Chronic vagal nerve stimulation improves baroreflex neural arc function in heart failure rats

2014 ◽  
Vol 116 (10) ◽  
pp. 1308-1314 ◽  
Author(s):  
Toru Kawada ◽  
Meihua Li ◽  
Can Zheng ◽  
Shuji Shimizu ◽  
Kazunori Uemura ◽  
...  
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Vagal Stimulation ◽  
Statistical Significance ◽  
Open Loop ◽  
Sprague Dawley ◽  
Baroreflex Control ◽  
Response Range ◽  
Sprague Dawley Rats ◽  
The Difference

We tested whether 6-wk vagal stimulation (VS) treatment improved open-loop baroreflex function in rats after myocardial infarction (MI). The following three groups of Sprague-Dawley rats were examined: normal control (NC, n = 9), MI with no treatment (MI-NT, n = 8), and MI treated with VS (MI-VS, n = 7). Under anesthesia, a stepwise input ranging from 60 to 180 mmHg was imposed on isolated carotid sinus baroreceptor regions, while the responses in splanchnic sympathetic nerve activity (SNA) and arterial pressure (AP) were measured. The response range of percent SNA was greater in the MI-VS than in the MI-NT group (63.8 ± 4.9% vs. 33.1 ± 3.8%, P < 0.01). The slope of the AP response to percent SNA was not different between the MI-VS and MI-NT groups (0.611 ± 0.076 vs. 0.781 ± 0.057 mmHg/%). The difference in the response range of AP between the MI-VS and MI-NT groups did not reach statistical significance (40.7 ± 6.2 vs. 26.4 ± 3.5 mmHg). In conclusion, the 6-wk VS treatment significantly improved the baroreflex control of SNA, but the effect was limited for the baroreflex total-loop function due to the lack of significant improvement in the AP response to percent SNA.

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity

1985 ◽  
Vol 249 (5) ◽  
pp. H922-H928 ◽  
Author(s):  
F. M. Sharabi ◽  
G. B. Guo ◽  
F. M. Abboud ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Urinary Osmolality ◽  
Arterial Baroreceptors ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
High Level

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

Adrenalectomy eliminates both fiber-type differences and starvation effects on denervated muscle

1988 ◽  
Vol 255 (6) ◽  
pp. E850-E856 ◽  
Author(s):  
R. R. Almon ◽  
D. C. Dubois
Keyword(s):  
Muscle Mass ◽  
Extensor Digitorum Longus ◽  
Fiber Type ◽  
Sprague Dawley ◽  
Denervated Muscle ◽  
Adrenalectomized Animal ◽  
Sprague Dawley Rats ◽  
Starvation Effects ◽  
The Difference ◽  
Denervated Muscles

This report describes changes in muscle mass of innervated and denervated pairs of muscles taken from intact and adrenalectomized 250-g male Sprague-Dawley rats provided with different diets. Diets ranged from a nutritionally complete liquid diet to starvation (water only). In the intact animals, muscles with a more tonic character (soleus) are less sensitive to starvation than are muscles with a more phasic character (extensor digitorum longus), whereas the opposite is true of denervation. In the intact animals, starvation greatly increased the amount of atrophy following denervation. In the adrenalectomized animals, starvation had no effect on the amounts of atrophy following denervation. Furthermore, adrenalectomy virtually eliminated the fiber-type differences in the amount of atrophy following denervation. In addition, a comparison between denervated muscles from intact animals and adrenalectomized animals subjected to starvation demonstrates that all denervated muscles from the adrenalectomized animals atrophy less. Finally, it was observed that although an adrenalectomized animal can tolerate 6 days of starvation, an adrenalectomized-castrated animal cannot tolerate even short periods of starvation. The difference appears to be due to low amounts of corticosterone of testicular origin.

Vagal stimulation-induced gastric damage in rats

1991 ◽  
Vol 261 (1) ◽  
pp. G104-G110
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson
Keyword(s):  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Vagal Afferents ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagus Nerves ◽  
Sprague Dawley Rats ◽  
Series Of Experiments ◽  
Stimulation Of

The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.

scholarly journals Arcuate nucleus injection of an anti-insulin affibody prevents the sympathetic response to insulin

2013 ◽  
Vol 304 (11) ◽  
pp. H1538-H1546 ◽  
Author(s):  
Brittany S. Luckett ◽  
Jennifer L. Frielle ◽  
Lawrence Wolfgang ◽  
Sean D. Stocker
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arcuate Nucleus ◽  
Insulin Receptors ◽  
Ventromedial Hypothalamus ◽  
Intracerebroventricular Injection ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sympathetic Response ◽  
Sprague Dawley Rats

Accumulating evidence suggests that insulin acts within the hypothalamus to alter sympathetic nerve activity (SNA) and baroreflex function. Although insulin receptors are widely expressed across the hypothalamus, recent evidence suggests that neurons of the arcuate nucleus (ARC) play an important role in the sympathoexcitatory response to insulin. The purpose of the present study was to determine whether circulating insulin acts directly in the ARC to elevate SNA. In anesthetized male Sprague-Dawley rats (275–425 g), the action of insulin was neutralized by microinjection of an anti-insulin affibody (1 ng/40 nl). To verify the efficacy of the affibody, ARC pretreatment with injection of the anti-insulin affibody completely prevented the increase in lumbar SNA produced by ARC injection of insulin. Next, ARC pretreatment with the anti-insulin affibody attenuated the lumbar sympathoexcitatory response to intracerebroventricular injection of insulin. Third, a hyperinsulinemic-euglycemic clamp increased lumbar, but not renal, SNA in animals that received ARC injection of a control affibody. However, this sympathoexcitatory response was absent in animals pretreated with the anti-insulin affibody in the ARC. Injection of the anti-insulin affibody in the adjacent ventromedial hypothalamus did not alter the sympathoexcitatory response to insulin. The ability of the anti-insulin affibody to prevent the sympathetic effects of insulin cannot be attributed to a general inactivation or nonspecific effect on ARC neurons as the affibody did not alter the sympathoexcitatory response to ARC disinhibition by gabazine. Collectively, these findings suggest that circulating insulin acts within the ARC to increase SNA.

Loss of hypoxic pulmonary vasoconstriction in chronic pneumonia is not mediated by nitric oxide

1993 ◽  
Vol 265 (5) ◽  
pp. H1523-H1528 ◽  
Author(s):  
D. G. McCormack ◽  
N. A. Paterson
Keyword(s):  
Nitric Oxide ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Sprague Dawley ◽  
Absolute Increase ◽  
Pulmonary Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Inflammatory Processes ◽  
The Difference

In pulmonary inflammatory processes such as pneumonia there is diminished hypoxic pulmonary vasoconstriction (HPV). We investigated whether the attenuated HPV in pneumonia is a due to excess nitric oxide (NO) release. Sprague-Dawley rats were anesthetized, and a slurry (0.06 ml) of infected agar beads (containing 6 x 10(5) Pseudomonas aeruginosa organisms) or control (sterile) beads was then injected into a distal bronchus through a tracheotomy. After the establishment of a chronic P. aeruginosa pneumonia (7-10 days later) animals were instrumented for hemodynamic monitoring, and the response to exposure to hypoxic gas (fraction of inspired O2 = 0.08) was recorded before and after the administration of NG-monomethyl-L-arginine (L-NMMA; 50 mg/kg), an inhibitor of NO synthesis. The hypoxic pressor response, as assessed by the absolute increase in pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR), was reduced in infected animals compared with control animals. The change in PAP and TPR was 8.5 +/- 0.7 and 0.053 +/- 0.007, respectively, in control animals compared with 5.9 +/- 0.5 and 0.041 +/- 0.011 in infected animals. After L-NMMA the increase in PAP and TPR during hypoxia was greater in both control and infected animals. However, treatment with L-NMMA did not affect the difference between control and infected animals. We conclude that excess release of NO does not account for the attenuated hypoxic pressor response in pneumonia.

HEXAFLUORODIETHYL ETHER (INDOKLON) CONVULSIONS IN CORPUS-CALLOTOMIZED WHITE RATS

1964 ◽  
Vol 42 (5) ◽  
pp. 609-621 ◽  
Author(s):  
H. R. Butler ◽  
S. J. Manax ◽  
G. W. Stavraky
Keyword(s):  
Sprague Dawley ◽  
White Rats ◽  
Sprague Dawley Rats ◽  
Maximal Sensitivity ◽  
The Difference

The convulsant threshold of 24 corpus-callotomized Sprague–Dawley rats exposed to Indoklon vapor once a week was found to be significantly lower than that of 24 sham-operated controls in the second, third, and fourth exposures; the sensitivity of both groups of animals increased progressively and levelled out at the fifth exposure. Repetition of the experiment after 3 weeks of rest, with exposures spaced at 48-hour intervals, further lowered the convulsant threshold of the animals, both groups exhibiting a similar, and possibly maximal, sensitivity to Indoklon at the second exposure. When in another series, 60 corpus-callotomized rats and 60 sham-operated controls were injected intraperitoneally with CD10 of Indoklon at weekly intervals, the susceptibility of both groups to convulsions again increased rapidly during the first four injections; at the second injection, the corpus-callotomized rats were significantly more sensitive to Indoklon than the controls. During the fifth to eighth injection, the convulsibility of the animals reached a plateau, 62.2% to 78.5% of the rats convulsing; the difference between the two groups at this stage became less marked, though the convulsions in corpus-callotomized animals continued to be of longer duration than in the controls. Repetition of the injections, spaced at 48-hour intervals, after 3 months of rest, demonstrated a continuing high and equal sensitivity of the two groups of rats to Indoklon with some depression setting in during the second half of a series of 12 injections.

Strain Differences Occurring in an Experimental Study of Punishment

1965 ◽  
Vol 16 (2) ◽  
pp. 531-536 ◽  
Author(s):  
Morton H. Kleban
Keyword(s):  
Experimental Study ◽  
Empirical Evidence ◽  
Wistar Rats ◽  
Strain Differences ◽  
Training Procedure ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Y Maze ◽  
Minimum Number ◽  
The Difference

Forty-three Sprague-Dawley and 43 Wistar rats were given reward training for 40 trials in a Y-maze. On the next 20 trials, control groups were continued under the same training procedure, and 50% shock trials were introduced in the training of the remaining rats. For the extinction training, the reward was shifted to the opposite arm and 50% shock was continued for the no-delay and 30-sec. delay shock groups. The most significant results were that in the 30-sec. delay groups, the delay helped the Sprague-Dawley rats reverse in a minimum number of trials, whereas the Wistar rats showed strong indications of response stereotypy. The findings with respect to the Sprague-Dawley rats supported the empirical evidence on the effectiveness of delay in overcoming response persistence and the findings on the Wistar rats supported the empirical evidence on omission in punishment. The difference in response to punishment between the two albino strains emphasizes the need for experimental study of strain factors. Experiments should be repeated with several animal strains to remedy over-generalization from single strains and to help elaborate our understanding of the interaction present between punishment and strains.

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