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Penetrating artery

Lacunar stroke is characterized by occlusion of a small penetrating artery creating a small deep infarct. Lacunar strokes have the lowest early recurrence risk and best survival rates, but may still cause significant functional morbidity. Although subgroup analyses are available from secondary prevention trials in lacunar stroke, few clinical trial data are available regarding nonthrombolytic antithrombotic therapy for lacunar stroke in the acute setting. [Pg.152]

Oliveria-Filho et al. (2000) 67 Clinical syndrome consistent with infarct of small penetrating artery Conventional MRI does not identify the clinically relevant infarct in almost 25% of patients with acute lesions on DWI... [Pg.199]

MCA stenosis causes subcortical stroke either by occlusion of a single penetrating artery to produce a small lacunar infarct or by artery to artery embolism with impaired clearance of emboli that produces multiple small cerebral infarcts, mainly in borderzone regions (Wong et al. 2002). [Pg.212]

Medullary infarcts can be medial, lateral or combined (Fig. 14.6). The medial territory is supplied by penetrating vessels from the anterior spinal artery and the distal vertebral artery. The lateral territory main arterial supply comes from penetrating arteries from the distal vertebral artery and the posterior inferior cerebellar artery. The small posterior territory is supplied by the posterior spinal artery and the posterior inferior cerebellar artery. Medial... [Pg.217]

The small penetrating arteries of the brain, less than 0.5 mm in diameter, include the lenticulostriate branches of the middle cerebral artery, the thalamoperforating branches... [Pg.60]

ICA, the MCA stem, the branch points of the major MCA branches, the ACA, A1 and A2 branches, the PI and P2 segment of the PCA, the distal vertebral artery, the vertebral artery origin, the vertebrobasilar junction, and the basilar artery. Microatherosclerotic plaques can occur as described above in the proximal portion of the penetrator arteries arising from the major vessels at the base of the brain. They are not seen in the leptomeningeal vessels over the cortex [20]. [Pg.30]

Patients who have had a stroke or transitory ischemic attack associated with intracranial artery stenosis (>50%) have a 12-14% risk of subsequent stroke in the 2-year period after the initial event, regardless of treatment with antithrombotic medications. Atherosclerosis in the intracranial portion of the ICA and the MCA is more common in the African-American, Hispanic, and Asian populations for unknown reasons. The proportion of patients hospitalized for ischemic strokes with symptomatic intracranial stenosis ranges from 1% in non-Hispanic whites to as high as 50% in Asian populations [21, 22]. Atherosclerosis in the intracranial portion of the carotid and in the MCA often causes multiple strokes in the same vascular territory. It may also cause slow stroke syndrome, in which there is progressive worsening of focal cortical ischemic symptoms over days or weeks. In addition, the penetrator arteries flowing to the deep white matter and striatum originate from the MCA stem (Ml) and may be occluded in patients with severe MCA stenosis [20]. [Pg.30]

Embohsm to the penetrating artery Evidence of other small emboli. No history of hypertension or atherosclerosis... [Pg.36]

P-Adrenoceptor Blockers. There is no satisfactory mechanism to explain the antihypertensive activity of P-adrenoceptor blockers (see Table 1) in humans particularly after chronic treatment (228,231—233). Reductions in heart rate correlate well with decreases in blood pressure and this may be an important mechanism. Other proposed mechanisms include reduction in PRA, reduction in cardiac output, and a central action. However, pindolol produces an antihypertensive effect without lowering PRA. In long-term treatment, the cardiac output is restored despite the decrease in arterial blood pressure and total peripheral resistance. Atenolol (Table 1), which does not penetrate into the brain is an efficacious antihypertensive agent. In short-term treatment, the blood flow to most organs (except the brain) is reduced and the total peripheral resistance may increase. [Pg.141]

Methyldopa, through its metaboHte, CX-methyInorepinephrine formed in the brain, acts on the postsynaptic tt2-adrenoceptor in the central nervous system. It reduces the adrenergic outflow to the cardiovascular system, thereby decreasing arterial blood pressure. If the conversion of methyldopa to CX-methyl norepinephrine in the brain is prevented by a dopamine -hydroxylase inhibitor capable of penetrating into the brain, it loses its antihypertensive effects. [Pg.142]

The vasculature is established by the 18th day of gestation in rats, and comes from the arterial supply as the anterior cerebral vessel, eventually entering the basal lamina via septal tributaries of the olfactory artery (Szabo, 1988). Unlike the MOE, the organ s capillaries penetrate in loops into the neuroepithelium. Blood from the vomeronasal complex arrives for collection in the vomeronasal vein, as described earlier [Fig. 2.11(a)]. The establishment of the highly vascular columnar complexes seen in the ophidian organ has not been correlated with functional development (c.f. Wang and Halpem, 1980 Holtzman and Halpem, 1990). [Pg.81]

The penis consists of three components, two dorsolateral corpora cavernosa and a ventral corpus spongiosum that surrounds the penile urethra and distally forms the glans penis. The corpora cavernosa consist of blood-filled sinusoidal or lacunar spaces, which are lined with endothelial cells, supported by trabecular smooth muscle, and surrounded by a thick fibrous sheath called the tunica albuginea. The caver-nosal arteries, which are branches of the penile artery, penetrate the tunica albuginea and supply blood flow to the penis. [Pg.780]

A highly complex network of arteries, arterioles, and capillaries penetrates the dermis from below and extends up to the surface of, but not actually into, the epidermis. A matching venous system siphons the blood and returns it to the central circulation. Blood flow through the vasculature is linked to the production and movement of lymph through a complementary dermal lymphatic system. The dermis is laced with tactile, thermal, and pain sensors. [Pg.195]

In the final study to be mentioned in regard to the possible penetration of pyrldinium oximes into brain, anesthetized, atropi-nized cats were given intravenous injections of sarin at 27/tg/kg. 12 Thirty minutes later, to allow clearance of unreacted sarin from the tissues, some cats received saline injections into one common carotid artery and others received similar injections of 1 at 15 mg/kg. The cholinesterase activity of cerebral cortex was measured. In animals given 1, nearly 20% of the cholinesterase in their cerebral cortices that had been inhibited by sarin was calculated to have been reactivated by the oxime. [Pg.288]

Familial dysbetalipoproteinemia (type III) is characterized by the accumulation of chylomicron and VLDL remnants, which are enriched in cholesterol compared to their precursors. The primary molecular cause of familial dysbetalipoproteinemia (type III) is the homozygous presence of the apolipoprotein E2 (apoE2) isoform, which is associated with recessive inheritance of the disorder [62]. However, only 1 in 50 homozygotes for apoE2 will develop type III hyperlipoproteinemia, which is clinically characterized by palmar and tuberous xanthomas, arcus lipoides, and premature atherosclerosis of coronary, peripheral, and cerebral arteries. Precipitating factors include diabetes mellitus, renal disease, hemochromatosis, but also familial hypercholesterolemia. In addition, some rare mutations in the apoE gene have been found to cause dominant and more penetrant forms of type III hyperlipoproteinemia. [Pg.506]

We are interested in ACAT-1 inhibitors, which are expected to affect macrophages directly. In the early stages of atherosclerogenesis, macrophages penetrate the intima, efficiently take up modified LDL, store cholesterol and fatty acids as a form of neutral lipids such as CE and TG in the cytosolic lipid droplets, and are converted into foam cells, leading to the development of atherosclerosis in the arterial wall. We established an assay system of lipid droplet formation using intact mouse macrophages and searched for microbial inhibitors of the for-... [Pg.360]


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