Role of Alpha-adrenoceptor Activity in Regulation of Coronary Blood Flow During Myocardial Ischemia

1991 ◽  
pp. 61-77
Author(s):  
Masatsugu Hori ◽  
Masafumi Kitakaze ◽  
Akira Kitabatake ◽  
Takenobu Kamada ◽  
Michitoshi Inoue
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow ◽  
Alpha Adrenoceptor

scholarly journals Role of nitric oxide in regulation of coronary blood flow during myocardial ischemia in dogs

1996 ◽  
Vol 27 (7) ◽  
pp. 1804-1812 ◽  
Author(s):  
Masafumi Kitakaze ◽  
Koichi Node ◽  
Tetsuo Minamino ◽  
Hiroaki Kosaka ◽  
Yoshiro Shinozaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow

scholarly journals Myocardial Ischemia and Diabetes Mellitus: Role of Oxidative Stress in the Connection between Cardiac Metabolism and Coronary Blood Flow

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Paolo Severino ◽  
Andrea D’Amato ◽  
Lucrezia Netti ◽  
Mariateresa Pucci ◽  
Fabio Infusino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Risk Factors ◽  
Blood Flow ◽  
Ion Channels ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow ◽  
Myocardial Metabolism ◽  
Diabetic Patients

Ischemic heart disease (IHD) has several risk factors, among which diabetes mellitus represents one of the most important. In diabetic patients, the pathophysiology of myocardial ischemia remains unclear yet: some have atherosclerotic plaque which obstructs coronary blood flow, others show myocardial ischemia due to coronary microvascular dysfunction in the absence of plaques in epicardial vessels. In the cross-talk between myocardial metabolism and coronary blood flow (CBF), ion channels have a main role, and, in diabetic patients, they are involved in the pathophysiology of IHD. The exposition to the different cardiovascular risk factors and the ischemic condition determine an imbalance of the redox state, defined as oxidative stress, which shows itself with oxidant accumulation and antioxidant deficiency. In particular, several products of myocardial metabolism, belonging to oxidative stress, may influence ion channel function, altering their capacity to modulate CBF, in response to myocardial metabolism, and predisposing to myocardial ischemia. For this reason, considering the role of oxidative and ion channels in the pathophysiology of myocardial ischemia, it is allowed to consider new therapeutic perspectives in the treatment of IHD.

scholarly journals Computational Analysis of Coronary Blood Flow: The Role of Asynchronous Pacing and Arrhythmias

Mathematics ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 1205
Author(s):  
Timur Gamilov ◽  
Philipp Kopylov ◽  
Maria Serova ◽  
Roman Syunyaev ◽  
Andrey Pikunov ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Long Qt Syndrome ◽  
Premature Ventricular Contraction ◽  
Cardiac Pacing ◽  
Long Qt ◽  
Computational Evaluation ◽  
Qt Syndrome

In this work we present a one-dimensional (1D) mathematical model of the coronary circulation and use it to study the effects of arrhythmias on coronary blood flow (CBF). Hydrodynamical models are rarely used to study arrhythmias’ effects on CBF. Our model accounts for action potential duration, which updates the length of systole depending on the heart rate. It also includes dependency of stroke volume on heart rate, which is based on clinical data. We apply the new methodology to the computational evaluation of CBF during interventricular asynchrony due to cardiac pacing and some types of arrhythmias including tachycardia, bradycardia, long QT syndrome and premature ventricular contraction (bigeminy, trigeminy, quadrigeminy). We find that CBF can be significantly affected by arrhythmias. CBF at rest (60 bpm) is 26% lower in LCA and 22% lower in RCA for long QT syndrome. During bigeminy, trigeminy and quadrigeminy, respectively, CBF decreases by 28%, 19% and 14% with respect to a healthy case.

Role of cardiac mast cells in complement C5a-induced myocardial ischemia

1993 ◽  
Vol 264 (5) ◽  
pp. H1346-H1354 ◽  
Author(s):  
B. R. Ito ◽  
R. L. Engler ◽  
U. del Balzo
Keyword(s):  
Blood Flow ◽  
Mast Cell ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow ◽  
Cell Activation ◽  
Mast Cell Degranulation ◽  
Mast Cell Activation ◽  
Coronary Vein ◽  
Arterial Blood ◽  
Complement C5a

Activated complement component C5a causes myocardial ischemia mediated by thromboxane (Tx) A2 and leukotrienes C4/D4. Blood cells are not involved in either the mediator release or the myocardial effects of C5a, suggesting that a C5a-sensitive, cardiac resident inflammatory cell is responsible. The goals of this study were to determine whether 1) cardiac mast cell activation accompanies the C5a response, 2) inhibition of mast cell degranulation inhibits the response, and 3) histamine release plays a role in the C5a-induced myocardial ischemia. The left anterior descending coronary artery (LAD) of open-chest pigs (n = 13) was perfused with arterial blood at constant pressure (95 mmHg). Coronary blood flow (CBF) was measured (in-line flowmeter) and regional function [percent segment shortening (%SS)] determined with sonomicrometry. A coronary vein was cannulated for measurement of plasma TxB2 and histamine (a marker of mast cell degranulation). Intracoronary C5a (500 ng) decreased coronary blood flow (45% of preinfusion levels) and LAD %SS (65% of preinfusion) and was accompanied by increases in coronary venous TxB2 (delta 63.3 ng/ml) and histamine (delta 200 nM). Mast cell inhibition with lodoxamide (2 mg/kg iv, n = 8) attenuated the C5a-induced fall in CBF (14 vs. 53% decrease, P < 0.01) and %SS (10 vs. 38% decrease, P < 0.01) and also reduced the C5a-induced increase in both coronary venous histamine (delta 26 vs. 278 nM, P < 0.05) and TxB2 (delta 0.34 vs. 63.3 ng/ml, P < 0.01). However, histamine H1 (pyrilamine) and H2 (ranitidine) receptor blockade had no effect on the C5a-induced fall in CBF or LAD %SS.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Blood Flow and Myocardial Ischemia

2007 ◽  
pp. 439-449
Author(s):  
Robert J. Henning ◽  
Ray A. Olsson
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow

Adenosine potentiates insulin-stimulated myocardial glucose uptake in vivo

1988 ◽  
Vol 254 (5) ◽  
pp. H970-H975 ◽  
Author(s):  
W. R. Law ◽  
R. M. Raymond
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Coronary Blood Flow ◽  
Metabolic Regulation ◽  
Metabolic Response ◽  
Dose Response Relationship ◽  
Circumflex Artery ◽  
Myocardial Glucose Uptake

Myocardial adenosine (ADO) has long been regarded as a regulator of coronary blood flow. In other tissues, such as adipose and skeletal muscle, much attention has focused on the role of ADO as a metabolic regulator of the actions of insulin. In the present study, we determined the effect of ADO infusion on insulin-stimulated myocardial glucose uptake (MGU). Mongrel dogs of either sex were instrumented to obtain arterial-coronary sinus differences for glucose, lactate, and oxygen. These were multiplied by circumflex artery blood flow (Q) to obtain uptake values. Measurements were made before and during hyperinsulinemic (4 U/min)-euglycemic clamp (clamp) with intracoronary infusions of saline, ADO, adenosine deaminase (ADA), or nitroprusside (NP). During clamp, MGU increased from a basal value of 3.0 +/- 0.8 mg/min (mean +/- SE) to 5.53 +/- 0.8 mg/min. Adenosine infusion potentiated this response, raising MGU further to 9.02 +/- 1.1 mg/min while not significantly affecting lactate or oxygen uptakes. Infusion of ADA confirmed the specificity of the response by blocking the metabolic effect of exogenously infused ADO. When NP was infused, Q increased significantly without altering MGU, indicating that the metabolic response to ADO was independent of the changes it caused in Q. A dose-response relationship existed between ADO and insulin-stimulated MGU. The metabolic response to ADO was more sensitive than the vasodilator response. It is concluded that ADO acts as a regulator of insulin in heart. This metabolic regulation occurs independent of changes in coronary blood flow.

Behavioral Influences on Coronary Blood Flow and Susceptibility to Arrhythmias

Physiology ◽  
1990 ◽  
Vol 5 (3) ◽  
pp. 108-112
Author(s):  
RL Verrier
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Vagus Nerve ◽  
Eye Movement ◽  
Coronary Blood Flow ◽  
Protective Action ◽  
Tonic Activity ◽  
Electrical Instability ◽  
Behavioral Influences ◽  
Sympathetic Discharge

Both stress and poststress states can induce myocardial ischemia and electrical instability by enhancing sympathetic discharge. Tonic activity of the vagus nerve exerts a protective action. The rapid-eye-movement phase of sleep can also cause coronary vasoconstriction. This observation may help to elucidate mechanisms responsible for nocturnal angina.

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