scholarly journals Activities in a single sensory fiber of the aortic depressor nerve were derived from multiple encoders (1132.8)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Jun Liu ◽  
Nana Song ◽  
Shifu Tian ◽  
Juan Guardiola ◽  
Mary Proctor ◽  
...  
1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.


2000 ◽  
Vol 279 (5) ◽  
pp. R1922-R1933 ◽  
Author(s):  
Barry R. Dworkin ◽  
Xiaorui Tang ◽  
Alan J. Snyder ◽  
Susan Dworkin

To determine the relationship between blood pressure (BP) variability and the open-loop frequency domain transfer function (TF) of the baroreflexes, we measured the pre- and postsinoaortic denervation (SAD) spectra and the effects of periodic and step inputs to the aortic depressor nerve and isolated carotid sinus of central nervous system-intact, neuromuscular-blocked (NMB) rats. Similar to previous results in freely moving rats, SAD greatly increased very low frequency (VLF) (0.01–0.2 Hz) systolic blood pressure (SBP) noise power. Step response-frequency measurements for SBP; interbeat interval (IBI); venous pressure; mesenteric, femoral, and skin blood flow; and direct modulation analyses of SBP showed that only VLF variability could be substantially attenuated by an intact baroreflex. The −3-dB frequency for SBP is 0.035–0.056 Hz; femoral vascular conductance is similar to SBP, but mesenteric vascular conductance has a reliably lower and IBI has a reliably higher −3-dB point. The overall open-loop transportation lag, of which ≤0.1 s is neural, is ≈1.07 s. Constrained algebraic solution, over a range of frequencies, of the pre- and postSAD endogenous noise spectra and the independently determined relative frequency and absolute lag measurements was used to calculate the absolute gain for the open-loop TF. The average gain at 0.02 Hz, the frequency of maximum sensitivity, was 1.47 (95% confidence interval = ±0.48), which agrees well with estimates for the dog reversible sinus. We found that, in the NMB rat, the effects of SAD on the BP noise spectrum were accounted for by the open-loop properties of the baroreflex.


2000 ◽  
Vol 279 (5) ◽  
pp. R1910-R1921 ◽  
Author(s):  
Barry R. Dworkin ◽  
Susan Dworkin ◽  
Xiaorui Tang

To characterize the baroreflex in central nervous system-intact neuromuscular-blocked rats, we measured the vascular and cardiac responses and compared direct stimulation of the aortic depressor nerve (ADN) with a capacitance electrode (differentially activating either A or A + C fibers) to carotid sinus pressure with a micro-balloon (SINUS). One-thousand-two-hundred-ninety-seven open-loop measurements of systolic blood pressure (SBP), heart rate, venous pressure (VBP), and mesenteric (msBF), femoral (fmBF), and skin (skBF) blood flow were completed; the linear range of the effects was determined for each response and stimulus mode. The rats were sinoaortic denervated (SAD). The open-loop stimulation effect was very stable; e.g., the mean effect of 790 ADN stimulations during >7 days was −9.8 mmHg, with an average drift of +0.001 mmHg/h. In contrast, there was large variability of the SBP baseline (e.g., SD = ±10.9), which was due to SAD (±6.3 to ±16.3 mmHg, t = −13.9, df = 4, P < 0.0002) and was reversed by ganglionic block (±10.8 to ± 2.9 mmHg, t = −12.9, df = 3, P < 0.001). The ADN stimuli produced larger depressor responses than sinus stimuli (−66 vs. −45 mmHg); all component responses paralleled the magnitude of the SBP effect, except interbeat interval (IBI), for which the ADN ΔIBI was ≈10 times that of SINUS. For all stimuli, fmBF increased and msBF did not. Mesenteric and femoral vascular conductance both increased, whereas VBP decreased and skBF followed SBP. We found that for all baroreflex response components, with the exception of SINUS-elicited ΔIBI, there was an orderly, substantially linear, relationship between stimulus strength and response magnitude.


1963 ◽  
Vol 205 (4) ◽  
pp. 771-774 ◽  
Author(s):  
Eduardo Moacyr Krieger ◽  
Ricardo Francisco Marseillan

In 51 rats the distribution of the aortic depressor fibers which travel in the cervical region with the vagus, sympathetic, laryngeal, or as a separate aortic nerve was investigated by recording the action potential or by stimulating these nerves. A separate aortic depressor nerve was found in only 20% of the rats on the left side and in 5% on the right side. In these animals no depressor fibers were identified in the sympathetic trunk but the laryngeal nerves usually still exhibited depressor fiber activity. In those rats with no separate aortic depressor nerve the aortic fibers were present almost equally in the sympathetic trunk and laryngeal nerves, and on both sides of the neck. Only exceptionally was depressor activity found in the vagus trunk, and stimulation elicited depressor instead of pressor effects in 2 out of 12 rats. Optimal stimuli for obtaining hypotensive effects from the aortic depressor fibers were 80–150 per frequency and 1–2-msec duration.


2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Milena Menezes Amorim ◽  
Jaci Airton Castania ◽  
Helio Cesar Salgado ◽  
Valéria Paula Sassoli Fazan

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Harald Martin Stauss ◽  
Donald A Morgan ◽  
Kamal Rahmouni

2002 ◽  
Vol 97 (6) ◽  
pp. 1550-1556 ◽  
Author(s):  
Anthony E. Pickering ◽  
Hidefumi Waki ◽  
P. Max Headley ◽  
Julian F.R. Paton

Background The inadvertent systemic administration of bupivacaine has been associated with fatal cardiovascular collapse. Systemic bupivacaine may affect neural control of the cardiovascular system in addition to having toxic actions on the heart. The study tested the hypothesis that systemic bupivacaine has toxic effects on brainstem cardiorespiratory control. Methods The working heart-brainstem preparation (WHBP) of rat was used to examine the actions of bupivacaine administered either by arterial injection or brainstem microinjection. The WHBP is a decerebrate rostral-half of a bisected rat, which is artificially perfused with a carbogenated Ringer solution via the aorta. Phrenic nerve activity, perfusion pressure, and electrocardiographic results were recorded. Results Systemic bupivacaine (3 microg/ml) evoked a prolonged pressor response (10.5 +/- 5 mmHg) associated with marked bradycardia (-45 +/- 22 beats/min) and prolonged the PR and QRS intervals of the electrocardiogram. The amplitude of respiratory sinus arrhythmia was attenuated (64 +/- 15%) by bupivacaine without affecting activity recorded from the phrenic nerve. Bupivacaine selectively attenuated the baroreflex gain (55 +/- 19%) but had no effect on the peripheral chemoreflex-evoked bradycardia. The bradycardia elicited by stimulation of the aortic depressor nerve was inhibited by bupivacaine, indicating baroreflex inhibition within the brainstem. Furthermore, bilateral microinjections of bupivacaine in the nucleus of the solitary tract reversibly inhibited the baroreflex. Conclusions These results demonstrate that arterial concentrations of bupivacaine that previously were shown to be cardiotoxic can selectively affect key cardiovascular control processes within the brainstem. Such impairment of neural cardiovascular control may contribute to the cardiovascular collapse associated with systemic bupivacaine.


1995 ◽  
Vol 269 (3) ◽  
pp. H923-H933 ◽  
Author(s):  
L. F. Hayward ◽  
R. B. Felder

The caudal nucleus tractus solitarius (NTS) is the primary termination site for baroreceptor afferents, but distinct pulse phasic activity is rarely recorded from NTS neurons. In the present study cross-correlation analysis was used to identify pulse phasic activity in NTS neurons in the anesthetized rabbit. Cross-correlation analysis demonstrated that 19 of 38 pressure-sensitive neurons had activity that correlated with the cardiac cycle, including 5 of 11 neurons activated by aortic depressor nerve stimulation, and 12 of 28 pressure-sensitive NTS neurons had activity that correlated with renal sympathetic nerve activity. Autocorrelation analysis identified 17 of 38 pressure-sensitive neurons that had rhythmic activity not related to the cardiac cycle (mean frequency 14.1 +/- 2 Hz). The results indicate that many NTS neurons do have pulse phasic activity consistent with baroreceptor input, but this activity is difficult to detect because it is distributed throughout the cardiac cycle.


2003 ◽  
Vol 285 (2) ◽  
pp. H516-H526 ◽  
Author(s):  
Hidehiko Komine ◽  
Kanji Matsukawa ◽  
Hirotsugu Tsuchimochi ◽  
Jun Murata

To examine whether the central characteristics of the aortic baroreflex alter from moment to moment during static exercise, we identified the dynamic changes in the sizes of the bradycardia and depressor response evoked by stimulation of the aortic depressor nerve (ADN). Three conscious cats were trained to voluntarily extend the right forelimb and press a bar for 31 ± 1 s with a peak force of 337 ± 22 g while maintaining a sitting posture. The ADN stimulation-induced bradycardia was attenuated at the initial period of exercise (up to 8 s from the exercise onset) to 62 ± 5% of the preexercise bradycardia and remained blunted until the end of exercise. The most blunted bradycardia was observed immediately before or when the forelimb was extended before force development. The baroreflex-induced bradycardia was suppressed again at cessation of exercise when the forelimb was retracted and recovered within a few seconds. In contrast, static exercise did not affect the ADN stimulation-induced depressor response. The ADN stimulation-induced bradycardia was also blunted at the beginning of naturally occurring body movement such as spontaneous postural change or grooming behavior. Thus it is likely that the central characteristics of the aortic baroreflex dynamically change from moment to moment during voluntary static exercise and during natural body movement and that particularly a central inhibition of the cardiac component of the aortic baroreflex is induced by central command at the onset of static exercise, whereas the central property of the vasomotor component of the baroreflex is preserved.


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