The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.

Animals↗

PubMedDate not supplied

Effect of steroid on ischemic brain edema. Analysis of cytotoxic and vasogenic edema occurring during ischemia and after restoration of blood flow.

Mongolian gerbils were observed for the effects of beta-methasone on ischemic brain edema which developed during ischemia or after blood flow restoration. The severity of brain edema was determined by measuring water content of the ischemic cerebral hemisphere, using the wet and dry methods. Sodium and potassium ions were extracted from homogenized brains with 0.75N HNO2 and ion concentration measured by flame photometry. Passage of RISA from blood into the cerebral parenchyma, as an indicator of blood-brain barrier change, was determined with a gamma-scintillation counter. In the cytotoxic edema model, animals were killed after 9 h permanent ischemia or 3 h after 1 h ischemia. In the simultaneous cytotoxic and vasogenic edema model, the animals were killed either 20 h or 3 days following 1 h ischemia, or 3 h after blood flow restoration following 6 h ischemia. Steroid treatment was ineffective in ischemic brain edema of the cytotoxic or vasogenic type.

Animals↗

PubMedDate not supplied

Transient appearance of "no-reflow" phenomenon in Mongolian gerbils.

We investigated the existence of the "no-reflow" phenomenon in focal cerebral ischemia. Regional cerebral blood flow was studied in Mongolian gerbils perfused with a carbon-black particle suspension after cerebral ischemia prior to decapitation and compared with 14C-antipyrine autoradiographic images. The correlation between the occurrence of the "no-reflow" phenomenon and systemic arterial blood pressure change was also examined. We found that the phenomenon was transient in character and that its manifestation was related to the transient fall in arterial blood pressure observed immediately after clip release and with stagnation of venous blood flow. The phenomenon disappeared in animals in which the arterial blood pressure was artificially increased after clip release.

Animals↗

PubMedDate not supplied

Effect of hypertension on blood-brain barrier. Change after restoration of blood flow in post-ischemic gerbil brains. An electronmicroscopic study.

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.

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PubMedDate not supplied

CT enhancement after prolonged high-dose contrast infusion in the early stage of cerebral infarction.

To demonstrate the BBB break-down on the CT image in the acute stage of cerebral infarction, a 3 hour continuous drip infusion of 200 ml of meglumine amidotrizoate, rather than the conventional bolus injection, was used. In this study, 22 examinations were carried out in 18 patients in whom cerebral infarction due to temporary or permanent obstruction of the cerebral artery was diagnosed by CT and angiography on admission. With each examination, the first CT was obtained prior to contrast infusion, and second immediately after the end of 3 hours of continuous contrast infusion. The EMI number was calculated at 3 regions of interest in the infarction. Within 3 days after stroke episode, 4 out of 5 patients with temporary vascular obstruction demonstrated enhancement, as well as 6 out of 9 patients with permanent vascular obstruction. Between 4 and 14 days after the stroke episode, all of 8 patients showed enhancement. To further clarify the extravasation of the contrast medium during the first 3 days of a cerebral infarction, a third CT scan was performed 3-hrs after finishing the contrast infusion in 4 patients. In these latter patients, blood was sampled at the time of each of the 3 CT series. The EMI number of the blood samples was also measured. In all 4 patients, the Gado's tissue-blood ratio (the EMI number of the CT lesion divided by that of the blood sample) was higher than 17.2% in the second, and higher than 54.7% in the third CT scan. Thus break-down of the BBB which was demonstrated by prolonged contrast infusion is an earlier event in human cerebral infarction than is usually accepted.

Blood-Brain Barrier↗

PubMedDate not supplied

[Application of transcranial Doppler ultrasonography in the assessment of cerebrovascular reactivity studies and cerebral vascular reserve estimation in patients with focal brain injury].

Cerebrovascular reactivity and cerebrovascular reserve were studied using transcranial Doppler sonography (TCD). Investigations were carried out in acute cases--8 patients with severe head injury within 5 days after trauma and in chronic cases with brain tissue defect (12 patients), and in cases with cerebral circulation insufficiency (15 patients). In acute cases the pCO2 cerebrovascular response was studied and in chronic cases cerebrovascular reserve was estimated using acetazolamide. TCD was found suitable for local vascular reactivity disturbances determination independently in three intracranial compartments--both hemispheres and infratentorial space. In patients with local brain tissue defect cerebrovascular reserve remained within normal range. In cerebral circulation insufficiency vascular reserve disturbances were limited to one compartment in cases with local vascular lesion they were found in all three compartments in cases with generalized atheromatosis.

Acetazolamide↗