scholarly journals Effects of sympathetic nerves on cerebral vessels in dog, cat, and monkey

1978 ◽  
Vol 235 (5) ◽  
pp. H544-H552 ◽  
Author(s):  
D. D. Heistad ◽  
M. L. Marcus ◽  
P. M. Gross
Keyword(s):  
Blood Brain Barrier ◽  
Severe Hypertension ◽  
Species Difference ◽  
Cerebral Vessels ◽  
Brain Barrier ◽  
Sympathetic Stimulation ◽  
Acute Hypertension ◽  
Important Species ◽  
Blood Brain ◽  
Cervical Sympathetic

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.

Heterogeneity of brain blood flow and permeability during acute hypertension

1985 ◽  
Vol 249 (3) ◽  
pp. H629-H637 ◽  
Author(s):  
G. L. Baumbach ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Blood Brain Barrier ◽  
Regional Differences ◽  
Severe Hypertension ◽  
Brain Barrier ◽  
Acute Hypertension ◽  
Blood Brain ◽  
The Brain ◽  
Increased Blood Flow

The purpose of this study was to examine regional autoregulation of blood flow in the brain during acute hypertension. In anesthetized cats severe hypertension increased blood flow more in cerebrum (159%) and cerebellum (106%) than brain stem (58%). In contrast to the heterogeneous autoregulatory response, hypocapnia produced uniform vasoconstriction in the brain. We also compared vasodilatation during severe hypertension with vasodilatation during hypercapnia. During hypercapnia, blood flow increased as much in brain stem, as in cerebrum and cerebellum. Thus regional differences in autoregulation appear to be specific for autoregulatory stimulus and are not secondary to nonspecific differences in vasoconstrictor or vasodilator capacity. To determine whether the blood-brain barrier is more susceptible to hypertensive disruption in regions with less effective autoregulation, permeability of the barrier was quantitated with 125I-albumin. Severe hypertension produced disruption of the barrier in cerebrum but not in brain stem. Thus there are parallel differences in effectiveness of autoregulation and susceptibility to disruption of the blood-brain barrier in different regions of the brain.

Protection of the blood-brain barrier by hypercapnia during acute hypertension

1986 ◽  
Vol 251 (2) ◽  
pp. H282-H287
Author(s):  
G. L. Baumbach ◽  
W. G. Mayhan ◽  
D. D. Heistad
Keyword(s):  
Blood Brain Barrier ◽  
Severe Hypertension ◽  
Venous Pressure ◽  
Sympathetic Nerves ◽  
Brain Barrier ◽  
Acute Hypertension ◽  
Blood Brain ◽  
Cerebral Vasodilatation ◽  
Fluorescent Dextran ◽  
Incremental Increase

The purpose of this study was to examine effects of hypercapnia on susceptibility of the blood-brain barrier to disruption during acute hypertension. Two methods were used to test the hypothesis that cerebral vasodilatation during hypercapnia increases disruption of the blood-brain barrier. First, permeability of the blood-brain barrier was measured in anesthetized cats with 125I-labeled serum albumin. Severe hypertension markedly increased permeability of the blood-brain barrier during normocapnia, but not during hypercapnia. The protective effect of hypercapnia was not dependent on sympathetic nerves. Second, in anesthetized rats, permeability of the barrier was quantitated by clearance of fluorescent dextran. Disruption of the blood-brain barrier during hypertension was decreased by hypercapnia. Because disruption of the blood-brain barrier occurred primarily in pial venules, we also measured pial venular diameter and pressure (with a servo-null method). Acute hypertension increased pial venular pressure and diameter in normocapnic rats. Hypercapnia alone increased pial venular pressure and pial venular diameter, and acute hypertension during hypercapnia further increased venular pressure. The magnitude of increase in pial venular pressure during acute hypertension was significantly less in hypercapnic than in normocapnic rats. We conclude that hypercapnia protects the blood-brain barrier. Possible mechanisms of this effect include attenuation of the incremental increase in pial venular pressure by hypercapnia or a direct effect on the blood-brain barrier not related to venous pressure.

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