scholarly journals The Impact of Aging on Vasa Nervorum, Nerve Blood Flow and Vasopressin Responsiveness

Author(s):  
Mikihiro Kihara ◽  
Mitsuaki Shioyama ◽  
Kazuto Okuda ◽  
Mitsuo Takahashi

Abstract:Objective:Aging impacts microvessels in a number of tissue beds. Vasopressin acts as a vasoconstrictor in most blood vessels but may also cause vasodilation. We evaluated the role of aging and vasopressin in the regulation of nerve blood flow (NBF) in rat peripheral nerve.Methods:We undertook a dose-response study to examine the impact of aging on resting NBF and its vasoreactivity to vasopressin. Nerve blood flow was measured using microelectrode hydrogen polarography. Argininevasopressin was administered both intra-arterially and topically.Results:In young adult rats (two months old) topical epineurial application of arginine-vasopressin produced a concentration-dependent reduction of NBF (ED50= 3.8 X 10-5 mol/L). Intra-arterial arginine-vasopressin also reduced NBF. Nerve blood flow was lower in aged rats (12 months old) and less responsive to topically applied vasopressin. The aging group had significantly higher concentrations of vasopressin in plasma than did the younger group.Conclusions:The results suggest that vasopressin constricts vessels in peripheral nerve and that there is an age related decline in the vasoconstrictive response to vasopressin. There may be a reduction in receptor sensitivity in vascular smooth muscle cells in peripheral nerve with increasing age.

1993 ◽  
Vol 16 (12) ◽  
pp. 1383-1389 ◽  
Author(s):  
Mikihiro Kihara ◽  
Paula J. Zollman ◽  
James D. Schmelzer ◽  
Phillip A. Low

1996 ◽  
Vol 8 (4) ◽  
pp. 342
Author(s):  
H. Hino ◽  
G. Lu ◽  
O. Tajiri ◽  
H. Nagashuna ◽  
V. Kvetan

2001 ◽  
Vol 172 (2) ◽  
pp. 398-406 ◽  
Author(s):  
Ahmet Höke ◽  
Hong S. Sun ◽  
Tessa Gordon ◽  
Douglas W. Zochodne

1994 ◽  
Vol 266 (6) ◽  
pp. E980-E985 ◽  
Author(s):  
M. Kihara ◽  
P. J. Zollman ◽  
I. L. Smithson ◽  
T. D. Lagerlund ◽  
P. A. Low

Insulin administration can cause or worsen experimental and human diabetic neuropathy ("insulin neuritis"). In this study, we tested the hypothesis that insulin administration impairs tissue oxygenation. We infused insulin under nonhypoglycemic conditions and evaluated its effect on endoneurial oxygen tension, nerve blood flow, and the oxyhemoglobin dissociation curve of peripheral nerve in normal and diabetic rats. Intravenous insulin infusion resulted in a dose-dependent reduction in endoneurial oxygen tension in normal nerves (from 26% at 0.04 U/kg insulin to 55% at 32 U/kg). The nerves of rats with streptozotocin-induced diabetes were resistant, but with control of hyperglycemia this susceptibility to the endoneurial hypoxic effect of insulin returned. The reduction in endoneurial oxygen tension regressed with glycosylated hemoglobin (Y = 53.8-2.7X, where Y = %reduction in endoneurial oxygen tension and X = HbA1; r = 0.87; P = < 0.001). Diabetes or insulin administration resulted in only minimal and physiologically insignificant alterations in the oxygen dissociation curve and 2,3-diphosphoglycerate of sciatic nerve. Instead, insulin administration resulted in a reduction in nerve nutritive blood flow and an increase in arteriovenous shunt flow. When the latter was eliminated by the closure of arteriovenous shunts (infusion of 5-hydroxytryptamine), endoneurial oxygen reverted to normal. These findings indicate a deleterious vasoactive effect of insulin and may explain the development of insulin neuritis.


1963 ◽  
Vol 204 (2) ◽  
pp. 327-329 ◽  
Author(s):  
Morris J. Mandel ◽  
Francesco Arcidiacono ◽  
Leo A. Sapirstein

Rb86 and Iodo131 antipyrine were injected together by vein in rats. The brain, spinal cord, and nerve contents of each label were measured 30 or 60 sec later. Iodoantipyrine values were used to calculate blood flow to these portions of the nervous system. The ratio of Rb86 to iodoantipyrine uptake was used as an index of the efficacy of the hematoneural barrier. The barrier is most complete in the brain, less complete in the spinal cord, and absent in peripheral nerve. Blood flow values per gram are: brain .41 ml/g min; cord .28 ml/g min, and nerve .11 ml/g min. It is suggested that the blood-brain barrier is an anatomical entity rather than a functional one.


1993 ◽  
Vol 250 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Arnoud C. Kappelle ◽  
Geert J. Biessels ◽  
Theo Van Buren ◽  
D. Willem Erkelens ◽  
Dick J. De Wildt ◽  
...  

1999 ◽  
Vol 11 (4) ◽  
pp. 309
Author(s):  
Shunichi Takagi ◽  
Koji Tateishi ◽  
Takaaki Kilano ◽  
Gabriel Lu ◽  
Vladmir Kvetan ◽  
...  

1977 ◽  
Vol 33 (3) ◽  
pp. 347-352 ◽  
Author(s):  
Donald R. Smith ◽  
Arthur I. Kobrine ◽  
Hugo V. Rizzoli

1987 ◽  
Vol 253 (4) ◽  
pp. E349-E353 ◽  
Author(s):  
M. Takeuchi ◽  
P. A. Low

We studied the dynamic effects of exsanguination of approximately one-third of rat blood volume over 3-12 min on energy metabolism and blood flow in rat sciatic nerves. Nerve high-energy phosphate compounds were relatively well maintained. There was a modest stimulation of anaerobic metabolism at slow rates of exsanguination, and glucose stores were slightly increased. These findings indicate that when stressed because of significant blood loss, compensatory mechanisms, presumably adrenosympathetic mediated, are effective in vivo. We recorded nerve blood flow (NBF), endoneurial oxygen tension, and mean arterial pressure simultaneously; NBF was linearly related to blood pressure (BP) over a wide range of BPs, confirming that NBF does not significantly autoregulate. Endoneurium underwent oxygen-exchange, indicating that peripheral nerve microvasculature is physiologically nutritive. NBF fell before and at a faster rate than BP, indicating that it is a capacitive system. Nerves also adapted to declining oxygen supplies, presumably by reducing their oxygen consumption. The physiological implications of such a system are discussed.


Author(s):  
Jiabin Zhang ◽  
Yaqiong Zhu ◽  
Nan Li ◽  
Feihong Dong ◽  
Jingyi Yin ◽  
...  

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