrees C in either minimum essential medium or Wisconsin solution. Fresh segments served as the control group. After 1 month, the specimens were rapidly thawed (37 degrees C) and processed for biomechanical, ultrastructural, morphological and immunohistochemical (MMP-1, MMP-2, MMP-3 and MMP-9) analysis. Visualisation of apoptotic cells was performed by TUNEL method. For the mechanical distension analysis, an in vitro circuit was designed. RESULTS: The cryopreserved segments showed a 42% incidence of spontaneous fracture and the appearance of microfractures which affected the endoluminal third of the vessel. An accumulation of liquid in the subelastica was observed. An increased expression of wall-degradative enzymes (mainly MMP-2) was also observed following cryopreservation. No significant differences were detected in the proportional elasticity module or tensile strength of the specimen groups. No differences in mechanical distension were observed between groups after the vessel segments were subjected to the pulsatile circuit flow for 72 h. Cell damage was most intense in the specimens cryopreserved in Wisconsin solution. CONCLUSIONS: Cryopreservation in both the solutions employed, followed by rapid thawing, induce changes in the permeability which increase the fragility of the cryopreserved arterial wall. Both increased expression of wall-degradative enzymes and accumulation of liquid may contribute to graft failure after implantation.  (+info)

Abnormalities in the cerebral arterial system in osteogenesis imperfecta. (4/14)

A 9-year-old girl with osteogenesis imperfecta (OI) type 4 was admitted to the hospital because of choreatic movement. Cerebral angiography demonstrated bilateral symmetrical stenosis of the proximal cavernous segment of internal carotid artery, prethrombotic occlusion of the M1 segment of left middle cerebral artery, and moyamoya-like collateral vascular structure arising from the right lenticulostriate arteries. After a literature review, these findings were interpreted as vasculopathic changes secondary to vascular fragility caused by the collagen abnormality in OI.  (+info)

Microvascular and capillary perfusion following glycocalyx degradation. (5/14)

Systemic parameters and microvascular and capillary hemodynamics were studied in the hamster window chamber model before and after hyaluronan degradation by intravenous injection of Streptomyces hyaluronidase (100 units, 40-50 U/ml plasma). Glycocalyx permeation was estimated using fluorescent markers of different molecular size (40, 70, and 2,000 kDa), and electrical charge. Systemic parameters (blood pressure, heart rate, blood gases) and microhemodynamics (vascular tone, velocity, and blood flow) remained statistically unchanged after injection of hyaluronidase, compared with inactivated hyaluronidase. Conversely, capillary hemodynamics were drastically affected. Functional capillary density, the capillaries perfused with red blood cells (RBCs), decreased by 35%, capillary Hct of the remaining functional capillaries increased from 16 to 27%, and penetration of 70-kDa fluorescent marker increased. Furthermore, plasma-only perfused capillaries statistically increased 30 min after hyaluronidase. The decrease in functional capillary density accounted for an increased RBC flux in the remainder of the capillaries, since the same number of RBCs had to traverse a reduced number of capillaries. Flux balances showed a reduction from baseline of 11% for the RBC flux and 20% for the plasma flux after treatment. These discrepancies are within the margin of error of the techniques used and could be explained by accounting for RBC over-velocity compared with plasma. These findings suggest that the decrease in the glycocalyx leads to capillary perfusion impairments.  (+info)

Peritubular capillaritis in renal allografts: prevalence, scoring system, reproducibility and clinicopathological correlates. (6/14)

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Physiological responses of erythrocytes of goats to transportation and the mondulatory role of ascorbic acid. (7/14)

Experiments were performed with the aim of investigating the effect of road transportation for 12 hr on erythrocytes of goats during the hot-dry season and the modulatory role of ascorbic acid. Forty 2.5-3-year-old Red Sokoto goats weighing 23-25 kg and belonging to both sexes served as the subjects of the study. Twenty of the goats served as the experimental group and were administered ascorbic acid (AA) per os at a dosage rate of 100 mg/kg body weight; the other 20 served as controls and were given 10 ml each of sterile water. Forty minutes after the administration and loading, the goats were transported for 12 hr. EDTA blood samples collected before loading, after loading, immediately after transportation and subsequently on the 3rd and 7th days of post-transportation were used to determine the red blood cell (RBC) count, packed cell volume (PCV), hemoglobin (Hb), erythrocyte osmotic fragility (EOF), hematimetric (intrinsic) indices and hemoglobin index levels. The obtained results showed that handling, loading and transportation of the control goats induced significant (P<0.05) increases in RBC, Hb, EOF and hypochromic erythrocytes and a decrease (P<0.05) in the volume and average Hb content in RBCs. AA administration ameliorated all these changes. The present results suggest that road transportation for 12 hr during the hot-dry season could induce serious stress, resulting in hemolysis of erythrocytes, which was ameliorated by AA administration. In addition, the results demonstrated that EOF could be used as a diagnostic tool in road transportation stress.  (+info)

Rupture of the internal elastic lamina and vascular fragility in stroke-prone spontaneously hypertensive rats. (8/14)

We studied a possible relation between stroke and an enhanced susceptibility to rupture of the arterial internal elastic lamina by comparing stroke-prone spontaneously hypertensive rats with spontaneously hypertensive rats, which have a very low incidence of stroke. We quantified interruptions in the internal elastic lamina in certain arteries and studied the effect of beta-aminopropionitrile, an inhibitor of cross-link formation in collagen and elastic fibers, on rupture of the internal elastic lamina and on mortality in these two substrains. To eliminate any influence of higher blood pressure in the stroke-prone rats on the parameters studied, we used antihypertensive treatment to obtain equivalent blood pressures in the two substrains. Results showed that stroke sensitivity was associated with an enhanced early spontaneous rupture of the internal elastic lamina in the caudal artery, an increased susceptibility to beta-aminopropionitrile-induced rupture of the internal elastic lamina, and earlier mortality, mainly from aortic rupture, under beta-aminopropionitrile treatment. These findings suggest that stroke-prone rats have an enhanced minor connective tissue defect that is expressed by rupture of the internal elastic lamina and may be related, at least in part, to their greater vascular fragility and increased susceptibility to stroke.  (+info)