Myocardium contractility

Nonionic contrast media are intrinsically ion-free but iohexol, iopentol, and iodixanol, for example, contain cations at subplasma concentration levels to avoid negative effects on myocardium contractility, electric conduction, and red blood cell aggregation during coronary arteriography. An oxygenated iohexol solution (350 mg I/mL) containing (in mM/L) Na-" 30, Ca + 0.15, 0.9, and Mg - 0.1,... 

S100A1 is the most abundant in the myocardium but is also expressed in brain and other tissues. S100A1 was found to stimulate Ca2+-induced Ca2+-release (CICR) in skeletal muscle terminal cisternae. In the presence of nanomolar Ca2+-concentrations, S100A1 binds to the ryanodine receptor increasing its channel open probability, and was shown to enhance SR Ca2+-release and contractile performance. Several animal models (over expressing S100A1 or S100A1-deficient mice) have... 

Przyklenk, K. and Kloner, R.A. (1986). Superoxide dismutase plus catalase improve contractile function in the canine model of the stunned myocardium. Circ. Res. 58, 148-156. 

Intravenous or oral doses of a P-blocker should be administered early in the care of a patient with STE ACS, and then oral agents should be continued indefinitely. Early administration of a P-blocker to patients lacking a contraindication within the first 24 hours of hospitalization is a quality care indicator.2,3 In ACS the benefit of P-blockers mainly results from the competitive blockade of P,-adrenergic receptors located on the myocardium. Pi-Blockade produces a reduction in heart rate, myocardial contractility, and blood pressure, decreasing myocardial oxygen demand. As a result of these effects, P-blockers reduce the risk for recurrent ischemia, increase in infarct size and risk of reinfarction, and occurrence of ventricular arrhythmias in the hours and days following MI.39... 

Length of diastole Venous return (preload) Contractility of the myocardium Afterload Heart rate... 

The contractility of the myocardium determines the ejection fraction of the heart, which is the ratio of the volume of blood ejected from the left ventricle per beat (stroke volume) to the volume of blood in the left ventricle at the end of diastole (end-diastolic volume) ... 

Ca++-channel blockers. Verapamil has powerful effects on the heart, decreasing heart rate and myocardial contractility ( l CO) and causing some vasodilation. On the other hand, nifedipine is a more potent vasodilator (1 TPR) with weaker myocardial effects. The effects of diltiazem are somewhat intermediate, in that this drug has moderate inhibitory effects on the myocardium and vascular smooth muscle. 

Two forms of xanthine oxidoreductase namely XO and XDH are present in many human and animal cells and plasma, XDH and XO are the predominant species in cytoplasma and serum, respectively [39]. Damaging effects of XO-catalyzed superoxide production in post-ischemic tissues were demonstrated by many authors. For example, Chambers et al. [40] and Hearse et al. [41] have shown that the suppression of superoxide production by the administration of XO inhibitor allopurinol or SOD resulted in the reduction of infarct size in the dog and of the incidence of reperfusion-induced arrhythmia in the rat. Similarly, Charlat et al. [42] has also shown that allopurinol improved the recovery of the contractile function of reperfused myocardium in the dog. However, the use of allopurinol as the XO inhibitor has been questioned because this compound may affect oxygen radical formation not only as a XO inhibitor but as well as free radical scavenger [43]. Smith et al. [44] also showed that gastric mucosal injury depends on the oxygen radical production catalyzed by XO and iron. 

For example, Ide et al. [43] demonstrated the involvement of oxygen radicals produced by mitochondria in heart failure myocytes from adult mongrel dogs, which could be responsible for contractile dysfunction and structural damage to the myocardium. In a subsequent study... 

The benefits result from blockade of //j receptors in the myocardium, which reduces heart rate, myocardial contractility, and BP, thereby decreasing myocardial oxygen demand. The reduced heart rate increases diastolic time, thus improving ventricular filling and coronary artery perfusion. 

Figure 22.17 Summary of mechanisms to maintain the ATP/ADP concentration ratio in hypoxic myocardium. A decrease in the ATP/ADP concentration ratio increases the concentrations of AMP and phosphate, which stimulate conversion of glycogen/ glucose to lactic acid and hence ATP generation from glycolysis. The changes also increase the activity of AMP deaminase, which increases the formation and hence the concentration of adenosine. The latter has two major effects, (i) It relaxes smooth muscle in the arterioles, which results in vasodilation that provides more oxygen for aerobic ATP generation (oxidative phosphorylation). (ii) It results in decreased work by the heart (i.e. decrease in contractile activity), (mechanisms given in the text) which decreases ATP utilisation.

Amlodipine is a calcium-channel blocker that blocks the intracellular movement of calcium ions and hence slows the contractility of the myocardium and relaxes the vascular smooth muscle. The negative inotropic effects are rarely seen at therapeutic doses since amlodipine has a greater selectivity for vascular smooth muscle than for the myocardium. 

Several studies have indicated that n-butane sensitizes the myocardium to epinephrine-induced cardiac arrhythmias. In anesthetized dogs, 5000 ppm caused hemodynamic changes such as decreases in cardiac output, left ventricular pressure, and stroke volume, myocardial contractility, and aortic pressure. Exposure of dogs to 1-20% butane for periods of 2 minutes to 2 hours hypersen-... 

Propranolol is a prototype of this series of drugs and is the oldest and most widely used nonselective )3-adrenoblocker. It possesses antianginal, hypotensive, and antiarrhythmic action. Propranolol is a cardiac depressant that acts on the mechanic and electrophysio-logical properties of the myocardium. It can block atrioventricular conductivity and potential automatism of sinus nodes as well as adrenergic stimulation caused by catecholamines nevertheless, it lowers myocardial contractility, heart rate, blood pressure, and the myocardial requirement of oxygen. 

Verapamil possesses antiarrhythmic, antianginal, and hypotensive activity. It reduces the myocardial need for oxygen by reducing contractility of the myocardium and slowing the frequency of cardiac contractions. It causes dilation of coronary arteries and increased coronary blood flow. It reduces tonicity of smooth musculature, peripheral arteries, and overall peripheral vascular resistance. It provides antiarrhythmic action in supraventricular arrhythmia. 

Residual trapping of metabolic analogues by hibernating myocardium, such as FDG [46-48], "Carbon ("Q acetate [49-52], and "C palmitate [53-55] reflects sufficient integrity of myocytes and their metabolism to allow recovery of myocardial contractile function after revascularization. 

For patients with chronic CAD, nuclear imaging is essential for addressing the following major clinical issues (i) detection of ischemic myocardium, (ii) differentiation between viable hibernating or stunned myocardium and scar tissue in mechanically dysfunctional regions, and (ill) risk stratification for future major adverse events. Such information provides the basis for percutaneous coronary intervention (PCI) or coronary artery bypass (CAB) surgery and assessing their outcomes based on detection of residual ischemia and recovery of contractile function. 

Much of the research on myocardial viability has focused on measuring pathological changes, cellular metabolism, or myocardial contractility without defining how much of the myocardium is involved, its relation to LV systolic function, and clinical outcomes. PET currently provides the best answer to the following questions (a) How much myocardium is scarred or viable as a percent of the zone at risk distal to a stenosis and as a percent of the whole heart (b) What amount of viable tissue justifies revascularization ... 

The effects of phenytoin on the cardiovascular system vary with the dose, the mode and rate of administration, and any cardiovascular pathology. Rapid administration can produce transient hypotension that is the combined result of peripheral vasodilation and depression of myocardial contractility. These effects are due to direct actions of phenytoin on the vascular bed and ventricular myocardium. If large doses are given slowly, dose-related decreases in left ventricular force, rate of force development, and cardiac output can be observed, along with an increase in left ventricular end-diastolic pressure. 

Enflurane (Ethrane) depresses myocardial contractility and lowers systemic vascular resistance. In contrast to halothane, it does not block sympathetic reflexes, and therefore, its administration results in tachycardia. However, the increased heart rate is not sufficient to oppose enflurane s other cardiovascular actions, so cardiac output and blood pressure fall. In addition, enflurane sensitizes the myocardium to catecholamine-induced arrhythmias, although to a lesser extent than with halothane. Enflurane depresses respiration through mechanisms similar to halothane s and requires that the patient s ventilation be assisted. 

Because of the extensive presence of )Si-ARs in the non-failing myocardium, the heart can be defined as a jSi-AR organ. The )Si// 2-AR ratio within the ventricles of the healthy human heart is 80/20 and the average jS-AR density (Bmax) in atria and ventricles is normally 70-100 fmol/mg protein [89], In the heart, Pt-AR agonists are responsible for the increase in cardiac contractility and heart rate, whereas bronchodilation and vasodepression can be mediated by / 2-selective agonists. 

Calcium channel blockers depress the contractility of the myocardium and decrease the cardiac work and the requirement of oxygen. This effect proves to be beneficial in the treatment of angina pectoris. 

Isoflurane has a dose-dependent depressant effect on the myocardium. In vitro studies indicate that it reduces myocardial contractility to a similar extent as halothane. In vivo, isoflurane appears to be less of a cardiovascular depressant than other volatile agents. 

The net result of the action of therapeutic concentrations of a cardiac glycoside is a distinctive increase in cardiac contractility (Figure 13-5, bottom trace). In isolated myocardial preparations, the rate of development of tension and of relaxation are both increased, with little or no change in time to peak tension. This effect occurs in both normal and failing myocardium, but in the intact patient the responses are modified by cardiovascular reflexes and the pathophysiology of heart failure. 

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