The electrical and mechanical recordings of the frog heart were first observed during normal heart activity. Ventricular and atrial contractions are the systole and diastole portions of the cardiac cycle that represent mechanical activity. The collections of action potentials elicited by pacemaker cells represent the electrical activity. Excitation of cardiac tissue is caused by pacemaker activity that is normally located in the sinus venosus of the frog heart. The heart contracts or beats rhythmically as a result of action potentials that are generated by itself as a result of the pacemaker activity. Autorhythmic pacemaker cells do not contract but are specialized for initiating and conducting the action potentials (Sherwood, 2007, p. 309). There are different phases of the action potential unique to pacemaker cells. At phase 0, there is a rapid influx of Ca2+ that induces depolarization. Phase 1 and phase 2 are only presnt in cardiac muscle. During phase 3, there is a rapid repolarization caused by K+ efflux. At phase 4, the resting potential does not stay constant but slowly drifts toward threshold. The slow drift to threshold is called pacemaker potential activity and triggers beating without nervous stimulation (Sherwood, 2007, p. 309). The action potentials for contractile cardiac muscle also consist of different phases. At phase 0, there is a rapid depolarization caused by Na+ influx. Immediately following that is phase 1, inactivation of Na+ channels causes rapid repolarization. During phase 2, there is a plateau due to slow Ca2+ influx and decreased K+ permeability. At phase 3, fast K+ efflux and Ca2+ channel inactivation causes repolarization. Lastly, phase 4 is the constant resting membrane potential.
In order to get contraction, electrical activity has to be carried over to mechanical activity and the time period required for this happen is called latency (Sherwood, 2007). The latency is the time between the onset of electrical and the beginning of ventricular activity. In this experiment, the latency was ~ 0.20 seconds. The mechanical activity lags from electrical because mechanical activity ensures muscle fibers are coordinated to contract as a unit to pump efficiently while electrical spreads throughout the heart at a very fast rate. The fluctuations among Na+, K+, and Ca2+ is the result of what is observed on the electrical traces which lead to mechanical activity.
Once the muscle cells are electrically activated, they enter an effective refractory period where the cell cannot fire another action potential. The cardiac muscle has this effective refractory period so a second action potential cannot be triggered until the excitable membrane has recovered from the preceding action potential (Sherwood, 2007, p. 316). The effective refractory period is long because of the prolonged plateau phase of the action potential in the cardiac muscle. Following the effective refractory period is the relative refractory period where an action potential can occur. This is a protective mechanism to allow the heart to have efficient periods of contraction and relaxation. Thus, the cardiac muscle cannot be re-stimulated until the contraction is almost over.
Late diastole and early systole corresponds to the effective refractory period. Early diastole and late systole corresponds to the relative refractory period. In our experiment, we were unable to elicit an extrasystolic contraction during late diastole because of the effective refractory period. Comparatively, we should be able to elicit an extrasystolic contraction during early diastole because that is within the relative refractory period. Our TA told us to stimulate the heart at early systolic by mistake, so our data did not show a lot of extrasystole. However, there is one point around ~ 139 seconds into the data which showed extrasystole. With this extrasystole, we can analyze the ventricular contraction amplitude. We were unable to measure the contraction force because our data values displayed negative tension values. The systolic contraction before the extrasystole has an amplitude of 0.246 grams, which then increases to 0.277 grams at extrasystole. Extrasystole is a premature ventricular contraction often caused by depolarization in the ventricle. Following the extrasystole is a compensatory pause, which is the time period after the extrasystolic contraction and the following ventricular contraction. We measured the compensatory pause to be 0.890 seconds, which is the time before ventricular filling occurs to compensate for the premature ventricular contraction. After this period, the rhythm of heart beat catches up and resumes the amplitude at 0.246 grams.
The heart is innervated by the autonomic nervous system which can modify the rate of contraction. Stimulation of the parasympathetic nerve causes the heart rate to decrease. We stimulated the vagal nerve at 0.75 volts and caused the heart to enter cardiac arrest before we could see bradycardia. Acetylcholine is released from the parasympathetic axons on the sinus venosus cells and slows the heart rate. In similar experiments, acetylcholine works as an inhibitor by stopping the generation of pacemaker action potentials and cardiac arrest is seen when the heart stops beating as the sinus venosus is permanently hyperpolarized (Bywater et al, 1990). The duration of cardiac arrest was 20,000 msec before a small contraction was seen again. During vagal escape, other pacemaker cells will take over control of the heart rate. This will generally occur at a slower heart rate because the pacemaker activity will be set by the next fastest pacemaker cell. Vagal escape is followed by an irregular frequency and force of tension where the muscle cells try to coordinate an organized contraction for efficient pumping (Bywater et al, 1990). After vagal stimulation was stopped, the heart contractions returned with the amplitude of contractions increasing from 0.180 g to 0.197 g. The idea of vagal escape agrees with our data because the heart rate prior to cardiac arrest was at 40 bpm and then decreased to 26 bpm when slower pacemaker cells take over.
Another way for the autonomic nervous system to change heart rate is through sympathetic activity. Under resting conditions, parasympathetic discharge dominates because acetylcholine suppresses sympathetic activity by inhibiting the release of norepinephrine from neighboring sympathetic nerve endings (Sherwood, 2007, p. 327). Sympathetic activity increases heart rate, stroke volume, and causes dilation of the coronary arteries (Purves et al, 2008, p. 514). Sympathetic stimulation and epinephrine enhance the hearts contractility, which is the strength of contraction of end diastolic volume. The heart contracts more forcefully and squeezes out a greater percentage of blood it contains, leading to a more complete ejection (Sherwood, 2007, p. 329). The rate of depolarization is increased and the increase in intracellular Ca2+ enables greater contractions of the heart (Shepherd et al, 1986). In this experiment, epinephrine was applied on the surface of the heart at first but did not cause a change in heart rate. Then a second application of epinephrine was applied and there was a very small increase in heart rate from 45 bpm to 50 bpm. At this point, the baseline for tension has changed due to movement of the frog tray from its original location. So the data for contraction amplitude is unreliable but we should expect to see an increase in tension and amplitude. Futhermore, epinephrine was injected and this generated a greater response. The heart rate increased to 70 bpm and the amplitude also increased from 0.973 to 0.991. Injection elicited a greater response because this allows the epinephrine to reach the sinus venosus quicker.
The innervations of the autonomic nervous system of the heart follow the Frank-Starling Law. The law follows the concept that increased venous return results in increased contractility, enabling the heart to pump back out the same volume of blood; the end diastolic volume of frog heart is load dependant (Sanjay et al, 1993, p. 297). The heart pumps blood out during systole and the volume of blood returned to it is during diastole. If the heart is filled to a greater extent during diastole, it will contract with more force during systole. More ventricular filling causes an increase in end diastolic volume. More force contraction causes an increase in stroke volume. An increase in venous return results in an increase of stroke volume (Sherwood, 2007, p. 328).
Despite the other important functional organs within the body, the heart is vital to maintain life. The main purpose of the heart is to transport oxygen and nutrients within blood to tissues while removing waste products and metabolites. In homeostasis, the heart can accommodate with changes in body activity by providing the sufficient amount of blood to meet the body's demands. The mechanical and electrical activity of the heart enables contraction and relaxation to occur rhythmically and efficiently. Although complications may occur that can alter heart rate, the pacemaker activity can react to maintain heart contractibility. Pacemaker cells taking control of heart rate after cardiac arrest was seen during vagal stimulation. The heart manages to function as a unit to keep a body healthy and alive.