EFFECTS OF STRETCHING-MEDIATED TENSION ON VENTRICULAR CONTRACTION OF TOAD HEART
INTRODUCTION
Heart contraction is produced by stretching of sarcomere units, which produces strokes between myosin head and actin monomers located in the thin filament of sarcomere (Robinson, Dong et al. 2004). Changes in the resting tension of heart muscle affect the range of heart contraction. The heart has the capacity to adjust its contraction force as result of variations in ventricular filling (end-diastole), this effect is known as the Frank–Starling Law (Sequeira and van der Velden 2015). An increased systolic contraction is the results of the ventricle stretching due to greater end-diastolic volume happens (Schneider, Shimayoshi et al. 2006). However,
…show more content…
Three ECG leads were attached in the toad body. A thin wire attached to the alligator clip of the positive lead was inserted through the muscle wall of the ventricle, far enough to avoid touching the bend pin. The negative lead was attached to right collar bone. Finally, the earth lead as attached to right hind-limb.
Data was recording using the LabChart software. Tension was increased on the heart with the micro positioner until the signal was strong enough to be read. Data for “Control”, also known as “baseline data” was collected before increasing tension on the heart. In this case, tension of baseline was set at 30 mm. Data was recorded during 2 minutes. After control data was recorded, tension on heart was increased by 5 mm and data was collected during 2 minutes until 45 mm was reached. A total of 3 replicates were recorder for each condition.
After data was recorder, amplitude of contraction force was calculated for each condition and its average was calculated. Averages calculated from LabChart was used in Graph prism software to analyze and compare each condition. Finally, statistical analysis was performed using one-way ANOVA with multiple comparisons. P-value threshold stablished was 0.05.
RESULTS
As shown in Figure 1, comparison between control group (13.09 ± 2.769 mN) and condition at 35 mm (mean=14.58 mN and SEM=±1.757 mN) showed no difference (p-value=0.9603). Comparison between control group and condition with
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).
A 30cm piece of thread was placed around the heart at the Atrioventricular groove (AV groove) and tied in a knot but left loose so as to not interrupt the normal function of the heart. The heart was allowed to beat for about 15 seconds with no pressure. After 15 seconds the knot was slowly tightened while taking care to stay on the AV groove while tightening. Data was observed and recorded.
contraction, and this reduction in tension production is the cause of the loss of strength. Her muscles are actually
DROGMAN G, RAEMAEKERS L & CASTEELS R 1977, ‘Electro- and pharmomechanical coupling in the smooth muscle cells of the rabbit ear artery’, Journal of General Physiology, vol. 70, no. 2, pp. 129-148
Contractility is the pumping of the heart muscle. It is measured as the ejection fraction. Contractility directly influences stroke volume. Increased contractility will increase stroke volume with any amount of preload. Diseases that disrupt myocyte activity reduce contractility. Myocardial infarction is the most common. Others include, but are not limited to, cardiomyopathies, degenerative valve disease, and myocarditis (Francis & Tang, 2003). Secondary causes of decreased contractility, such as myocardial ischemia and increased myocardial workload, contribute to neurohumoral , immune, and inflammatory changes and can cause ventricular remodeling. Ventricular remodeling occurs when the size, shape, and function of the affected chamber is distorted. Ventricular remodeling causes hypertrophy and dilation of the heart muscle and causes progressive myocyte contractile dysfunction over a period of time. When contractility is decreased, stroke
Once the patient was correctly hooked up to the EKG the BIOPAC Student Lab Program was started. Lesson five is the one we used for this experiment and once it had been chosen we label it and started the experiment. There were four conditions we needed to measure; the first being lying down. The subject was lying down relaxing on the cot. We clicked record and let it run for 20 seconds. The data resembled the chart below. If it did not we would have had to repeat the steps until it did.
The purpose of arterial pressure and the pulse lab is to determine the effect of posture and exercise on systolic and diastolic pressure and the heart rate. And also in order to find the differences in the reading taken under these condition compares to the baseline reading. The Sphygmomanometer and stethoscope are used to measure the systolic and diastolic blood pressure, counting the beat on the radial artery will give the reading for pulse rate and by using the lab scribe software and IWX214, the blood pressure will be measured. In the heart, the aorta and the carotid arteries have baroreceptors and the chemoreceptors that identify the changes in arterial pressure and the changes in
of atria and ventricle. Impulses not being transmitted from atria to the ventricle; no whole number relationship between atrial and ventricular contractions was demonstrated.
Pittiruti, M., Scoppettuolo, G., LaGreca, A., Emoli, A., Brutti, A., Migliorini, I., et al. (2008). The EKG
The term “ventricular remodelling” includes a complex of anatomic, functional, cellular, and molecular changes in the myocardium in response to the injury Markers of cardiac remodelling are hemodynamic and echocardiographic changes which correlate with cardiac impairment (Cohn et al., 2000; Kubanek et al., 2013). In HF animal models, the process of left ventricular (LV) remodelling begins rapidly, and continues to progress; LV are a greater cardiac chamber dilation, a greater increase in systolic and diastolic volume index and a progressive decline in the ejection fraction (EF) (Eaton et al., 1981; Korup et al., 1997; Cohn et al., 2000; Kubanek et al., 2013).
In the first part of the practical, we will dissect the heart of a sheep and observe its anatomical structure. We will also examine the structure of blood vessels at a microscopic level. My hypothesis is that by examining the anatomy of the cardiovascular system, we will be able to detect differences in both vessels and the chambers of the heart. In the second part of the practical we will examine the electrical activity of the heart. In doing so my aim will be to produce a familiar ECG reading containing a P wave, QRS complex and T wave. Futhermore, we will take blood pressure readings by listening to the korotkoff sounds of the heart using a sphygmomanometer and stethoscope. We hypothesis that the higher the arm position is from the ground, the smaller the blood pressure reading will
Cardiac muscle- Found in the wall of the heart in the myocardium. The cardiac muscle’s contractions help force blood through the blood vessels such as the aorta to the whole. This therefore delivers oxygen and nutrients to the body while removing other waste products, e.g. lactic acid. This muscle is responsible for pumping blood through the heart chambers and into the blood vessels the heart beats non-stop about 100,000 times each day, it can do this because of the cardiac muscle. It does this by contracting when it is relaxed it fills your heart with blood. Unlike other muscles the cardiac muscles never gets tired, it works constantly without pausing to rest. It consists of specialised fibres which do not tire. The cardiac muscle is also
Both of these muscles expand and contract as they have complex structures so it is essential how they do this. The cardiac muscle needs the contractions to occur in order to pump blood out of the atria and into the ventricles and round the circulatory system so the structure of this muscle shows the systole of the heart. The contractions of the skeletal muscle also depend on its structure. The binding and releasing of two strands of sarcomere is how the repeated pattern of contractions occurs. ATP is used to prepare myosin for binding to allow the contractions to happen. The skeletal and cardiac muscle also both has elasticity. The elasticity is used to restore the muscles back to their original lengths which enable them to resume back to their original length once they have contracted and been stretched.
The purpose of these lab exercises is to understand the function and importance of an electrocardiogram. This lab will demonstrate how stress levels or different elevations can affect human heart rate. Furthermore, the equipment used in the experiment will show the functions in the right and left arm; as well as, in the right and left ankles. Finally, the lab will serve a purpose as a way to know how to read an electrocardiogram and calculate the heart rate.
Thus far into my first semester of being admitted into the Respiratory program here at Wallace community college, it has been a very hardcore, yet valuable learning experience. One that has taught me many lessons but also helped me to grow into a better college student. There have been many valuable and important lessons taught thus far into the program. But one that stood out to me the most and one that I had the least amount of trouble with but was still yet challenging, was the electrophysiology of the heart.