Effects of Sympathetic Nerve Stimulation on Long Posterior Ciliary Artery Blood Flow in Cats

2002 ◽  
Vol 18 (2) ◽  
pp. 115-125
Author(s):  
Michael C. Koss
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Artery Blood Flow ◽  
Sympathetic Nerve Stimulation ◽  
Posterior Ciliary Artery ◽  
Ciliary Artery

Arteriolar network response to pressure reduction during sympathetic nerve stimulation in cat skeletal muscle

1994 ◽  
Vol 266 (3) ◽  
pp. H1251-H1259 ◽  
Author(s):  
P. Ping ◽  
P. C. Johnson
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Similar Degree ◽  
Sartorius Muscle ◽  
Pressure Reduction ◽  
Third Order ◽  
Sympathetic Nerve Stimulation ◽  
Resistance Change

Previous studies in this laboratory have shown that autoregulation of blood flow and dilation of midsized (second-order) arterioles were significantly enhanced during sympathetic nerve stimulation of cat sartorius muscle apparently because of a greater myogenic response of the arterioles. Quite typically, blood flow increased with arterial pressure reduction to 80, 60, and 40 mmHg (superregulation) during sympathetic nerve stimulation. To determine the contribution of the various orders of arterioles to the enhanced autoregulation, we measured diameters in all orders of arterioles and measured red cell velocity in first-, second-, and third-order arterioles. Without sympathetic nerve stimulation, all orders of arterioles except the first order dilated to pressure reduction, but flow autoregulation was weak. With sympathetic nerve stimulation, arteriolar dilation to pressure reduction was significantly enhanced in all six orders of arterioles, and flow rose significantly. The resistance change in the arteriolar network during pressure reduction as calculated from diameter changes was greatest in third- and fourth-order arterioles. Experimentally determined flow changes to pressure reduction and to sympathetic nerve stimulation were quantitatively similar to those predicted from diameter changes in a model of the arteriolar network. Calculated wall shear stress (from viscosity and shear rate) for first-, second-, and third-order arterioles decreased during pressure reduction with and without sympathetic nerve stimulation. We concluded that endothelium-mediated dilation due to shear stress would tend to oppose autoregulation of blood flow to a similar degree under both circumstances.

Presynaptic inhibitory effects of sotalol, propranolol, and acebutolol on noradrenaline release upon cardiac sympathetic nerve stimulation in anesthetized dogs

1986 ◽  
Vol 64 (8) ◽  
pp. 1076-1084 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Michel Naud ◽  
Daniel Lamontagne ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Inhibitory Effect ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Flow Response ◽  
Anesthetized Dogs ◽  
Na Release

Effect of sotalol (STL) was compared with that of (±)-propranolol, (+)-propranolol (PPL), and acebutolol (ABL) on noradrenaline (NA) release as measured in coronary sinus (CS) blood during postganglionic stimulation (2 Hz, 30 s) of the left cardiac sympathetic nerves in anesthetized dogs. In control dogs receiving saline, increasing responses of CS-NA concentration, mean CS blood flow, and CS-NA output to repetitive stimulation were relatively stable throughout a given experimental period. Both STL (1, 2.5, and 5 mg/kg, i.v.) and (±)-PPL (0.5 and 2.5 mg/kg, i.v.) diminished the increased CS-NA concentration by approximately 35 (P < 0.05) to 60% (P < 0.01) in a dose-dependent fashion. However, (+)-PPL (0.02–2.5 mg/kg, i.v.) and ABL (0.5–5 mg/kg, i.v.) did not significantly alter the increasing response of CS-NA concentration upon stimulation. STL, (±)-PPL, and ABL markedly inhibited the CS blood flow response to stimulation at all doses tested, while (+)-PPL did not significantly diminish the flow response even at the highest dose tested. Consequently, CS-NA output decreased significantly (p < 0.01) in the presence of STL, (±)-PPL, and ABL at all doses tested but not with (+)-PPL at any dose tested. The inhibitory effect of STL and (±)-PPL on the increasing response of CS-NA concentration upon stimulation could be related to their beta-blocking effect, which exerts presumably on postulated presynaptic β-adrenoceptors, as (+)-PPL did not at all diminish the response. On the other hand, ABL does not seem to exert a similar presynaptic inhibitory effect, owing presumably either to its β-1 selectivity or to its intrinsic sympathetic activity. The results support the existence of facilitatory presynaptic β-adrenoceptors in the normal dog heart under in vivo conditions. The findings also suggest that NA release upon cardiac sympathetic nerve stimulation may be reflected more precisely by CS-NA concentration than by NA output.

Effect of Sympathetic Nerve Stimulation on Cutaneous Small Vein and Small Artery Pressures, Blood Flow and Hindpaw Volume in the Dog

1956 ◽  
Vol 185 (3) ◽  
pp. 453-464 ◽  
Author(s):  
William D. Kelly ◽  
Maurice B. Visscher
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Cardiac Contraction ◽  
Intraluminal Pressure ◽  
Small Artery ◽  
Sympathetic Nerve Stimulation ◽  
Abrupt Decrease ◽  
Average Value ◽  
Small Vein

Electrical stimulation of the lumbar sympathetic chain in dogs produced a variety of response patterns in pressures measured in the femoral artery, a small cutaneous artery (saphenous) and a small cutaneous vein. The preponderant response in the small vein during stimulation was a rise from an average control value of 17 mm Hg to an average value of 30 mm Hg. Shortly after cessation of stimulation a secondary pressure rise occurred to an average value of 42 mm Hg. The average small artery pressure changed from 99 mm Hg to 138 mm Hg during stimulation and fell to 55 mm Hg shortly after stimulation ended. Both pressures then gradually returned to control levels. Hindpaw volume and saphenous artery blood flow invariably showed an abrupt decrease during sympathetic nerve stimulation. An increase in small vein pressure associated with decreased blood flow is interpreted to be due to an increase in resistance to run off from the venous bed. Marked increases in small vein pressure occurred following sympathetic stimulation for as long as ten minutes after cessation of respiration and cardiac contraction. Control experiments excluded changes in cardiac output, central venous pressure and skeletal muscle movement as significant factors in the observed changes. Therefore the small veins as well as the small arteries of the skin of the hindpaw in the dog are capable of constricting in response to sympathetic nerve stimulation to produce marked increases in intraluminal pressure. The small vein can react independently of the small artery.

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