OBJECTIVETo investigate the general pattern of cholinergic nerve distribution and M(2) receptors in adult rat heart.

METHODSKarnovsky-Roots histochemical staining combining point counting method and immunochemical SABC method with image analysis were used to identify the cholinergic nerves and M(2) receptors, respectively, in adult rat heart.

RESULTSPositive staining of cholinergic nerves and M(2) receptors was found in all regions of the rat heart, and the point count of cholinergic nerves in the atria was 4.6 times as much as that in ventricles, and the area of immunoreactive substance for M(2) receptors two-fold higher in the atria than in the ventricles. The point counts of the cholinergic nerves in the medial-layer myocardium were fewer than that in subepicardial and endocardial tissues of the left ventricular free wall. However, M(2) receptors were comparable among the 3 layers of the left free ventricular wall.

CONCLUSIONCholinergic nerves and M(2) receptors are located in both rat atria and ventricles, but their density is much higher in the atria than in the ventricles. Transmural heterogeneity characterizes cholinergic nerve innervation in the left ventricular free wall without significant differences in M(2) receptor density.

Animals ; Cholinergic Fibers ; metabolism ; Female ; Heart ; innervation ; Heart Atria ; innervation ; metabolism ; Heart Ventricles ; innervation ; metabolism ; Immunohistochemistry ; Male ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Muscarinic M2 ; analysis

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization (TDR) under acute myocardial ischemia in intact canine was investigated. Using the monophasic action potential (MAP) recording technique, MAPs of the epicardium (Epi), mid-myocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall under acute myocardial ischemia in 12 open-chest dogs. MAPD90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization (EAD) before autonomic nervous stimulation and during autonomic nervous stimulation were compared. It was found that 10 min after acute myocardial ischemia, TDR was increased from 55 +/- 8 ms to 86 +/- 15 ms during sympathetic stimulation (P < 0.01). The TDR (53 +/- 9 ms) during parasympathetic stimulation was not significantly different from that of the control (55 +/- 8 ms) (P > 0.05). The EAD was elicited in the Mid of 2 dogs (16%) 10 min after acute myocardial ischemia, but the EAD were elicited in the Mid of 7 dogs (58%) during sympathetic stimulation (P < 0.01). It was concluded that: (1) Sympathetic stimulation can increase the transmural dispersion of repolarization and induce early afterdepolarizations in the Mid under acute myocardial ischemia, which provide the opportunity for the ventricular arrhythmia developing; (2) Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.
Action Potentials/physiology ; Autonomic Nervous System/*physiopathology ; Electric Stimulation ; Heart Ventricles/innervation ; Heart Ventricles/*physiology ; Myocardial Ischemia/*physiopathology ; Neuromuscular Junction

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.
Action Potentials ; physiology ; Animals ; Autonomic Nervous System ; physiology ; Dogs ; Electric Stimulation ; Electrocardiography ; Electrodes ; Endocardium ; innervation ; physiology ; Heart Ventricles ; innervation ; Myocardium ; cytology ; Neuromuscular Junction ; Pericardium ; innervation ; physiology ; Ventricular Function

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.
Action Potentials/physiology ; Autonomic Nervous System/*physiology ; Electric Stimulation ; Electrocardiography ; Electrodes ; Endocardium/innervation ; Endocardium/physiology ; Heart Ventricles/innervation ; Heart Ventricles/*physiology ; Myocardium/cytology ; Neuromuscular Junction ; Pericardium/innervation ; Pericardium/physiology

Autonomic nervous system plays an important role in the regulation of mammalian heart, and it is divided into the sympathetic and parasympathetic (vagal) subsystems. The parasympathetic (vagal) control of the atria involves modulation of chronotropic, dromotropic and inotropic activities, but the role of the parasympathetic innervation of the ventricles is still unclear. There is a common misconception that the sympathetic nerves innervate all over the heart; while the parasympathetic nerves only innervate the superventricular part of the heart, but not the ventricles. Recent evidence indicates that the cholinergic innervation of the left ventricle is functionally very important in some mammalian species. The present article reviews the evidence of vagal control in the ventricles from the anatomy and histochemistry, molecular biology, and function areas. Additionally we overview the vagal (muscarinic) regulation of cardiac contractile function and its signal transduction.
Animals ; Heart Ventricles ; anatomy & histology ; innervation ; metabolism ; Humans ; Myocardial Contraction ; physiology ; Receptors, Muscarinic ; metabolism ; Signal Transduction ; physiology ; Vagus Nerve ; physiology

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization (TDR) under acute myocardial ischemia in intact canine was investigated. Using the monophasic action potential (MAP) recording technique, MAPs of the epicardium (Epi), mid-myocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall under acute myocardial ischemia in 12 open-chest dogs. MAPD90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization (EAD) before autonomic nervous stimulation and during autonomic nervous stimulation were compared. It was found that 10 min after acute myocardial ischemia, TDR was increased from 55 +/- 8 ms to 86 +/- 15 ms during sympathetic stimulation (P < 0.01). The TDR (53 +/- 9 ms) during parasympathetic stimulation was not significantly different from that of the control (55 +/- 8 ms) (P > 0.05). The EAD was elicited in the Mid of 2 dogs (16%) 10 min after acute myocardial ischemia, but the EAD were elicited in the Mid of 7 dogs (58%) during sympathetic stimulation (P < 0.01). It was concluded that: (1) Sympathetic stimulation can increase the transmural dispersion of repolarization and induce early afterdepolarizations in the Mid under acute myocardial ischemia, which provide the opportunity for the ventricular arrhythmia developing; (2) Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.
Action Potentials ; physiology ; Animals ; Autonomic Nervous System ; physiopathology ; Dogs ; Electric Stimulation ; Female ; Heart Ventricles ; innervation ; Male ; Myocardial Ischemia ; physiopathology ; Neuromuscular Junction ; Ventricular Function

AIMTo study the importance of blood pressure variability in organ protection for long-term treatment with fosinopril in-sinoaortic-denervated (SAD) rats.

METHODSFosinopril (15 mg.kg-1.d-1) was given in rat chow for 16 weeks after SAD surgery. Blood pressure variability (BPV) was recorded during 24 h in conscious state. Histopathological changes were evaluated with light microscope and computer-assisted image analysis.

RESULTSLong-term treatment with fosinopril significantly decreased BPV in SAD rats. The thickness of the left ventricular wall, collagen fraction of the left ventricle and glomerulosclerosis score were all positively related to BPV in untreated and fosinopril-treated SAD rats. Fosinopril markedly prevented the damages of target organs in SAD rats.

CONCLUSIONLong-term treatment with fosinopril showed obvious organ protection in SAD rats. The decrease in BPV may significantly contribute to organ protection.

Animals ; Antihypertensive Agents ; administration & dosage ; pharmacology ; Blood Pressure ; drug effects ; Denervation ; methods ; Fosinopril ; administration & dosage ; pharmacology ; Heart Ventricles ; pathology ; Kidney ; pathology ; Male ; Myocardium ; pathology ; Protective Agents ; pharmacology ; Rats ; Sinoatrial Node ; innervation ; Time Factors