Dynamic peripheral nerve metabolic and vascular responses to exsanguination

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.

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

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.


1995 ◽  
Vol 15 (8) ◽  
pp. 4648-4656 ◽  
Author(s):  
M H Paalman ◽  
S L Henderson ◽  
B Sollner-Webb

We show that the mouse ribosomal DNA (rDNA) spacer promoter acts in vivo to stimulate transcription from a downstream rRNA gene promoter. This augmentation of mammalian RNA polymerase I transcription is observed in transient-transfection experiments with three different rodent cell lines, under noncompetitive as well as competitive transcription conditions, over a wide range of template concentrations, whether or not the enhancer repeats alone stimulate or repress expression from the downstream gene promoter. Stimulation of gene promoter transcription by the spacer promoter requires the rDNA enhancer sequences to be present between the spacer promoter and gene promoter and to be oriented as in native rDNA. Stimulation also requires that the spacer promoter be oriented toward the enhancer and gene promoter. However, stimulation does not correlate with transcription from the spacer promoter because the level of stimulation is not altered by either insertion of a functional mouse RNA polymerase I transcriptional terminator between the spacer promoter and enhancer or replacement with a much more active heterologous polymerase I promoter. Further analysis with a series of mutated spacer promoters indicates that the stimulatory activity does not reside in the major promoter domains but requires the central region of the promoter that has been correlated with enhancer responsiveness in vivo.


1985 ◽  
Vol 248 (4) ◽  
pp. G432-G436 ◽  
Author(s):  
I. R. Holzman ◽  
B. Tabata ◽  
D. I. Edelstone

We chronically catheterized 15 newborn lambs (9.5 +/- 2.8 days) and measured intestinal blood flow (Qi) by the radionuclide microsphere technique at hematocrit levels ranging from 10 to 55%. Seven animals were made progressively anemic and eight polycythemic by means of exchange transfusions. Using the Fick principle, we calculated intestinal oxygen delivery (Di o2), oxygen consumption (Vi o2), and oxygen extraction. Initial base-line values were Qi = 195.5 ml . min-1 . 100 g intestine-1, Di o2 = 22.1 ml . min-1 . 100 g-1, Vi o2 = 4.8 ml . min-1 . 100 g-1, and O2 extraction = 22.5%. As the hematocrit was lowered, Di o2 decreased and O2 extraction increased and vice versa when the hematocrit was raised. Vi o2 remained constant, but Qi did not correlate with changes in hematocrit. However, intestinal blood flow, as a percent distribution of total blood flow, decreased with lower hematocrit levels. At no time was there any evidence of anaerobic metabolism as measured by excess lactate production. Our data indicate that the intestines of neonatal lambs are capable of maintaining their metabolic needs over a wide range of oxygen availability induced by a changing hematocrit. The primary mechanism is through alteration of oxygen extraction. Within the range of our experiments, no critically low oxygen availability was attained at which anaerobic metabolism became significant.


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.


Electronics ◽  
2021 ◽  
Vol 10 (15) ◽  
pp. 1867
Author(s):  
Florian Kolbl ◽  
Yannick Bornat ◽  
Jonathan Castelli ◽  
Louis Regnacq ◽  
Gilles N’Kaoua ◽  
...  

Electrical stimulation of the nervous system is commonly based on biphasic stimulation waveforms, which limits its relevance for some applications, such as selective stimulation. We propose in this paper a stimulator capable of delivering arbitrary waveforms to electrodes, and suitable for non-conventional stimulation strategies. Such a system enables in vivo stimulation protocols with optimized efficacy or energy efficiency. The designed system comprises a High Voltage CMOS ASIC generating a configurable stimulating current, driven by a digital circuitry implemented on a FPGA. After fabrication, the ASIC and system were characterized and tested; they successfully generated programmable waveforms with a frequential content up to 1.2 MHz and a voltage compliance between [−17.9; +18.3] V. The system is not optimum when compared to single application stimulators, but no embedded stimulator in the literature offers an equivalent bandwidth which allows the wide range of stimulation paradigms, including high-frequency blocking stimulation. We consider that this stimulator will help test unconventional stimulation waveforms and can be used to generate proof-of-concept data before designing implantable and application-dedicated implantable stimulators.


2021 ◽  
Author(s):  
Sara Cadoni ◽  
Charlie Demene ◽  
Matthieu Provansal ◽  
Diep Nguyen ◽  
Dasha Nelidova ◽  
...  

Remote, precisely controlled activation of the brain is a fundamental challenge in the development of brain machine interfaces providing feasible rehabilitation strategies for neurological disorders. Low-frequency ultrasound stimulation can be used to modulate neuronal activity deep in the brain, but this approach lacks spatial resolution and cellular selectivity and loads the brain with high levels of acoustic energy. The combination of the expression of ultrasound-sensitive proteins with ultrasound stimulation (sonogenetic stimulation) can provide cellular selectivity and higher sensitivity, but such strategies have been subject to severe limitations in terms of spatiotemporal resolution in vivo, precluding their use for real-life applications. We used the expression of large-conductance mechanosensitive ion channels (MscL) with high-frequency ultrasonic stimulation for a duration of milliseconds to activate neurons selectively at a relatively high spatiotemporal resolution in the rat retina ex vivo and the primary visual cortex of rodents in vivo. This spatiotemporal resolution was achieved at low energy levels associated with negligible tissue heating and far below those leading to complications in ultrasound neuromodulation. We showed, in an associative learning test, that sonogenetic stimulation of the visual cortex generated light perception. Our findings demonstrate that sonogenetic stimulation is compatible with millisecond pattern presentation for visual restoration at the cortical level. They represent a step towards the precise transfer of information over large distances to the cortical and subcortical regions of the brain via an approach less invasive than that associated with current brain machine interfaces and with a wide range of applications in neurological disorders.


1987 ◽  
Vol 252 (2) ◽  
pp. H439-H441
Author(s):  
H. Sugimoto ◽  
W. W. Monafo ◽  
S. Shimazaki

The regional blood flow in the sciatic nerves (NBF), biceps femoris muscles (MBF), and hind limb skin (SBF) was measured simultaneously in anesthetized, normal rats, in other rats immediately after 15 min of electrical stimulation of one sciatic trunk (10 shocks/s), and in a group of similarly stimulated but previously curarized rats. These experiments were done to quantitate NBF during direct nerve stimulation in both the presence and absence of associated vigorous limb twitching, as these relationships have not previously been examined. Tissue blood flows were measured by an “indicator-fractionation” technic, using the distribution of [14C]butanol. NBF in normal controls was 11.1 +/- 1.4 ml X min-1 X 100 g-1; MBF was 6.8 +/- 0.6 ml X min-1 X 100 g-1. In the stimulated limb of noncurarized rats, NBF rose to 19.8 +/- 3.5 ml X min-1 X 100 g-1. MBF was elevated approximately tenfold. SBF also rose. In stimulated limbs of curarized rats, NBF was also approximately double the resting normal value, 23.2 +/- 4.8 ml X min-1 X 100 g-1, but MBF was then only slightly increased. We conclude that sciatic NBF increases appreciably when this nerve is stimulated, irrespective, for the most part, of whether limb motor activity is increased. The vascular mechanisms which regulate NBF differ from and are largely independent of those regulating MBF.


2008 ◽  
Vol 26 (3) ◽  
pp. 145-148 ◽  
Author(s):  
Motohiro Inoue ◽  
Tatsuya Hojo ◽  
Miwa Nakajima ◽  
Hiroshi Kitakoji ◽  
Megumi Itoi ◽  
...  

Objective To investigate the mechanism of the clinical effect of electroacupuncture of the pudendal nerve on the lumbar and lower limb symptoms caused by lumbar spinal canal stenosis, we studied changes in sciatic nerve blood flow during electrical stimulation of the pudendal nerve in the rat. Methods Using rats (n=5), efferent electrical stimulation to the pudendal nerve was performed and sciatic nerve blood flow was measured with laser Doppler flowmetry. Simultaneously, changes in the blood pressure and cardiac rate were measured. Furthermore, the effect of atropine on these responses to the stimulation was also studied. Results Electrical stimulation of the pudendal nerve significantly increased blood flow in the sciatic nerve transiently without increasing heart rate and systemic blood pressure. The significant increase in the sciatic nerve blood flow disappeared after administration of atropine. Conclusion Electrical stimulation of the pudendal nerve causes a transient and significant increase in sciatic nerve blood flow. This response is eliminated or attenuated by administration of atropine, indicating that it occurs mainly via cholinergic nerves.


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