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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have tested the hypothesis that blood-borne substances released from a site of vascular thrombosis can lead to acute alterations in the blood-brain barrier. The right common carotid artery of rats was photothrombosed using a dye/light insult. Rats were given the photosensitizing dye rose bengal and irradiated for 4 minutes with an argon laser beam focused onto the exposed common carotid artery. During the irradiation, 3 ml of blood was taken from the right external carotid artery. After 10 minutes, the blood was infused into the external carotid artery of a recipient rat that had received horseradish peroxidase. Fifteen minutes after blood infusion, bilateral peroxidase extravasation was noted within cortical and subcortical areas of recipient rats, being most intense ipsilaterally. Ultrastructural studies demonstrated peroxidase reaction product within numerous endothelial vesicles of arteriolar segments. Infusion of blood from control rats did not produce similar changes. Thus, photoinduced vascular thrombosis of a large feeding artery leads to the formation of blood-borne factors that acutely alter cerebral vascular permeability.
Stroke 1988 Jul
PMID:Photochemically stimulated blood-borne factors induce blood-brain barrier alterations in rats. 338 56

Alterations in the blood-brain barrier to proteins, and regional water and electrolyte content were documented in a rat model of photochemically induced small-vessel thrombosis leading to infarction. Horseradish peroxidase (HRP) or Evans blue was given immediately following a 2-min photochemical sensitization period. At 5 min following irradiation, multifocal sites of peroxidase extravasation were noted within the irradiated area. Ultrastructural examination revealed endothelial cells filled with HRP which in some cases extended into the basal lamina and extracellular spaces. At 15 min, protein leakage was more pronounced within the irradiated zone and reaction product was also apparent within the subarachnoid and perivascular spaces of brain regions remote from the site of irradiation. Widespread staining on the surface of the irradiated hemisphere was apparent in rats perfused 8 h following Evans blue infusion. Water content increased significantly by 15 min within the irradiated zone but not in brain regions remote from this site. Although vasogenic edema is an early event in this stroke model, increases in water content are restricted to the irreversibly damaged site. In contrast, protein tracer escaping from microvessels coursing within the irradiated zone was widely distributed. These findings implicate endothelial barrier dysfunction in the genesis of tissue injury in this model. Morphological evidence for the capability of macromolecules to escape from a site of evolving infarction and to migrate to distances remote from the area of primary microvascular damage is also discussed.
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PMID:Photochemically induced cerebral infarction. II. Edema and blood-brain barrier disruption. 357 88

The location of the postganglionic parasympathetic cell bodies projecting to cerebral arteries is unknown. Using axonal tracing techniques, we examined whether the sphenopalatine ganglia (associated with the seventh cranial nerve) and otic ganglia (associated with ninth cranial nerve) contain perikarya which send axons to the feline middle cerebral artery (MCA). The tracers horseradish peroxidase (HRP: 3 cats) or wheat germ agglutinin (WGA: 6 cats) were applied to the MCA in a slow release polymeric system. Three days later the SPG, otic ganglia, and rete mirabile were harvested bilaterally and processed for tracer by the TMB method (HRP) or immunohistochemistry (WGA). In a given animal, approximately equal numbers of cells containing axonal tracer were found in both SPG. Labeled fibers occasionally could be seen extending into the vidian nerve. Positive cells were also found in the otic ganglia and in the walls of the internal rete mirabile. These results provide the first identification of parasympathetic cell bodies projecting to cerebral blood vessels.
Stroke
PMID:Cerebrovascular projections from the sphenopalatine and otic ganglia to the middle cerebral artery of the cat. 371 48

Intravascular platelet aggregation induced by ADP injection into the carotid artery of rabbits caused ipsilateral cerebrovascular injuries. We have observed the details of these in vivo vascular changes under the electron microscope. Intracytoplasmic vacuole (1.0-2.0 micron in diameter) formation and partial deendothelialization followed by platelet thrombus formation were characteristic changes in the middle cerebral artery. These vacuoles did not contain horseradish peroxidase (HRP) which was used as a marker of vascular permeability change. Compared with these phenomenon, increased vesicular (0.05-0.2 micron in diameter) transport was prominent, and vacuole formation was rarely seen in small vessels, namely, capillaries and arterioles in the cortex. Endothelial cell damage seemed to be more prominent in large arteries, but only the smaller vessels show marked extravasation of HRP-reaction product and perivascular edema. Blood levels of TXB2 and 6-keto PGF1 alpha were significantly increased 3 min after the ADP injection and returned to pre-injection levels at 60 min after. These results suggest that vasoactive substances resulting from platelet activation may play an important role in producing cerebrovascular injuries caused by platelet aggregation induced with ADP.
Stroke
PMID:Cerebrovascular injuries induced by activation of platelets in vivo. 397 62

Topographic distribution of barrier function in normal canine cervico-cephalic arteries was studied using horseradish peroxidase (HRP) and Evans blue as tracers. The carotid sinus of the internal carotid artery (ICA) was conspicuously permeable to HRP when compared to other areas of major cervical arteries. The cavernous portion of the ICA also showed prominent permeation of HRP, especially through the outer surface, which is covered with venous endothelial cells. On the luminal side of the cavernous portion of the ICA, barrier deficiency was noted at angulated segments such as the carotid siphon. Intracranial segments of both ICA and vertebral arteries demonstrated incomplete barrier function of the first 1 to 4 mm from the origin of the intradural segments. These areas were considered to be transitional sites in barrier function between extra- and intracranial arteries. Focal, but definite, barrier disruption was also noted at the distal ends of the ICA and other arterial branching sites of major intracranial arteries. While opening of the interendothelial junctions was considered to be one of the mechanisms causing increased permeability in the cavernous ICA, the mechanisms for the permeation of HRP into the major cerebral arteries could not be confirmed ultrastructurally.
Stroke
PMID:Topographical distribution of barrier function in cervico-cephalic arteries of dog. Major cerebral arteries possess definite barrier function? 404 52

Permeability of brain capillaries of stroke-prone spontaneously hypertensive rats (SHRSP) was studied using labelling (horseradish peroxidase) and cytochemical techniques at the cellular level. In the cerebral capillary endothelium the tracer molecules were quickly transported by abundant transendothelial channels which directly connected the capillary lumen to the subendothelial space. Transendothelial channels are abundant and should be postulated as structural formations engaged in the increased transport of proteins across the capillary endothelium. Ultracytochemical studies revealed that the channels, bounded by indistinct delimiting membranes, initially had no acid phosphatase activity. With the passage of time, however, the channels showed acid phosphatase activity and were lined with distinct membranes. These observations suggested that the lysosomes might fuse with the transendothelial channels and might play an important part in the transport of macromolecules.
Stroke
PMID:Increased transendothelial channel transport of cerebral capillary endothelium in stroke-prone SHR. 665 37

The effect of induced hypertension on the blood-brain barrier (BBB) change in Mongolian gerbils exposed to various periods of ischemia was studied. Evans blue dye was used to determine the BBB change in animals subjected to different levels of hypertension after 3 h ischemia. Horseradish peroxidase (HRP) was used in electronmicroscopic studies of animals subjected to 30 min, 1, 3 or 6 h ischemia and subsequently exposed for 30 min to varying periods and sequences of normo- and hypertension. Furthermore, HRP-labeled vesicle counts were performed in animals from the 30-min ischemia group. Our findings revealed that hypertension, after blood flow restoration following ischemia, induces and/or accelerates BBB damage by enhancing endothelial vesicular and/or tubulo-channel transport.
Stroke
PMID:Effect of hypertension on blood-brain barrier. Change after restoration of blood flow in post-ischemic gerbil brains. An electronmicroscopic study. 721 66

The choriocapillaris is the fenestrated capillary bed in the choroid of the eye and is the major blood supply to the retinal pigment epithelium (RPE) and photoreceptor cells. Bruch's membrane (BM) is a multilaminated basement membrane that separates the choriocapillaris from the RPE. In a previous study (Pino RM, Essner E; Cell Tissue Res 208:21, 1980) we found that the choriocapillary endothelium restricted the egress of ferritin from the choriocapillaris. In the present study, hemeproteins were used to further establish the permeability characteristics of this capillary bed. Horseradish peroxidase (Einstein-Strokes radius (ESR), 30 A) rapidly crossed the capillary endothelium (less than 5 min) after intravenous administration and after 5 minutes filled BM and the basal infoldings of the RPE. In contrast, hemoglobin (Hg) (ESR, 32 A) and lactoperoxidase (LP) (ESR, approximately 40 A) are markedly restricted at the level of endothelial diaphragmed fenestrae, channels, and intercellular junctions. Little vesicular transport of these proteins was observed. The reaction product of the two hemeprotein activities was not demonstrable in BM for up to 30 min after injection; relatively low levels were detected after 75 min. HG and LP appear to be further restricted by BM, since their reaction products were not demonstrable between the RPE basal infoldings at this time. Catalase (ESR, 52 A) activity was not detected in BM for up to 4 hr after injection. These results indicate that the rat choriocapillary endothelium, unlike the fenestrated endothelia lining other vascular beds, substantially restricts the passage of large tracer molecules.
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PMID:Permeability of rat choriocapillaris to hemeproteins. Restriction of tracers by a fenestrated endothelium. 725 21

Permeability of intracranial extracerebral arteries of stroke-prone spontaneously hypertensive rats (SHRSP) was studied using labeling techniques (ferritin and horseradish peroxidase), at the cellular level. In the arterial endothelial cells, the tracer molecules were slowly but constantly transported by the plasmalemmal vesicles to the subendothelial space. This endothelial transportation of the tracers into these cerebral arteries did not seem to be significantly influenced by aging, increased blood pressure, hyperlipidemia or the existence of cerebral bleeding and infarction. Around the adventitia, there were a great number of periadventitial capillaries, especially near bifurcations. In the periadventitial capillaries, the tracer molecules were readily trapped by endothelial cells and were quickly transported to pericapillary spaces. The tracer molecules were then detected in the phagocytes adjacent to the deeper layers of the media, and further in the medial smooth muscle cells. The possibility that large amounts of plasma components are supplied to the media from periadventitial capillaries in the intracranial extracerebral arteries has to be considered in the pathogenic mechanisms of cerebrovascular lesions.
Stroke
PMID:Permeability of intracranial extracerebral vessels in stroke-prone SHR. 730 76

Air injection into the carotid artery of adult mongolian gerbils caused, within 10 minutes, multifocal brain lesions. The extracellular spaces were widened and neurons, oligodendrocytes and myelin sheaths remained unchanged. The "delayed" effects of air embolism (first seen after 3 h) were similar to those observed in gerbils after unilateral carotid ligation. The histologic alterations after 3 h consisted of astrocytic swelling and shrinkage/necrosis of neuronal soma. The observations reported here illustrate the temporal and spatial separations that exist between a) brain water retention, and b) intraparenchymal entry of horseradish peroxidase. Both alterations can be a consequence of either decreased blood flow or arterial air embolism. Edema and protein leakage in each situation may be initiated by different mechanisms.
Stroke
PMID:Arterial air embolism: structural effects on the gerbil brain. 731 63


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