scholarly journals Electrophysiological effects of right and left vagal nerve stimulation on the ventricular myocardium

2014 ◽  
Vol 307 (5) ◽  
pp. H722-H731 ◽  
Author(s):  
Kentaro Yamakawa ◽  
Eileen L. So ◽  
Pradeep S. Rajendran ◽  
Jonathan D. Hoang ◽  
Nupur Makkar ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Regional Differences ◽  
Left Ventricular Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Ventricular Pressure ◽  
Electrophysiological Effects

Vagal nerve stimulation (VNS) has been proposed as a cardioprotective intervention. However, regional ventricular electrophysiological effects of VNS are not well characterized. The purpose of this study was to evaluate effects of right and left VNS on electrophysiological properties of the ventricles and hemodynamic parameters. In Yorkshire pigs, a 56-electrode sock was used for epicardial ( n = 12) activation recovery interval (ARI) recordings and a 64-electrode catheter for endocardial ( n = 9) ARI recordings at baseline and during VNS. Hemodynamic recordings were obtained using a conductance catheter. Right and left VNS decreased heart rate (84 ± 5 to 71 ± 5 beats/min and 84 ± 4 to 73 ± 5 beats/min), left ventricular pressure (89 ± 9 to 77 ± 9 mmHg and 91 ± 9 to 83 ± 9 mmHg), and dP/d tmax (1,660 ± 154 to 1,490 ± 160 mmHg/s and 1,595 ± 155 to 1,416 ± 134 mmHg/s) and prolonged ARI (327 ± 18 to 350 ± 23 ms and 327 ± 16 to 347 ± 21 ms, P < 0.05 vs. baseline for all parameters and P = not significant for right VNS vs. left VNS). No anterior-posterior-lateral regional differences in the prolongation of ARI during right or left VNS were found. However, endocardial ARI prolonged more than epicardial ARI, and apical ARI prolonged more than basal ARI during both right and left VNS. Changes in dP/d tmax showed the strongest correlation with ventricular ARI effects ( R2 = 0.81, P < 0.0001) than either heart rate ( R2 = 0.58, P < 0.01) or left ventricular pressure ( R2 = 0.52, P < 0.05). Therefore, right and left VNS have similar effects on ventricular ARI, in contrast to sympathetic stimulation, which shows regional differences. The decrease in inotropy correlates best with ventricular electrophysiological effects.

In vivo detection of endogenous acetylcholine release in cat ventricles

1994 ◽  
Vol 266 (3) ◽  
pp. H854-H860 ◽  
Author(s):  
T. Akiyama ◽  
T. Yamazaki ◽  
I. Ninomiya
Keyword(s):  
Nerve Stimulation ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Left Ventricular Myocardium ◽  
Ach Release ◽  
Vagal Nerves ◽  
Dialysis Technique

To detect and monitor endogenous acetylcholine (ACh) release in the in vivo heart, we applied a dialysis technique to the hearts of anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium and were perfused with Krebs-Henseleit solution containing Eserine (10(-4) M) at 3 microliters/min. Dialysate ACh concentration was measured with high-performance liquid chromatography. In four cats, the response to vagal stimulation was studied. Electrical stimulation of efferent vagal nerves (10 Hz) significantly increased dialysate ACh concentration from 596 +/- 118 (control) to 12,210 +/- 1,661 pM. After stimulation, dialysate ACh concentration significantly decreased to 382 +/- 80 pM below control. The influence of ganglionic blocker was determined in six cats. Control vagal nerve stimulation (10 Hz) increased dialysate ACh concentration from 582 +/- 136 to 9,102 +/- 754 pM. Local perfusion of hexamethonium (10(-4) M) did not affect this nerve stimulation-induced ACh increase (8,611 +/- 1,189 pM), and intravenous administration of hexamethonium (20 mg/kg) prevented this increase (340 +/- 88 pM). We examined the response to vagal nerve stimulation at different frequencies in three cats. Vagal nerve stimulation increased dialysate ACh concentration from a control of 588 +/- 211 to 1,227 +/- 195 pM at 2 Hz, 3,946 +/- 1,059 pM at 5 Hz, and 9,366 +/- 1,873 pM at 10 Hz. Dialysate ACh concentration reflects ACh release from postganglionic vagal nerves innervating the left ventricular myocardium; the dialysis technique permits estimation of relative changes in efferent cardiac vagal nerve activity.

Vagal Nerve Stimulation Evoked Heart Rate Changes and Protection from Cardiac Remodeling

2016 ◽  
Vol 9 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Rahul Agarwal ◽  
Eric Mokelke ◽  
Stephen B. Ruble ◽  
Craig M. Stolen
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Cardiac Remodeling ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation

Ivabradine augments high-frequency dynamic gain of the heart rate response to low- and moderate-intensity vagal nerve stimulation under beta-blockade

2021 ◽  
Author(s):  
Toru Kawada ◽  
Hiromi Yamamoto ◽  
Kazunori Uemura ◽  
Yohsuke Hayama ◽  
Takuya Nishikawa ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Moderate Intensity ◽  
Beta Blockade ◽  
Hcn Channels

Our previous study indicated that intravenously administered ivabradine (IVA) augmented the dynamic heart rate (HR) response to moderate-intensity vagal nerve stimulation (VNS). Considering an accentuated antagonism, the results were somewhat paradoxical; i.e., the accentuated antagonism indicates that an activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels via the accumulation of intracellular cyclic adenosine monophosphate (cAMP) augments the HR response to VNS, whereas the inhibition of HCN channels by IVA also augmented the HR response to VNS. To remove the possible influence from the accentuated antagonism, we examined the effects of IVA on the dynamic vagal control of HR under beta-blockade. In anesthetized rats (n = 7), the right vagal nerve was stimulated for 10 min according to binary white noise signals between 0 and 10 Hz (V0-10), between 0 and 20 Hz (V0-20), and between 0 and 40 Hz (V0-40). The transfer function from VNS to HR was estimated. Under beta-blockade (propranolol, 2 mg/kg, i.v.), IVA (2 mg/kg, i.v.) did not augment the asymptotic low-frequency gain but increased the asymptotic high-frequency gain in V0-10 (0.53 ± 0.10 vs. 1.74 ± 0.40 beats·min−1·Hz−1, P < 0.01) and V0-20 (0.79 ± 0.14 vs. 2.06 ± 0.47 beats·min−1·Hz−1, P < 0.001). These changes, which were observed under a minimal influence from sympathetic background tone, may reflect an increased contribution of the acetylcholine-sensitive potassium channel (IK,ACh) pathway after IVA, because the HR control via the IK,ACh pathway is faster and acts in the frequency range higher than the cAMP-mediated pathway.

scholarly journals Intravenous ivabradine augments the dynamic heart rate response to moderate vagal nerve stimulation in anesthetized rats

2019 ◽  
Vol 317 (3) ◽  
pp. H597-H606 ◽  
Author(s):  
Toru Kawada ◽  
Hiromi Yamamoto ◽  
Kazunori Uemura ◽  
Yohsuke Hayama ◽  
Takuya Nishikawa ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Heart Rate Response ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Corner Frequency ◽  
Moderate Intensity ◽  
Bradycardic Agent ◽  
Wistar Kyoto ◽  
White Noise Sequence

Ivabradine is a selective bradycardic agent that reduces the heart rate (HR) by inhibiting the hyperpolarization-activated cyclic nucleotide-gated channels. Although its cardiovascular effect is thought to be minimal except for inducing bradycardia, ivabradine could interact with cardiovascular regulation by the autonomic nervous system. We tested whether ivabradine modifies dynamic characteristics of peripheral vagal HR control. In anesthetized Wistar-Kyoto rats ( n = 7), the right vagal nerve was sectioned and stimulated for 10 min according to a binary white noise sequence with a switching interval of 500 ms. The efferent vagal nerve stimulation (VNS) trials were performed using three different rates (10, 20, and 40 Hz), and were designated as V0–10, V0–20, and V0–40, respectively. The transfer function from the VNS to the HR was estimated before and after the intravenous administration of ivabradine (2 mg/kg). Ivabradine increased the asymptotic dynamic gain in V0–20 [from 3.88 (1.78–5.79) to 6.62 (3.12–8.31) beats·min−1·Hz−1, P < 0.01, median (range)] but not in V0–10 or V0–40. Ivabradine increased the corner frequency in V0–10 [from 0.032 (0.026–0.041) to 0.064 (0.029–0.090) Hz, P < 0.01] and V0–20 [from 0.040 (0.037–0.056) to 0.068 (0.051–0.100) Hz, P < 0.01] but not in V0–40. In conclusion, ivabradine augmented the dynamic HR response to moderate VNS. At high VNS, however, ivabradine did not significantly augment the dynamic HR response, possibly because ivabradine reduced the baseline HR and limited the range for the bradycardic response to high VNS. NEW & NOTEWORTHY Ivabradine is considered to be a pure bradycardic agent that has little effect on cardiovascular function except inducing bradycardia. The present study demonstrated that ivabradine interacts with the dynamic vagal heart rate control in a manner that augments the heart rate response to moderate-intensity efferent vagal nerve stimulation.

Alterations in cardiac [14C]deoxyglucose uptake induced by two renal afferent stimuli

1986 ◽  
Vol 251 (5) ◽  
pp. R867-R877
Author(s):  
N. L. Herman ◽  
D. R. Kostreva
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nerve Stimulation ◽  
Ventricular Myocardium ◽  
Venous Occlusion ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Renal Nerve ◽  
Vein Occlusion ◽  
Renal Nerve Stimulation

The reflex effects of renal afferents on the heart were studied in pentobarbital-anesthetized rats (400-425 g) using 2-[14C]deoxyglucose (DG). Three groups of rats were given a single bolus injection of DG (100 mu Ci/kg) 1) six controls, 2) four with periodic electrical stimulation of the proximal end of a cut renal nerve (2 Hz, 0.5-ms width) and 1-mA current, and 3) six with intermittent renal venous occlusion (unilateral). Forty-five minutes after injection the heart was removed, cooled quickly, and frozen-sectioned. Sections 20 micron thick were exposed to film for 12 days. The resulting autoradiographs were scanned using a computerized densitometer, and these densities were converted to relative glucose utilization (GlU, mumol X 100 g-1 X min-1) using the lumped constant for rat brain. Both renal venous occlusion and renal afferent nerve stimulation resulted in a decrease in blood pressure of 6.7 +/- 0.6 mmHg (P less than 0.001) and 7.3 +/- 0.7 mmHg (P less than 0.001) and heart rate-blood pressure product of 5.6 +/- 0.7% (P less than 0.001) and 8.8 +/- 0.8% (P less than 0.001), respectively, and afferent renal nerve stimulation induced a decrease in heart rate of 7.2 +/- 0.9 beats/min (P less than 0.01). However, when compared with control, renal venous occlusion induced a significant increase in GlU in left ventricular myocardium (LV myo, P less than 0.05), endocardium (LV endo, P less than 0.001), and papillary muscle (LV pap, P less than 0.001), whereas afferent renal nerve stimulation induced a significant increase in GlU in LV endo (P less than 0.05) and LV pap (P less than 0.002) only. This study shows both a reflex increase in GlU for the rat heart and a decrease in heart rate with either renal vein occlusion or afferent renal nerve stimulation.

scholarly journals Changes of left ventricular pressure-diameter-velocity relations by alterations of heart rate in conscious dogs.

1984 ◽  
Vol 48 (12) ◽  
pp. 1312-1321 ◽  
Author(s):  
MASUAKI FUJIYAMA ◽  
YOH-ICHIRO FURUTA ◽  
JUN MATSUMURA ◽  
AKIHIRO TANABE ◽  
JUN OHBAYASHI ◽  
...  
Keyword(s):  
Heart Rate ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Ventricular Pressure
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