Frog Heart Lab, Animal Physiology

chemic and Environmental make on the nerve Introduction The eye is the centerpiece of the circulatory system, its muscular abridgments tot bothyow for the timely delivery of inbred gases and nutrients to virtually all cells of the trunk. The pressure created by the tenderness also plays a vital role in eliminating wastes done organs such as the kidney, thus the pith delivers and helps maintain nutrient and waste organisation throughout the body. The amount of money, like all muscular tissue cells, grows ionic calcium when stimulated which binds to troponin which in turn arouses tropomyosin to debunk the myosin-actin binding sites on the ponderosity.Temperature has effectuate on the metabolism and application of all cells. Warmer temperatures add the energizing energy of molecules in cells, providing more energy which allows metabolous processes to proceed more quickly. Cooler temperatures, on the other(a) hand, decrease molecular kinetic energy and pretend unh urried metabolic steps in cells and tissues, accordingly when a bear hibernates, its body temperature is some degree lower than it is during the bears active periods.The content is also susceptible to certain molecules for which are capable to bind to its receptors or diffuse across its tissue layer and affect intracellular activity and consequently nurture effects on the overall homeostatic discipline of the organism. The Sinoatrial Node (SA Node) acts as the pacemaker of the meat by providing a small, autorhythmic electric shivers that travel to the atrioventriclar guest (AV node) and through the Bundle of His and Purkinje Fibers through gap junctions at the intercalated disks which stimulate the cells of the totality to contract via calcium release.This contraction is kindred to a neuron in the sense that a threshold stimulus is needed to cause a contraction, a refractory period follows contraction at which time a new contraction brush offnot occur. Drugs that consec rank an effect on the tissues of the sum total, especially those where the SA Node resides sight have an effect on the frequency and force out of muscular contraction via causing a stimulus to occur and lowering the threshold needed to cause a contraction. The warmness is under both nervous and hormonal control.The brain is constantly receiving information from the body such as pH, CO2 levels, and many others that the hypothalamus and medulla play a role in translating and reacting to via the release of hormones such as epinephrine which affects the SA node, either by stimulating or inhibiting contraction position. Removal of the heart from the body would result in eventual cessation of beating as these sources are depleted from the adjacent environment, not to mention the absence of the appropriate ion levels needed to maintain resting cellular electrochemical gradients.All of the aforementioned aspects of heart control coordinate with Starlings Law of the Heart, which relate s to stroke volume, contractions lastingness, and frequency of heart contraction. This paper is interested in investigating what the effects of the alteration of temperature, chemical environments, and physical obtrusion have upon the faculty and frequency of cardiac muscle contractions. Decreasing the temperature of the hearts environment should hypothetically result in a decrease in both frequency and bearing of contractions due to the decreased ability of calcium ion channels to open and cause contraction.Various chemicals such as epinephrine and calcium ion solutions should correlate to both and increase in frequency and strength of the resultant contractions due to direct effects on the wagon mode of activation (SA node stimulus) and reassign order of magnitude the levels of available calcium needed to cause a contraction. Other chemicals such as Atropine should indirectly increase heart rate via the blocking of the effects of the para human system resulting in a predomin ation of likeable activity.Acetylcholine, which acts on the muscarinic receptors of the heart, should display inhibitory effects on the heart by decreasing available cantonment levels, which results in fewer phosphorylated Protein Kinases which are needed to open the calcium channels which result in contractions of all muscles of the body. Additionally, chemicals such as nicotine should have little to no effect on the effects of muscle contraction due to lack of receptors on the heart for such substrates as well as lack of nicotinic receptors on any body tissues that indirectly affect heart rate such as the brain.Methods mental process 1 The Heart compute The dissected frog, whose heart was left attached and embedded in the frog, was connected to a string at the most basal aspect of the heart, and wrapped around an electrical stress detector located 15cm above the heart to detect changes in pressure on the apparatus caused by heart contractions. Unless otherwise stated, all subs equent procedures will have the same setup to minimize variability in the results obtained. The resting heartbeat was then recorded via the described instrumentation. surgical operation 2 personal effects of parky TemperatureInitially, 10mL of room temperature tollmans solution was applied directly to the heart and allowed to contract freely for 15 seconds. The selective information obtained from the contractions was recorded. The heart was allowed 1 minute to recover from delineation to the solution. Next, 10mL of chilled Ringers solution was applied directly to the heart and allowed to contract freely for 15 seconds. This data was recorded. Procedure 3 Effects of Drugs Thirty seconds of frequent heart contractions were recorded at which time 2mL of epinephrine was dropped onto the heart itself.Contractions were allowed to proceed for 60 seconds during which time data was recorded. Following exposure to epinephrine, the heart was allowed to return to its resting state determin ed in procedure 1. This same procedure was repeated with the following chemicals 1) Acetylcholine, 2) Atropine, 3) calcium solution, 4) Nicotine solution, and 5) Caffeine solution. Procedure 4 The Refractory Period of the Heart Resting heart contractions were recorded for thirty seconds until the heart rate was less than 60 beats per minute. A stimulator electrode to be used was set to the following states bounteousness of 4. 0 Volts, a stimulus delay of 50ms, stimulus duration of 10ms, a frequency of 1. 0Hz, and a pulse number of 30. The electrode was then fixed in direct contact with the heart for 30 seconds at which time the data was find and recorded. Procedure 5 Effects of a ring-binder on the Heart 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 shape 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 slice taking care to stay on the AV groove while tightening. Data was observed and recorded. Results Procedure 1 The Heart Rate This test was carried out as noted about in Procedure 1. The resting heart rate was established and used as a baseline value from which to compare all future deviations. term data could not be exported from the computer to be definitively known, the relative rate and strength of the contractions were noted on a visual basis from which to compare the following experiments.Procedure 2 Effects of tatty Temperature As noted above in Procedure 1, technical data could not be obtained from this experiment and visual analysis had to suffice for data. Upon adjunct of room temperature Ringers solution, no notable change in contraction strength or frequency could be noted. Time was allowed for the heart to recover from the effects of the initial exposure. The application of cold Ringers solution resulted in a clear and discernable slowing of the heart rate, though no change in strength of the contractions could be detected.Procedure 3 Effects of Drugs Upon addition of epinephrine directly to the heart, the contraction rate showed a considerable increase in frequency. The strength or magnitude of distributively contraction also significantly increased as the heart real was lifting itself off of its resting place. Exposure of the heart to acetylcholine had clear effect on the heart as well. A warm decrease in heart rate was noticed upon exposure however the magnitude of contraction seemed to persevere somewhat constant.Addition of Atropine to the heart resulted in an increase in heart rate. The magnitude of each contraction showed a minor, but noticeable, increase in strength. A calcium solution was applied to the heart and showed a nuts increase in contraction rate with the magnitude of each contraction seemingly remaining constant. The addition of both nicotine and caffeine had negligible effects on the rate or st rength of heart contraction. send back 1 . Applied Chemical and Its Effect on Heart Contraction Rate and Strength Chemical Heart Rate Contraction StrengthNormal Ringers Control Rate Control Magnitude Cold Ringers Decrease No change Epinephrine profit Increase Acetylcholine Decrease Slight Decrease Atropine Increase Increase Calcium solution Increase No change Caffeine No change No change Nicotine No change No change Procedure 4 The Refractory Period of the Heart Upon exposure to a mild electric current, the heart rate was altered from the normal resting heart rate. While it definitely slowed, the contractions were sporadic at best.The heart lost its regularity and showed random contraction intervals, some ranging shorter than normal while others had peachyer time gaps mingled with contractions. Procedure 5 Effects of a Ligature on the Heart After the knot had been tied around the AV groove, no noticeable alterations were noticed to heart contraction. Upon tightening of the thre ad however, the heart appeared in clear distress. Beat irregularities ensued with an increase in magnitude of each pulse. The heart ceased functioning before the allotted time period had elapsed.Discussion Procedure 1 The Heart Rate The resting heart rate of the frog was perfectly normal. Steady, rhythmic contractions around 60 beats per minute were observed and used as a baseline for other experiments. The frog appeared healthy, showing no signs of beat irregularities or any other defects that may have impacted the experiments validity. Procedure 2 Effects of Cold Temperature The slowing of the heart in the presence of chilled Ringers solution was to be expected.All metabolic processes decrease in all cells upon exposure to cold due to the nature of chemical interactions. In the role of the frog heart, the cold solution probably decreased the rate at which calcium channels were able to open and thus, decrease the rate at which contractions were likely to occur since calcium entry to the cytosol initiates the cascade of reactions that leads to muscle contraction. Thus, the observational hypothesis was correct given that the rate at which the heart contracted decreased and the magnitude of each contraction also lowered.Procedure 3 Effects of Drugs Exposure to epinephrine increased both the rate and strength of each muscular contraction as was expected. The heart contains many adrenergic receptors which are antiphonary to epinephrine, especially near the SA node, which initiates the contractions of the heart. Epinephrine acts to increase the release time of calcium from the sarcoplasmic reticulum via a cascade of reactions. The fact that epinephrine had a positive impact on the heart indicates that the heart was healthy and responsive to normal physiological chemicals and pathways.Addition of acetylcholine predictably lowered the heart rate of the frog. Acetylcholine blocks the cAMP cascade pathway that last leads to calcium release, thus the frequency at w hich calcium is released is lowered and as a result, the contraction rate follows suit and lowers as well which is what you would expect from a fully functional heart. This part of the experiment was a success. The presence of Atropine, a parasympathetic system inhibitor, acted appropriately and increased the heart rate of the frog.The parasympathetic and sympathetic nervous system act antagonistically to one another and as a result, decreased activity in one serves to act as if an increase in the other had occurred. Addition of Atropine, in effect, should have had similar effects as the addition of epinephrine which it did. Exposure resulted in an increase in the rate of contraction and a mild but noticeable increase in the strength of contraction compared to the resting heart rate and magnitude which was what the response was predicted to have been.Neither caffeine nor nicotine had any visual effect on the hearts rate or strength of contraction. This was expected as both of these chemicals exert their effects by activating the release of neurotransmitters and hormones in the hypothalamus, specifically epinephrine, which then affects the heart. Because these tested chemicals were applied directly to the heart and not placed in the bloodstream where they could produce an indirect effect, it is honest that no effect was noticed from the heart upon exposure to these chemicals. Procedure 4 The Refractory Period of the Heart The SA node is the pacemaker of heart.It is produces electrical currents that travel to the AV node and through the Bundles of His and the Purkinje fibers and stimulates the cells of the atrium and ventricles to contract. This is electrical conduction that is carried through gap junction of the intercalated disks separating heart cells and thus it is reasonable to infer that applying an electric current directly to the heart would interfere with the even, rhythmic contractions normally observed in a healthy, undisturbed heart. Accordingly, as we applied a current to the heart, the cyclic contractions of the heart became erratic and unpredictable.No steady pattern was detectable in the muscular contractions. Some had longer periods between contractions while others had shorter time gaps between beats. This was expected as the heart would be receiving constant signals to contract along with the rhythmic electrical signals from the SA node itself and would result in interference and overlap of contraction signals which is exactly what was observed. This leads us to believe that both the electrical apparatus and the heart were working exactly as designed. Procedure 5 Effects of a Ligature on the HeartAfter placing the thread around the AV groove and tightening, the heart was clearly under a great deal of strength. Both the anterior and posterior segments of the heart swelled considerably, no doubt as a result of restriction of blood flow and buildup of pressure within the atriums and ventricles themselves. The AV node is a curiously sensitive portion of the heart to constriction as blood flow through the heart itself occurs at this junction. The heart contraction magnitude increased considerably while the contraction rate decreased substantially.Over the stock of time when the thread was tightened, the heart appeared to get weaker and weaker until it finally gave out itself. Using the electrical apparatus, we tried to liven the frog and succeeded, however, a steady and consistent heartbeat was never again established and was much weaker and slower than before the thread was utilized. This indicated that heart damage had occurred and it was unlikely that any more significant and reliable data could be obtained from the frogs heart and the experiment was finished as a result.Overall, the experiment can be considered a success as the appropriate responses to all the varying conditions were observed. While the experiment can be considered a success, the conditions with which the experiments were carr ied out were far from ideal. The experimental apparatus used was sufficient but just now the equipment of choice. Far from accurate and precision, as well as the lack of ability to export numbered data from the labs computers, it is rocky to really analyze the data and produce concrete results that reflect the true magnitudes of effect each experimental variable had on the heart.