In vivo detection of endogenous acetylcholine release in cat ventricles

Akiyama, Tsuyoshi; Yamazaki, Toji; Ninomiya, Ishio

doi:10.1152/ajpheart.1994.266.3.h854

Cited by 36 publications

(52 citation statements)

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“…A cardiac microdialysis is a powerful tool to estimate neurotransmitter levels in the myocardial interstitium in vivo (2,3,14,19,20,31). The present study demonstrated that hypothermia significantly attenuated the myocardial interstitial releases of NE and ACh in the ischemic region during the LAD occlusion.…”

Section: Discussionsupporting

confidence: 55%

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Hypothermia reduces ischemia- and stimulation-induced myocardial interstitial norepinephrine and acetylcholine releases

Kawada

Kitagawa

Yamazaki

et al. 2007

Journal of Applied Physiology

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though hypothermia is one of the most powerful modulators that can reduce ischemic injury, the effects of hypothermia on the function of the cardiac autonomic nerves in vivo are not well understood. We examined the effects of hypothermia on the myocardial interstitial norepinephrine (NE) and ACh releases in response to acute myocardial ischemia and to efferent sympathetic or vagal nerve stimulation in anesthetized cats. We induced acute myocardial ischemia by coronary artery occlusion. Compared with normothermia (n ϭ 8), hypothermia at 33°C (n ϭ 6) suppressed the ischemia-induced NE release [63 nM (SD 39) vs. 18 nM (SD 25), P Ͻ 0.01] and ACh release [11.6 nM (SD 7.6) vs. 2.4 nM (SD 1.3), P Ͻ 0.01] in the ischemic region. Under hypothermia, the coronary occlusion increased the ACh level from 0.67 nM (SD 0.44) to 6.0 nM (SD 6.0) (P Ͻ 0.05) and decreased the NE level from 0.63 nM (SD 0.19) to 0.40 nM (SD 0.25) (P Ͻ 0.05) in the nonischemic region. Hypothermia attenuated the nerve stimulation-induced NE release from 1.05 nM (SD 0.85) to 0.73 nM (SD 0.73) (P Ͻ 0.05, n ϭ 6) and ACh release from 10.2 nM (SD 5.1) to 7.1 nM (SD 3.4) (P Ͻ 0.05, n ϭ 5). In conclusion, hypothermia attenuated the ischemia-induced NE and ACh releases in the ischemic region. Moreover, hypothermia also attenuated the nerve stimulationinduced NE and ACh releases. The Bezold-Jarisch reflex evoked by the left anterior descending coronary artery occlusion, however, did not appear to be affected under hypothermia. vagal nerve; sympathetic nerve; cardiac microdialysis; cats HYPOTHERMIA IS ONE OF THE most powerful modulators that can reduce ischemic injury in the central nervous system, heart, and other organs. The general consensus is that hypothermia induces a hypometabolic state in tissues and balances energy supply and demand (25). With respect to the myocardial ischemia, the size of a myocardial infarction correlates with temperature (6), and mild hypothermia can protect the myocardium against acute ischemic injury (9). The effects of hypothermia on the function of the cardiac autonomic nerves in terms of neurotransmitter releases, however, are not fully understood. Because autonomic neurotransmitters such as norepinephrine (NE) and ACh directly impinge on the myocardium, they would be implicated in the cardioprotection by hypothermia.In previous studies from our laboratory, Kitagawa et al. (16) demonstrated that hypothermia attenuated the nonexocytotic NE release induced pharmacologically by ouabain, tyramine, or cyanide. Kitagawa et al. (15) also demonstrated that hypothermia attenuated the exocytotic NE release in response to vena cava occlusion or to local administration of high K ϩ . The effects of hypothermia on the ischemia-induced myocardial interstitial NE release, however, were not examined in those studies. In addition, the effects of hypothermia on the ischemia-induced myocardial interstitial ACh release have never been examined. Because both sympathetic and parasympathetic nerves control the heart, simultaneous monitoring of the m...

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Section: Discussionsupporting

confidence: 55%

“…The materials and properties of the dialysis probe have been described previously (2,3). Briefly, we designed a transverse dialysis probe.…”

Section: Dialysis Techniquementioning

confidence: 99%

Hypothermia reduces ischemia- and stimulation-induced myocardial interstitial norepinephrine and acetylcholine releases

Kawada

Kitagawa

Yamazaki

et al. 2007

Journal of Applied Physiology

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“…Accordingly, whether ANG II affects the vagal control over the ventricle remains unknown. The aim of the present study was to examine the effect of ANG II on the vagal stimulation-induced ACh release in the left ventricular myocardium by measuring the interstitial ACh levels directly using a cardiac microdialysis technique (1,(13)(14)(15). We also explored the possible sites of action for the effect of ANG II on the stimulation-induced ACh release by administering losartan systemically from the femoral vein or locally through the dialysis fiber.…”

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confidence: 99%

Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation

Kawada¹,

Yamazaki²,

Akiyama³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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exerts a variety of effects on the cardiovascular system, its effects on the peripheral parasympathetic neurotransmission have only been evaluated by changes in heart rate (an effect on the sinus node). To elucidate the effect of ANG II on the parasympathetic neurotransmission in the left ventricle, we measured myocardial interstitial ACh release in response to vagal stimulation (1 ms, 10 V, 20 Hz) using cardiac microdialysis in anesthetized cats. In a control group (n ϭ 6), vagal stimulation increased the ACh level from 0.85 Ϯ 0.03 to 10.7 Ϯ 1.0 (SE) nM. Intravenous administration of ANG II at 10 g ⅐ kg Ϫ1 ⅐ h Ϫ1 suppressed the stimulation-induced ACh release to 7.5 Ϯ 0.6 nM (P Ͻ 0.01). In a group with pretreatment of intravenous ANG II receptor subtype 1 (AT1 receptor) blocker losartan (10 mg/kg, n ϭ 6), ANG II was unable to inhibit the stimulation-induced ACh release (8.6 Ϯ 1.5 vs. 8.4 Ϯ 1.7 nM). In contrast, in a group with local administration of losartan (10 mM, n ϭ 6) through the dialysis probe, ANG II inhibited the stimulation-induced ACh release (8.0 Ϯ 0.8 vs. 5.8 Ϯ 1.0 nM, P Ͻ 0.05). In conclusion, intravenous ANG II significantly inhibited the parasympathetic neurotransmission through AT1 receptors. The failure of local losartan administration to nullify the inhibitory effect of ANG II on the stimulation-induced ACh release indicates that the site of this inhibitory action is likely at parasympathetic ganglia rather than at postganglionic vagal nerve terminals. cardiac microdialysis; cats; losartan ANG II HAS a variety of effects on the cardiovascular system (22): it acts on the vascular beds to increase peripheral vascular resistance and also on the adrenal cortex to cause volume retention. These direct effects of ANG II contribute to the maintenance of arterial pressure (AP). Aside from these direct effects, ANG II has been shown to modulate the sympathetic nervous system both centrally (7, 9) and peripherally (10). With respect to the sympathetic regulation in the heart, however, exogenous ANG II does not facilitate stimulation-and ischemia-induced norepinephrine release in the porcine left ventricle (18). Compared with a number of reports on the sympathetic system, only a few reports are available as to the effects of ANG II on the parasympathetic system. In 1982, Potter (23) demonstrated that ANG II (5-10 g iv, body wt not reported) inhibited bradycardia induced by vagal stimulation in dogs. In that study, administration of ACh reduced the heart rate to an identical degree in the presence or absence of ANG II, suggesting that the inhibition of bradycardia by ANG II was attributable to the inhibition of the ACh release from the vagal nerve terminals. In contrast, Andrews et al. (3) reported that ANG II (500 ng/kg iv) did not inhibit bradycardia induced by vagal stimulation in ferrets. In a rat heart failure model, ANG II receptor subtype 1 (AT 1 receptor) antagonist losartan enhanced the bradycardic response to vagal stimulation (5). In pithed rats, an angiotensin-converting enzyme (ACE) inhibitor...

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“…We measured the concentration of ACh in the dialysate sample as an index of myocardial interstitial ACh level (10)(11)(12)(13). Materials and properties of the dialysis probe have been reported previously (2). Briefly, we designed a transverse dialysis probe.…”

Section: Methodsmentioning

confidence: 99%

“…We have measured myocardial interstitial acetylcholine (ACh) levels by using a cardiac microdialysis technique in anesthetized cats (2,(10)(11)(12)(13). The ACh levels measured by the cardiac microdialysis were able to detect changes in the ACh kinetics in the vagal nerve terminals induced by pharmacological interventions, arterial baroreflex, or Bezold-Jarisch reflex (13).…”

mentioning

confidence: 99%

Disruption of vagal efferent axon and nerve terminal function in the postischemic myocardium

Kawada¹,

Yamazaki

Akiyama

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Despite the importance of vagal control over the ventricle, little is known regarding vagal efferent conduction and nerve terminal function in the postischemic myocardium. To elucidate postischemic changes in the cardiac vagal efferent neuronal function, we measured myocardial interstitial acetylcholine (ACh) levels by using in vivo cardiac microdialysis and examined the ACh responses to electrical stimulation of the vagi or local administration of ouabain in anesthetized cats. Sixty-minute occlusions of the left anterior descending coronary artery (LAD) followed by 60-min reperfusion abolished electrical stimulation-induced ACh release (20.4 Ϯ 3.9 vs. 0.9 Ϯ 0.4 nmol/l; means Ϯ SE, P Ͻ 0.01). In different groups of animals, 60-min LAD occlusion followed by 60-min reperfusion decreased but did not completely abolish ouabain-induced release of ACh (9.2 Ϯ 1.8 vs. 3.9 Ϯ 0.7 nmol/l; P Ͻ 0.05). These results indicate that function of the vagal efferent axon was completely interrupted, whereas the local ACh release was partially suppressed in the postischemic myocardium. The postischemic disruption of vagal efferent neuronal function might exert deleterious effects on cardiac regulation. cardiac microdialysis; vagal stimulation; ouabain; cats; acetylcholine AUTONOMIC DERANGEMENT ASSOCIATED with acute myocardial ischemia or infarction has deleterious effects on the heart (3, 6). The autonomic derangement occurs during postischemic as well as ischemic periods. Elucidating the underlying mechanisms of autonomic disturbance during the postischemic period is important to understand the pathophysiology of postischemic events such as those occurring after thrombolytic therapies. In the sympathetic nervous system, nerve terminal function as assessed by tyramine-induced norepinephrine release recovers 60-120 min after reperfusion of the coronary artery (1, 14). On the other hand, the myocardial response to electrical stimulation of sympathetic efferent neurons remains impaired up to 2 h after reperfusion, despite a preserved myocardial response to exogenous norepinephrine (5). Therefore, injury to sympathetic efferent axons (4, 8) is considered to be responsible for sympathetic denervation in the postischemic myocardium. However, conduction of the postganglionic axons in response to electrical stimulation of the epicardial sites was unaffected by regional ventricular ischemia (9), suggesting that the intrinsic cardiac fibers in the epicardial region were resistant to myocardial ischemia. We speculate that changes in the environment surrounding the postganglionic axons traveling through the midcardium affected the axonal conduction (15) even if the axon itself was not injured.In contrast to the sympathetic efferent nervous system, little is known regarding vagal efferent neuronal function in the postischemic myocardium in vivo. We have measured myocardial interstitial acetylcholine (ACh) levels by using a cardiac microdialysis technique in anesthetized cats (2, 10-13). The ACh levels measured by the cardiac microdialysis were ab...

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In vivo detection of endogenous acetylcholine release in cat ventricles

Cited by 36 publications

References 0 publications

Hypothermia reduces ischemia- and stimulation-induced myocardial interstitial norepinephrine and acetylcholine releases

Hypothermia reduces ischemia- and stimulation-induced myocardial interstitial norepinephrine and acetylcholine releases

Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation

Disruption of vagal efferent axon and nerve terminal function in the postischemic myocardium

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