Vagal afferent innervation and remodeling in the aortic arch of young-adult fischer 344 rats following chronic intermittent hypoxia

Neuroscience ◽  
2009 ◽  
Vol 164 (2) ◽  
pp. 658-666 ◽  
Author(s):  
J. Ai ◽  
R.D. Wurster ◽  
S.W. Harden ◽  
Z.J. Cheng
Keyword(s):  
Young Adult ◽  
Aortic Arch ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Vagal Afferent ◽  
Afferent Innervation

Selective impairment of central mediation of baroreflex in anesthetized young adult Fischer 344 rats after chronic intermittent hypoxia

2007 ◽  
Vol 293 (5) ◽  
pp. H2809-H2818 ◽  
Author(s):  
He Gu ◽  
Min Lin ◽  
Jianyu Liu ◽  
David Gozal ◽  
Karie E. Scrogin ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Maximum Amplitude ◽  
Logistic Function ◽  
Stimulus Onset ◽  
Chronic Intermittent Hypoxia ◽  
Baroreflex Control ◽  
Maximum Slope ◽  
Peak Response ◽  
Fischer 344 ◽  
Arterial Blood

Baroreflex control of heart rate (HR) is impaired after chronic intermittent hypoxia (CIH). However, the location and nature of this response remain unclear. We examined baroreceptor afferent, vagal efferent, and central components of the baroreflex circuitry. Fischer 344 (F344) rats were exposed to room air (RA) or CIH for 35–50 days and were then anesthetized with isoflurane, ventilated, and catheterized for measurement of mean arterial blood pressure (MAP) and HR. Baroreceptor function was characterized by measuring percent changes of integrated aortic depressor nerve (ADN) activity (Int ADNA) relative to the baseline value in response to sodium nitroprusside- and phenylephrine-induced changes in MAP. Data were fitted to a sigmoid logistic function curve. HR responses to electrical stimulation of the left ADN and the right vagus nerve were assessed under ketamine-acepromazine anesthesia. Compared with RA controls, CIH significantly increased maximum baroreceptor gain or maximum slope, maximum Int ADNA, and Int ADNA range (maximum − minimum Int ADNA), whereas other parameters of the logistic function were unchanged. In addition, CIH increased the maximum amplitude of bradycardic response to vagal efferent stimulation and decreased the time from stimulus onset to peak response. In contrast, CIH significantly reduced the maximum amplitude of bradycardic response to left ADN stimulation and increased the time from stimulus onset to peak response. Therefore, CIH decreased central mediation of the baroreflex but augmented baroreceptor afferent function and vagal efferent control of HR.

Initiation of cardiac hypertrophy in response to thyroxine is not limited by age

1993 ◽  
Vol 264 (4) ◽  
pp. H1041-H1047
Author(s):  
R. J. Tomanek ◽  
C. A. Butters ◽  
M. B. Zimmerman
Keyword(s):  
Young Adult ◽  
Cardiac Hypertrophy ◽  
Left Ventricular ◽  
Fischer 344 Rats ◽  
Tissue Levels ◽  
Fischer 344 ◽  
Lv Mass ◽  
Group A ◽  
And Control

We examined the role of age in the initiation of thyroxine-induced (T4) cardiac hypertrophy. T4 (0.4 mg/kg sc) was administered to prepubescent (2 mo), young adult (6 mo), and senescent (24 mo) Fischer 344 rats for 4 days. While significant increases in left ventricular (LV) mass and RNA/LV were evident at 4 days in all T4-treated groups, the elevation in RNA/LV occurred earlier (2 days) in the senescent group. A 0.2-mg/kg dose of T4 elevated RNA values within 24 h in senescent, but not in prepubescent, rats. LV norepinephrine levels were measured to determine whether it plays a role in this model of cardiac hypertrophy. When synthesis of this catecholamine was blocked with alpha-methyl-p-tyrosine, tissue levels fell significantly in all groups, and the decrement was similar in T4-treated and control rats in the two younger groups. We conclude that: 1) the initiation of T4-induced cardiac hypertrophy is not compromised in senescent rats, 2) hearts of senescent rats respond earlier and to a lower dose of T4 than young rats, and 3) the cardiac hypertrophy that occurs in hyperthyroidism is not due to enhanced levels of available cardiac norepinephrine.

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