scholarly journals Evidence That Acetylcholine Mediates Increased Cerebral Blood Flow Velocity in Crucian Carp through a Nitric Oxide—Dependent Mechanism

1995 ◽  
Vol 15 (3) ◽  
pp. 519-524 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Crucian Carp ◽  
Cerebral Blood Flow Velocity ◽  
Early Event ◽  
Brain Blood Flow ◽  
The Brain

Nitric oxide (NO)–dependent regulation of brain blood flow has not been proven to exist in fish or other ectothermic vertebrates. Using epi-illumination microscopy on the brain surface (optic lobes) of crucian carp ( Carassius carassius), we show that superfusing the brain with acetylcholine (ACh) induces an increase in cerebral blood flow velocity that can be completely blocked by the NO synthase inhibitors NG-nitro-l-arginine methylester (L-NAME) and NG-nitro-l-arginine. Also, sodium nitroprusside, which decomposes to liberate NO, causes an increase in cerebral blood flow velocity. By contrast, L-NAME does not block the increase in blood flow velocity caused by anoxia. The results suggest that NO is an endogenous vasodilator in crucian carp brain that mediates the effects of ACh. Because teleost fish deviated from other vertebrates 400 million years ago, these results suggest that NO-dependent brain blood flow regulation was an early event in vertebrate evolution.

scholarly journals Role of Nitric Oxide in the Elevation of Cerebral Blood Flow Induced by Acetylcholine and Anoxia in the Turtle

1996 ◽  
Vol 16 (2) ◽  
pp. 290-295 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson ◽  
Peter L. Lutz
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Freshwater Turtle ◽  
Brain Blood Flow ◽  
Brain Surface ◽  
Synthase Inhibitor ◽  
The Brain

Nitric oxide (NO)-dependent regulation of brain blood flow has hitherto not been studied in reptiles. By observing the brain surface (telencephalon) of the freshwater turtle (Trachemys scripta) with epiillumination microscopy, we show that topical application of acetylcholine (ACh) induces an increase in CBF velocity that can be completely blocked by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). The effect of L-NAME was reversed by L-arginine. Also, sodium nitroprusside (SNP), which decomposes to liberate NO, caused an increase in CBF velocity. By contrast, L-NAME could not block the increase in blood flow velocity caused by anoxia. Interestingly, superfusing the brain with ACh or SNP during anoxia had no effect on the blood flow velocity. The results suggest that NO is an endogenous vasodilator in the turtle brain, mediating the effects of ACh during normoxia. By contrast, anoxia does not rely on NO as a vasodilator.

Brain blood flow and blood pressure during hypoxia in the epaulette shark Hemiscyllium ocellatum, a hypoxia-tolerant elasmobranch

1999 ◽  
Vol 202 (7) ◽  
pp. 829-835 ◽  
Author(s):  
V. Soderstrom ◽  
G.M. Renshaw ◽  
G.E. Nilsson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Freshwater Turtles ◽  
Energy Depletion ◽  
Epaulette Shark ◽  
The Brain

The key to surviving hypoxia is to protect the brain from energy depletion. The epaulette shark (Hemiscyllium ocellatum) is an elasmobranch able to resist energy depletion and to survive hypoxia. Using epi-illumination microscopy in vivo to observe cerebral blood flow velocity on the brain surface, we show that cerebral blood flow in the epaulette shark is unaffected by 2 h of severe hypoxia (0.35 mg O2 l-1 in the respiratory water, 24 C). Thus, the epaulette shark differs from other hypoxia- and anoxia-tolerant species studied: there is no adenosine-mediated increase in cerebral blood flow such as that occurring in freshwater turtles and cyprinid fish. However, blood pressure showed a 50 % decrease in the epaulette shark during hypoxia, indicating that a compensatory cerebral vasodilatation occurs to maintain cerebral blood flow. We observed an increase in cerebral blood flow velocity when superfusing the normoxic brain with adenosine (making sharks the oldest vertebrate group in which this mechanism has been found). The adenosine-induced increase in cerebral blood flow velocity was reduced by the adenosine receptor antagonist aminophylline. Aminophylline had no effect upon the maintenance of cerebral blood flow during hypoxia, however, indicating that adenosine is not involved in maintaining cerebral blood flow in the epaulette shark during hypoxic hypotension.

Brain Blood Flow

PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 317-317
Author(s):  
NANCY B. HANSEN ◽  
BARBARA S. STONESTREET ◽  
TED S. ROSENKRANTZ ◽  
WILLIAM OH
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Brain Blood Flow ◽  
Flow Measurements ◽  
Correlation Data ◽  
Microsphere Method ◽  
Blood Flow Measurements

In Reply.— We appreciate Rosenfeld's comments on our paper on the validity of Doppler measurements of anterior cerebral artery blood flow velocity. Rosenfeld raised two points regarding the validity of our correlation data between Doppler technique and cerebral blood flow measurements by the microsphere method. (1) Rosenfeld correctly pointed out that when we relate brain blood flow to any of the parameters obtained in the measurement of cerebral blood flow velocity, there is considerable variation in the values observed.

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