Investigation on the Effect of Extracellular Calcium Concentration on Cardiac Function in the Langendorff Perfused Rat Heart

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

B. Part B. PowerPhys Experiment 4 – Effect of Exercise on Cardiac Output (13 points total)

Calculate the stroke volume of Suzie’s heart, and compare it to that of a normal individual. Her low calcium intake causes weaker heart contractions and that makes her stroke volume way lower than it should be.

To test these hypotheses I am using wild type mouse embryonic fibroblast (WT MEFs) to test changes in calcium uptake with and without KN93.To test the first hypothesis I am using calcium retention capacity assay to assess the uptake of calcium on three subgroups WT only, WT and DMSO, WT and KN93. This assay is used because it effectively compares calcium uptake between the subgroups. Considering that KN93 inhibits CaMKII I expect the WT+KN93 group to take up lower amounts of calcium and thus not reach calcium retention capacity. To test the second hypothesis, I am conducting MTT and propidium iodide testing on four different subgroups (WT, WT and H202, WT+H202+KN93, and WT+H202+DMSO) to compare the levels of cell viability and death respectively. I used MTT testing to assess cell viability post-exposure of H202 and I am also using propidium iodide staining to test for the measurements of cell death among the different groups. I decided to use propidium iodide staining to better test the cardioprotection of MEFs in ischemic like conditions that would better account for the confounding variable, cell-growth during the incubation

| An increase in heart rate will produce the following changes in each of the five other parameters:

Moreover, to learn this new analysis in the Prof. Hughson laboratory will allow that in the future we use this method together with other measurements (arterial blood pressure, heart rate and peripheral muscle deoxygenation) that will improve the evaluation of the central and peripheral cardiovascular interactions in health and

Results from the experiment can be found below in table 2. As apparent in the table, with an increase in the intensity of the exercise, the heart rate and blood pressure both increased. An important observation from the data is that the systolic blood pressure steadily increased as we increased the intensity. However, the diastolic blood pressure remained relatively constant as the intensity of the exercise increased. The heart rate steadily increased with the increase of intensity as well.

A fine line exists between the harmless enlargement of athlete’s heart and the harmful consequences of HCM. Found in 1/500 individuals, HCM causes a “thickened septum which separates the left and right ventricles” (“Causes of Sudden Cardiac Death”). The myofibrils, the “contractile elements of the heart,” lose their proper orientation and become disorganized, causing the heart to beat ineffectively and leading to the thickening of the walls and structural issues. The thickness can limit flow to the heart and lead to arrhythmias and sudden cardiac death (“Causes of Sudden Cardiac Death”). In both HCM and athlete’s heart the left ventricle thickens; however the wall hypertrophy in HCM may extend to more than 20mm, compared to less than 16mm in athlete’s heart (Maron, Pelliccia, and Spirito). Careful analysis of echocardiographic and clinical features almost always “permits this diagnostic differentiation” (Maron, Pelliccia, and Spirito). As mentioned before, left ventricular end-diastolic cavity dimensions greater than 55mm are not uncommon in trained athletes, yet the diastolic cavity dimension remains small (55mm, making it possible to distinguish athlete’s heart from HCM based on cavity measurement and borderline wall thickness (Maron, Pelliccia, and Spirito). However, ECGs, due to their wide variance, cannot provide sufficient evidence to distinguish between the two heart conditions (Maron, Pelliccia, and Spirito). Although there are numerous methods to distinguish and diagnose HCM, it remains the leading cause of sudden cardiac death (SCD) among

The two main parts to the cycle are systole and diastole. Systole is the contraction phase of the cycle, pumping the blood, and diastole is the relaxation phase of the cycle, blood filling the chambers (Reece 921). While the blood pumps out of the heart, the arteriole blood pressure is raised; however, during the relaxation phase, the aortic valve closes thus dropping the arteriole blood pressure (Harris-Haller 243). Because of this inconsistency in blood pressure during the cardiac cycle, the mean arterial pressure compensates for these fluctuations by calculating mean values (Harris-Haller 244). An electrocardiogram is a graph that represents “the electrical activity of the heart [and] plots sequential events of excitation and recovery of a heartbeat,” and it is summarized by four main parts to the heart wave (Harris-Haller 240). The P wave shows the depolarization of the wave over the atria, the QRS complex shows the ventricle depolarization process, and the T wave shows the repolarization of the ventricles (Harris-Haller 241). Exercise can also have an impact on the blood pressure and pulse by increasing both (Moeini 431). In addition, the respiratory rate when one is exercising can often increase as well in

Myocardial cells sustain their electrical gradient among their membrane, with the inside being slightly more negative. The resting potential is regulated by channels and pumps distributed inside and outside of the cell. As the cell depolarizes, the gate of the calcium channel opens, allowing calcium to enter the cell. The calcium flowing into the cell simultaneously results in initiating the action potential. With depolarization, the potassium channels then open, while the calcium channels close. Repolarization occurs when potassium leaves the cells, and then the whole cycle begins

Medications classified as dihydropyridines are procardia, norvasc, plendil, and cardene. These medications do not affect the cardiac conduction system. Dihydropyridines block calcium from moving into the cell membranes of the cardiac and smooth muscle. The cell tissue affected by these antihypertensive drugs is the cardiac muscle, SA & AV node, coronary arteries and arterioles, and the peripheral arterioles. Calcium channel blockers contract the heart by stopping calcium ions from going through the cell membrane during the plateau phase. This leads to failure of the calcium ions to release large amounts of calcium into the sarcoplasmic reticulum inside the cell. The calcium is needed to stimulate contractions by allowing the cross-bridge to form between the actin and myosin of

Person X’s heart and ventilation rate was normal before the test because they had not begun exercising and were at a resting rate. The reason their heart and ventilation

The presence of calcium in coronary arteries is known to be a strong indicator for coronary artery disease (CAD),It has been shown that quantification of coronary calcium enables the assessment of cardiac event risk stratification Dijkstra et

Anova 1, with values of each section of time after injection of Ringer's solution, shows a p-value of 0.9513. Thus, we are sure at more than 95% that values aren't significantly differents between the three groups. So Ringer's solution have no effect on heart rate or amplitude. Ringer it's our normal conditions control, it doesn't affect heart rate or amplitude (=force of heart contraction).

While contraction in skeletal muscle is triggered by motor neurons under central control, certain cardiac muscle variants exhibit autorhythmicity. This means that that they are capable of producing their own depolarizing electrical potential. The cardiomyocytes that are capable of producing their own electrical potentials are found in what is referred to as the electrical condition system of the heart. This system is comprised of specializes cardiomyocytes that are autorhythmic and are able to conduct electrical potentials rapidly. These specialized structures include the sinoatrial node, atrioventricular node and bundle, and Purkinje fibers.