Cardiovascular and respiratory effects of carotid sinus nerve section and vagotomy in dogs
Chiang, C.H.
Journal of the Formosan Medical Association 85(3): 222-233
1986
ISSN/ISBN: 0371-7682 PMID: 3462306 Document Number: 271528
The purpose of this study was to determine not only the cardiorespiratory effects of vagotomy or carotid sinus nerve section (C.S.N.S.), but also the combined effects of vagotomy and C.S.N.S. We also wanted to know whether the effects of vagotomy or carotid sinus nerve sections were influenced by previous carotid sinus nerve section or vagotomy. Studies were conducted in 14 anesthetized dogs with vagotomy and C.S.N.S. in which tidal volume (VT), respiratory frequency (f), inspiratory time (TI), systolic blood pressure (BPs), diastolic blood pressure (BPd) and heart rate (HR) were continuously measured. We performed the first experiment with 8 dogs, in the following 4 steps: 1. Left (Lt.) vagotomy 2. Right (Rt.) vagotomy 3. Lt. C.S.N.S. 4. Rt. C.S.N.S. and the second experiment with 6 dogs in the following 4 steps: 1. Lt. C.S.N.S. 2. Rt. C.S.N.S. 3. Lt. vagotomy 4. Rt vagotomy. The result of bilateral vagotomy showed significant increase in VT from 276 .+-. 54 and 75 .+-. 11 ml to 640 .+-. 77 and 233 .+-. 27 ml respectively in experiment I and II (P<0.001); TI from 1.06 .+-. 0.24 to 2.80 .+-. 0.41 sec. in experiment I (P<0.01); BPs from 151 .+-. 10 and 187 .+-. 12 mmHg to 169 .+-. 8 and 262 .+-. 16mmHg respectively in experiment I and II (P<0.05 and P<0.001); but f significantly decreased from 12.5 .+-. 2.2 and 17.6 .+-. 3.4 min-1 to 5.1 .+-. 0.6 and 10.3 .+-. 2.1 min-1 respectively in experiment I and II (P<0.01 and P<0.05). Only one side vagotomy showed the same cardiorespiratory changes as those of both sides, but in a less degree. Cardiorespiratory changes induced by vagotomy were not influenced by previous bilateral C.S.N.S. The vagotomy induced respiratory change was due to a loss of the inhibitory effect of Hering-Breuer reflex, whereas vagotomy induced HR and BPs increases were due to loss of parasympathetic effect and aortic baroreceptor reflex. Bilateral C.S.N.S. increased f from 4.7 .+-. 0.5 min-1 to 7.5 .+-. 1.1 min-1 in experiment I, but not significantly in experiment II. Bps increased from 156 .+-. 18 and 131 .+-. 40 mmHg to 233 .+-. 27 and 187 .+-. 12 mmHg respectively in experiment I and II (P<0.05 and P<0.01); BPd increased from 111 .+-. 17 and 88 .+-. 11 mmHg to 153 .+-. 18 and 144 .+-. 15 mmHg respectively in experiment I and II (P<0.05 and P<0.01); HR increased from 166 .+-. 9 and 158 .+-. 10 (bpm) to 177 .+-. 9 and 196 .+-. 11 (bpm) respectively in experiment I and II (P<0.05 and P<0.01); but VT significantly decreased from 574 .+-. 101 and 90 .+-. 12 ml to 490 .+-. 98 and 75 .+-. 11 ml respectively in experiment I and II (P<0.05). Unilateral C.S.N.S. showed the same changes, but in a less degree. More respiratory changes were found in C.S.N.S. after vagotomy than those in bilateral C.S.N.S. alone. Our result of respiratory change after C.S.N.S. was the same as that of Eldridge's studies which showed that the inhibition in the carotid chemoreceptor by NH4OH led to decreased tidal volume. The increase in HR and BP was due to a loss of carotid sinus baroreceptor reflex. Cardiorespiratory changes caused by the combination of vagotomy and C.S.N.S. showed significant increases in VT, TI, BPs, BPd, and Hr but not in f. In inducing respiratory pattern changes, carotid sinus nerve section had the opposite effect to vagotomy, but caused the same changes in circulation; although carotid sinus nerve section induced the opposite respiratory changes to vagotomy, because vagotomy induced more VT and f changes than those of C.S.N.S. The cardiorespiratory effects caused by the combination of vagotomy and carotid sinus nerve section were similiar to those caused by vagotomy alone.