Effect of an anion transport inhibitor on blood-brain barrier lesions during acute hypertension

1980 ◽  
Vol 51 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Jan Erik Hardebo ◽  
Barbro B. Johansson
1985 ◽  
Vol 248 (5) ◽  
pp. H712-H718 ◽  
Author(s):  
W. G. Mayhan ◽  
D. D. Heistad

We studied disruption of the blood-brain barrier (BBB) by acute hypertension and a hyperosmolar solution. The goals were to determine whether 1) disruption of the BBB occurs primarily in arteries, capillaries, or veins, and 2) transport of different-sized molecules is homogeneous or size dependent. Sprague-Dawley rats were studied using intravital fluorescent microscopy of pial vessels and fluorescein-labeled dextrans (FITC-dextran, mol wt = 70,000, 20,000, and 4,000 daltons). The site of disruption was determined by the appearance of microvascular leaky sites. Transport of different-sized molecules was calculated from clearance of FITC-dextran. During gradual hypertension and osmotic disruption, all leaky sites were venular. Rapid hypertension produced venular leaky sites and, in some experiments, diffuse arteriolar extravasation of FITC-dextran. Clearance of different-sized molecules was homogeneous during acute hypertension. In contrast, clearance of molecules during osmotic disruption was size dependent. The findings suggest that 1) venules and veins are the primary sites of disruption following acute hypertension and a hyperosmolar solution; 2) transport of different-sized molecules is homogeneous following acute hypertension, which suggests a vesicular mechanism; and 3) transport following hyperosmolar disruption is size dependent, which suggests that hyperosmolar disruption may involve formation of pores as well as vesicular transport.


1978 ◽  
Vol 235 (5) ◽  
pp. H544-H552 ◽  
Author(s):  
D. D. Heistad ◽  
M. L. Marcus ◽  
P. M. Gross

Cerebral vascular responses to sympathetic stimulation and denervation were examined in three species during acute severe hypertension as well as normal conditions. Cerebral blood flow (CBF) was measured with microspheres after the superior cervical sympathetic trunk was cut and during electrical stimulation of the superior cervical sympathetic ganglion. Sympathetic denervation did not increase CBF in anesthetized cats or monkeys. Under normal conditions, sympathetic stimulation decreased CBF significantly in monkeys (-26 +/- 3%) (mean +/- SE) but not in cats. During acute severe hypertension, decreases in CBF due to sympathetic stimulation were greatly augmented in cats (-29 +/- 7%, compared to -3 +/- 3%), only modestly augmented in dogs (-9 +/- 3%, compared to -1 +/- 2%), and not augmented in monkeys (-17 +/- 3%, compared to -23 +/- 4%). Disruption of the blood-brain barrier during hypertension was reduced by sympathetic stimulation. We conclude that 1) sympathetic tone to cerebral vessels is minimal because denervation does not increase CBF; 2) sympathetic stimulation decreases CBF under normal conditions in monkeys and during severe hypertension in cats, dogs, and monkeys, and it reduces disruption of the blood-brain barrier; and 3) there is an important species difference in responses to sympathetic stimulation under normal conditions and during acute hypertension.


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