Frog Disection Lab Report
The nervous system controls the heart which is regulated by medulla. The heart is innervated by parasympathetic and sympathetic nerve fibers that come to an end at the SA node. The sympathetic cardiac nerves have adrenergic neurons which produce norepinephrine and epinephrine in amphibians. The neurotransmitters released by these nerves influence the heart rate and the strength of contraction by either influencing the magnitude or timing of ion currents across the cell membrane. The parasympathetic cholinergic neurons are contained in vagus nerves that release acetylcholine at their end points. The central nervous system modifies the functions of the heart. The amount of acetylcholine produced by the autonomic nervous regulates the S-A node parasympathetic neurons. Acetylcholine, is the neurotransmitter used by nerve cells to control the heart, muscles and lungs.
Heartbeat arises from the muscle cells and is kept in place by the autonomic nervous system. The working mechanism of the heart of a frog is fundamentally similar to that of the human, apart from that the pacemaker is located in the sinus venosus wall. My hypothesis for the hot treatment is that inducing a hot solution will affect the rate of strength of cardiac muscle contraction. In addition, I hypothesized that the cold solution will have similar but opposite effect to hot treatment. My hypothesis for different pharmacological agents applied on the heart was as follows: Because acetylcholine is the neurotransmitter produced by the parasympathetic nervous system, its application to the heart would affect the cardiac muscle strength and hence heart rate.
Likewise, Atropine, other hormones and neurotransmitters were anticipated to affect the cardiac muscle strength and heart rate since they works by blocking or binding to acetylcholine receptors. Direct stimulation was hypothesized to affect refractory period while cardiac muscle contraction was hypothesized to be dependent on the intrinsic conduction. For Each chemical added at interval of 30seconds, contractile rate was measured and recorded at interval of 10 seconds accordingly. In addition, during the application of stimulus agents, we measured the ventricle contraction period as well as atria contraction and recorded accordingly to determine the refractory period. Finally, we disturbed the intrinsic conductance system by tying a ligature around the AV groove that separates the ventricle from atria and measured the contraction ratio for each observable degree change of heart block.
Results Table 2. Show average change in contractile strength and rate with different neurotransmitter and hormone treatments. 8 Digoxin 0. 0 Baseline 0. 2 Potassium 0. 8 Table 3. show the parameter of refractory period. show the change in the rate of contraction with temperature when frog heart is bathed in cold and hot frog ringer’s solution. Discussion i. Temperature It was predicted that cold treatment would lower the frequency with stronger contraction while hot will raise the frequency with weaker contraction. Our results predictions were positive for both hot and cold treatments but were negative for strength. Because frogs are ectothermic, their heart rate reflects metabolic rate which increases with increasing body temperature and vice versa. 141grams as illustrated in table 2 and figure1. Based on our prior prediction, first Acetylcholine predictions were supported while Atropine and second Acetylcholine predictions were not supported.
Based on known knowledge, it can be assumed that the counter evidence realized was due to chance and error. In summary, Acetylcholine produces parasympathetic effects by binding to muscarinic cholinergic receptors thereby activating G-proteins which in turn opens potassium channels (hyperpolarization), hence the decrease in rate of action potential which is seen as decreased heart rate. This process keeps the membrane close to equilibrium potential of potassium ions hence making depolarization almost impossible. According to Silverthorn (2012), epinephrine is a hormone secreted in the medulla by adrenal medulla as well as norepinephine which work by increasing the strength of contraction of the heart rate through binding to beta-1 adrenergic receptors. On the contrary, digoxin knocks out either Sodium or potassium pump thereby lowering the sodium ion gradient necessary to drive the calcium ions out of the cell.
Since calcium remains in cytosol, it causes stronger contractions. iv. Potassium chloride While the frequency predictions were supported; however, the strength predictions were not due to errors in potassium additions as timing was not accurate. Conclusion In summary, the initial hypotheses were partially correct, however, the results obtained strongly demonstrate that both contractile force and heart rate can be manipulated by imposing various factors as postulated in this experiment. In particular, by changing temperature fluctuations and administering pharmacological agents as well as increasing ventricular stretch, to monitor the cardiac muscle activity. Of great physiological importance was that the experiment demonstrated that cardiac muscles do not need rely on central nervous system’s commands to contraction but instead triggered by signals arising from the muscle itself.
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