SUMMARY Microangioarchitecture of the rat parietal cortex was studied by means of scanning electron microscopy and dark field microscopy. The richest supply of blood vessels in the parietal cortex was found in layer HI + IV and layer V, where 2 isolated plexuses of microressels were prominent. Tbe appearance of the plexuses was quite different between motor and sensory areas. In the motor area the capillary plexuses were narrow and compact, while in sensory area the plexuses were wide and diffuse.Characteristic ring formations, called ring-shaped-compressions in the present study, were frequently observed at branching sites of arterioles. The ring-shaped-compression probably corresponds to the precapillary sphincter. A similar structure was also seen in capillaries and venules and, therefore, it is likely that not only arterioles, but also capillaries and eren venules, can actively change diameter to control cerebral blood flow. Stroke, Vol 12, No 5, 1981BLOOD FLOW in the cerebral cortex changes under conditions such as cerebral thrombosis, 1 ' intracranial hypertension 4 '' and abnormal systemic blood pressure.* 17 It is important to understand the underlying mechanisms which control blood circulation within the cerebral cortex. There is a lack of morphological studies of small intracortical blood vessels which are responsible for cerebral microcirculation, although much has been known about extrinsic vessels and their neurogenic" 1 " and metabolic 10 ' " reactions. In the present study the basic differences of angioarchitecture of the somatomotor and somatosensory cortical areas have been studied by means of the scanning electron microscopy (SEM) and dark field microscopy. New information has been obtained about the active site in microvessels which constrict or dilate to control the cerebral microcirculation. Materials and MethodsTwenty albino rats of the Wistar strain (20O-250g) were used. The abdominal aorta and the inferior vena cava were cannulated with polyethylene catheters under sodium pentobarbital anesthesia (50 mg/kg, i.p.). The animals were then kept in an oxygen chamber filled with 95% O, and 5% CO,. Concurrently with exsanguination from the inferior vena cava, perfluochemical artificial blood" (Fluosol-43, The Green Cross Corporation) was injected through the abdominal aorta. The Po, and Pco, were kept at 400-500 mm Hg and 35-40 mm Hg, respectively. When the total circulating blood was exchanged with Fluosol-43, the animal was perfused with 250 ml of mixed solution of 4% glutaraldehyde and 4% paraformaldehyde in 0.1 M phosphate buffer (pH 7.4) for 7 m at room temperature. After perfusion fixation, the whole body of the animal was immersed in the same solution for 2 days (postfixation). The materials were further processed for dark field microscopy and SEM, as described below. Dark Field MicroscopyAfter fixation the brain was cut into coronal serial 80 nm thick sections with a vibratome. Serial sections were mounted on gelatine-coated glass slides and dried at room temperature. Sections were obser...

Two patients developed de novo vertebral artery dissecting aneurysm after contralateral vertebral artery occlusion. A 36-year-old man presented with brainstem ischemia and was treated non-surgically. Subsequent angiography showed spontaneous vertebral artery occlusion at the site of dissection. A 45-year-old man developed subarachnoid hemorrhage due to vertebral artery dissecting aneurysm. He underwent endovascular occlusion of the vertebral artery proximal to the dissecting aneurysm. These patients developed de novo dissecting aneurysm on the contralateral vertebral artery at 13 months and 11 days after unilateral vertebral artery occlusion, respectively. These cases strongly suggest that changes in hemodynamic stress due to unilateral vertebral artery occlusion are related to de novo dissecting aneurysm on the contralateral side. The risk of de novo dissecting aneurysm may be increased by proximal occlusion or trapping of dissecting aneurysm of the contralateral vertebral artery.

No abstract

We report 17 cases of intracranial arterial stenosis treated by percutaneous transluminal angioplasty (PTA), including 9 on the intracranial internal carotid (ICA), 4 on the middle cerebral (MCA), and 4 on vertebrobasilar artery (VBA) system. All patients had ischaemic brain symptoms and stenoses of more than 60% (calculated angiographically). We treated four patients by PTA for residual stenoses after thrombolysis for acute occlusion. We used PTA balloon catheters 2.0-3.5 mm in diameter for all procedures. As a rule, the balloon was inflated for 1 min at 6 atm. All arteries were successfully dilated (stenosis less than 50%) except for one treated by PTA for residual MCA stenosis after thrombolysis. The patient died of a massive infarct due to MCA reocclusion caused by arterial dissection. Stenosis recurred in 4 of 16 patients. Repeat PTA was successfully carried out in these cases. However, stenosis recurred in one of these patients 3 months after PTA, but the patient is being followed because he is asymptomatic. PTA of intracranial arteries is effective, but its indications should be based strictly on potential risks, such as acute occlusion derived from arterial dissection.