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.

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.

Selective AV nodal vagal stimulation improves hemodynamics during acute atrial fibrillation in dogs

2001 ◽  
Vol 281 (4) ◽  
pp. H1490-H1497 ◽  
Author(s):  
Don W. Wallick ◽  
Youhua Zhang ◽  
Tomotsugu Tabata ◽  
Shaowei Zhuang ◽  
Kent A. Mowrey ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Nerve Stimulation ◽  
Atrioventricular Node ◽  
Vital Role ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Ventricular Rate ◽  
Significant Deterioration ◽  
Vagal Nerves

Although the atrioventricular node (AVN) plays a vital role in blocking many of the atrial impulses from reaching the ventricles during atrial fibrillation (AF), a rapid irregular ventricular rate nevertheless persists. The goals of the present study were to explore the feasibility of novel epicardial selective vagal nerve stimulation for slowing of the ventricular rate during AF and to characterize the hemodynamic benefits in vivo. Electrophysiological-echocardiographic experiments were performed on 11 anesthetized open-chest dogs. Hemodynamic measurements were performed during three distinct periods: 1) sinus rate, 2) AF, and 3) AF with vagal nerve stimulation. AF was associated with significant deterioration of all measured parameters ( P < 0.025). The vagal nerve stimulation produced slowing of the ventricular rate, significant reversal of the pressure and contractile indexes ( P < 0.025), and a sharp reduction in one-half of the abortive ventricular contractions. The present study provides comprehensive evidence that slowing of the ventricular rate during AF by selective ganglionic stimulation of the vagal nerves that innervate the AVN successfully improved the hemodynamic responses.

Contribution of afferent pathway to vagal nerve stimulation-induced myocardial interstitial acetylcholine release in rats

2020 ◽  
Vol 319 (5) ◽  
pp. R517-R525
Author(s):  
Toru Kawada ◽  
Takashi Sonobe ◽  
Takuya Nishikawa ◽  
Yohsuke Hayama ◽  
Meihua Li ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Low Voltage ◽  
Low Frequency ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Afferent Pathway ◽  
Ach Release ◽  
Vagal Afferent ◽  
Wistar Kyoto

Vagal nerve stimulation (VNS) has been explored as a potential therapy for chronic heart failure. The contribution of the afferent pathway to myocardial interstitial acetylcholine (ACh) release during VNS has yet to be clarified. In seven anesthetized Wistar-Kyoto rats, we implanted microdialysis probes in the left ventricular free wall and measured the myocardial interstitial ACh release during right VNS with the following combinations of stimulation frequency (F in Hz) and voltage readout (V in volts): F0V0 (no stimulation), F5V3, F20V3, F5V10, and F20V10. F5V3 did not affect the ACh level. F20V3, F5V10, and F20V10 increased the ACh level to 2.83 ± 0.47 ( P < 0.01), 4.31 ± 1.09 ( P < 0.001), and 4.33 ± 0.82 ( P < 0.001) nM, respectively, compared with F0V0 (1.76 ± 0.22 nM). After right vagal afferent transection (rVAX), F20V3 and F20V10 increased the ACh level to 2.90 ± 0.53 ( P < 0.001) and 3.48 ± 0.63 ( P < 0.001) nM, respectively, compared with F0V0 (1.61 ± 0.19 nM), but F5V10 did not (2.11 ± 0.24 nM). The ratio of the ACh levels after rVAX relative to before was significantly <100% in F5V10 (59.4 ± 8.7%) but not in F20V3 (102.0 ± 8.7%). These results suggest that high-frequency and low-voltage stimulation (F20V3) evoked the ACh release mainly via direct activation of the vagal efferent pathway. By contrast, low-frequency and high-voltage stimulation (F5V10) evoked the ACh release in a manner dependent on the vagal afferent pathway.

β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

2014 ◽  
Vol 112 (11) ◽  
pp. 951-959 ◽  
Author(s):  
Morten Eriksen ◽  
Arnfinn Ilebekk ◽  
Alessandro Cataliotti ◽  
Cathrine Rein Carlson ◽  
Torstein Lyberg ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Sympathetic Nerves ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Β2 Adrenergic Receptor ◽  
Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

Vagal nerve stimulation causes noncholinergic dilatation of gastric arterioles

1986 ◽  
Vol 250 (5) ◽  
pp. G660-G664
Author(s):  
T. Morishita ◽  
P. H. Guth
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
In Vivo Microscopy ◽  
Vasodilator Effect ◽  
Splitting Technique

Vagal nerve stimulation causes prompt dilatation of gastric submucosal arterioles (the vessels that control gastric mucosal blood flow) in rats. In vivo microscopy was used to determine whether this direct vasodilator effect of vagal nerve stimulation on rat gastric submucosal arterioles is mediated by cholinergic fibers. Acetylcholine and atropine were topically applied to the submucosa. The distal end of the severed vagus nerve was electrically stimulated (8 V, 2 ms, 6 Hz, 20 s) subdiaphragmatically. Diameter changes of the submucosal arterioles were videotaped and measured with an image-splitting technique on playback of the videotapes. Acetylcholine, 10(-7) to 10(-5) M, dilated the arterioles dose dependently. Atropine prevented the acetylcholine-induced dilatation, 10(-5) M, nearly completely inhibiting the dilatation. Vagal nerve stimulation dilated the arterioles promptly, and this dilatation was not blocked by 10(-5) M atropine, a dose that blocked the acetylcholine-induced dilatation. These results indicate that vagal nerve stimulation causes atropine-resistant, noncholinergic dilatation of gastric submucosal arterioles in rats.

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.

Immuno-Enzyme Histochemistry of Creatine Phosphokinase

1977 ◽  
Vol 35 ◽  
pp. 446-447
Author(s):  
N. Baba ◽  
E.T. Poe ◽  
J. Scillian ◽  
T. Myser
Keyword(s):  
Creatine Phosphokinase ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Rabbit Muscle ◽  
Cytoplasmic Staining ◽  
Heart Muscle Cells ◽  
Diffuse Cytoplasmic Staining ◽  
Strong Staining

With a commercially available rabbit muscle (MM) type isoenzyme of the creatine phosphokinase (CPK) (Worthington Biochemical), anti-CPK antibody was produced in chicken and goat (Figure 1). Fab' fragments of the chicken and goat IgG were isolated and conjugated with a commercially available horseradish peroxidase (HRP) according to the Nakane method (J. Histochem. Cytochem,, 22:1084, 1974).Rabbit hearts were perfused in vivo with freshly prepared 2% paraformaldehyde solution, and the left ventricular myocardium was fixed for 30 minutes. Forty-micrometer-thick frozen sections of the myocardium were incubated with the Fab'-HRP conjugate overnight at 4°C. After a thorough rinse, the sections were stained for the peroxidase reaction.In an electron microscope, diffuse cytoplasmic staining of the heart muscle cells was noted, indicating the diffuse cytosol distribution of CPK (Figure 2). In addition, there was strong staining of the intermembranous and intracristal space of the mitochondria as well as the M-lines of the myofibrils (Figures 3 and 4).

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