Myocardial contractility, changes

Cardiovascular manifestations result in ECG changes characterized by a prolonged QT interval and symptoms of decreased myocardial contractility often associated with heart failure. 

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-... 

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 ... 

Dobutamine is widely used to increase myocardial contractility, cardiac output, and stroke volume in the peri-operative period. It is less likely to increase heart rate than dopamine. There is evidence that dobutamine can increase both myocardial contractility and coronary blood flow. This makes it particularly suitable for use in patients with acute myocardial infarction. Dobutamine is also suitable for treating septic shock associated with increased filling pressures and impaired ventricular function. Owing to the competing a and 3 activity there is usually little change in mean arterial pressure. 

When injected intravenously, kinins produce a rapid fall in blood pressure that is due to their arteriolar vasodilator action. The hypotensive response to bradykinin is of very brief duration. Intravenous infusions of the peptide fail to produce a sustained decrease in blood pressure prolonged hypotension can only be produced by progressively increasing the rate of infusion. The rapid reversibility of the hypotensive response to kinins is due primarily to reflex increases in heart rate, myocardial contractility, and cardiac output. In some species, bradykinin produces a biphasic change in blood pressure—an initial hypotensive response followed by an increase above the preinjection level. The increase in blood pressure may be due to a reflex activation of the sympathetic nervous system, but under some conditions, bradykinin can directly release catecholamines from the adrenal medulla and stimulate sympathetic ganglia. Bradykinin also increases blood pressure when injected into the central nervous system, but the physiologic significance of this effect is not clear, since it is unlikely that kinins cross the blood-brain barrier. 

Significant depression of myocardial contractility has been observed in individuals who acutely consume moderate amounts of alcohol, ie, at a blood concentration above 100 mg/dL. Myocardial biopsies in humans before and after infusion of small amounts of alcohol have shown ultrastructural changes that may be associated with impaired myocardial function. Acetaldehyde is implicated as a cause of cardiac dysfunction by altering myocardial stores of catecholamines. 

Blood pressure was reduced in dogs acutely exposed to high concentrations of 1,1,1-trichloroethane (>7,500 ppm) (Herd et al. 1974 Krantz et al. 1959). This effect was studied in detail by Herd et al. (1974), who reported that the decrease in blood pressure began within 15 seconds of the start of exposure and grew more pronounced as exposure continued. At 8,000-15,000 ppm, the decrease in blood pressure was accompanied by increased myocardial contractility and cardiac output. A decrease in total peripheral resistance was apparently responsible for the decrease in blood pressure at these concentrations. At 20,000-25,000 ppm, blood pressure depression was caused by reductions in myocardial contractility and cardiac output. Blood pressure returned to pre-exposure values within 15 minutes after exposure, but indices of cardiac output and contractility required 45 minutes to recover. The dogs died if the blood pressure dropped too low. Histopathological changes in the heart were not found upon necropsy. 

Answer B. Calcium channel antagonists decrease myocardial contractility by blocking the influx of Ca2+ ions through voltage-dependent L-type channels in the cardiac cell membrane. CCBs have no effects on Na+ channels, they do not change intracellular K+ levels, and they decrease not increase) conduction velocity. 

Given i.v. to anesthetized dogs, BAY K 8644 (41) caused increases in myocardial contractility, blood pressure, and peripheral vascular resistance. These changes were reversed by nifedipine but not by a- or 3-adrenoceptor blockade. BAY K 8644 Increased cardiac rate and contractility and also caused coronary vasoconstriction in an isolated cardiac preparation. This compound may be useful as a tool to ascertain the function of CEB in tissues. 

In the Soviet Union orotic acid has been studied for a long time in relation to arteriosclerosis, myocardial infarction [449-450] and various cardiopathogenic changes [451-455]. The effect of precursors of nucleic acid synthesis on myocardial contractile function was followed by Zharov and others [456,457]. However, the effect of orotic acid on the development of myocardial hypertrophy was also studied in other countries [458-463]. 

The development of practical methods for the assessment of myocardial contractility continues and while the ESP-ESV concept provides one approach for quantitating changes in the contractile state, it requires further modification in order that it may be employed for patient to patient comparison. The preliminary studies described here on the basis of the developed stress concept shows some promise, however, further studies are required to examine the relationships between peak systolic pressure and end diastolic volume in order to explore an alternative definition for developed stress. 

During an action potential, increased cytoplasmic calcium combines with troponin, the modulating myocardial protein. Troponin undergoes a conformational change that allows the myocardial contractile proteins, actin and myosin, to form a cross-brirlge. 

Dizziness. 4 Hallucinations. 4 Nervousness. Tachycardia. Tachypnea. Seizures. Lidocaine doesn t affect blood pressure, cardiac output or myocardial contractility. Lidocaine is ineffective against atrial arrhythmias. -0 Contraindicated in second- or third-degree AV block without pacing support Reduce drug dosage as ordered in patients with heart failure or liver disease. 0 Monitor patient closely for CNS changes. 

Figure 4.4 Effect of a free-radical scavenger M-(2-mercaptoproplonyl)-glycine (MPG) on the recovery of contractile function following 15 min of regional ischaemia in the dog heart, (a) MPG infused 1 min before reperfusion, (b) MPG infused 1 min after reperfusion. Contractile function was assessed as changes in ventricular wall thickening measured using an ultrasonic pulsed-Doppler epicardial probe. Note The free radical scavenger MPG can reduce myocardial stunning only when present during the first minute of reperfusion. Redrawn with permission from Bolli et af. (1989).

Changes in heart rate also affect the contractility of the heart. As heart rate increases, so does ventricular contractility. The mechanism of this effect involves the gradual increase of intracellular calcium. When the electrical impulse stimulates the myocardial cell, permeability to calcium is increased and calcium enters the cell, allowing it to contract. Between beats, the calcium is removed from the intracellular fluid and the muscle relaxes. When heart rate is increased, periods of calcium influx occur more frequently and time for calcium removal is reduced. The net effect is an increase in intracellular calcium, an increased number of crossbridges cycling, and an increase in tension development. 

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