Acute responses of blood pressure and turnover of norepinephrine in the brain to intracisternally injected guanethidine were studied in rats. Systolic blood pressure in guanethidine-treated rats showed a dose-relating rise for over 9 hrs, while norepinephrine contents in cortex-cerebellum, brain stem and heart were not affected. The endogenous norepinephrine in brain samples, however, did not decrease against alpha-methyl-p-tyrosine to result in regression coefficients significantly different from those in the saline-treated group whereas norepinephrine in heart was reduced similarly in the 2 groups, indicating a slowered turnover of norepinephrine selectively in the brain. The results may indicate that the retarded norepinephrine turnover in the brain is causatively related with an acute elevation in blood pressure.

Animals↗

PubMed1975

Brain circulation in cerebral transient ischemic attacks.

Cranial blood flow, mean cranial transit time and cranial blood volume were measured by the intravenous RISA technique in 10 patients with cerebral transient ischemic attacks (TIA) at the various time intervals from the onset of last attack. Cranial blood flow was subnormal in 5 out of 11 determinations and mean transit time trended to be prolonged in the diseased hemisphere in cases suggestive of the unilateral hemispheric lesion. A decrease in cranial blood flow was observed in TIA with lowering of heart rate below 60/min, or with atrial fibrillation, whereas no obvious correlation was present between heart rate and cranial blood flow either in 94 patients with, or with 62 patients without cerebrovascular diseases. Cardiac dysrhythmias including bradycardia, leading to reduce perfusion to the brain was discussed as a possible factor for producing TIA.

Adult↗

PubMed1975

An electron microscope study on permeability in cerebral venules in the rats with hypertensive encephalopathy.

Hypertensive encephalopathy was induced in the rat by clipping one renal artery and contralateral nephrectomy. The possible changes of vascular permeability of the cerebral blood capillaries and venules were investigated by using ferritin as a tracer. The uninephrectomized rats served as controls. In controls, ferritin was never seen in the basement membranes, within plasmalemmal vesicles on the basal surface of the endothelium, or in endothelial cell junctions of cerebral capillaries and venules up to 180 min after the injection. In venules of the brain in rats with hypertensive encephalopathy, a number of ferritin particles appeared in the basement membrane in 60 min after the injection. Many plasmalemmal vesicles in the endothelial cells of venules were labeled with ferritin. However, ferritin particles were never found in the endothelial cell junctions. The results suggested that leakage of macromolecules, such as serum proteins, occurred in venules mainly by increased vesicular transport.

Animals↗

PubMed1975