Atropine Contraction Lab

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In this lab, we assessed the impact of varying tensions and neurotransmitters on the heart’s rate and contractility. Prior to conducting the experiment, we hypothesized that the more the heart muscle stretches, the greater the force of contraction will be and that if a neurotransmitter can act on a muscarinic and nicotinic receptor without an antagonist present, the agonist will produce a parasympathetic (decrease in heart rate) and sympathetic response (increase in heart rate and contractility) respectably. After conducting the experiment, we can say with certainty that the majority of our results correspond with our hypothesis and the parts that don’t can be explained by human error; therefore, we must accept it.
For starters, the results …show more content…

In Figure 27, there is an increase of 10.3 % while there is an increase of 161.9%. Both demonstrate an anticipated increase in heart rate; however, the expected heart rate is substantially greater. This discrepancy is possible due to the numerous cold experimental treatments prior, the atropine being cold, and the control that the experimental group is being compared. Depending on the accuracy of the control, the experimental group can demonstrate either a positive or negative chronotropic response. It is also possible that dosage was the issue. According to a therapeutic review study conducted on bradycardia patients, a condition where the heart beats abnormally slow, atropine was administered to increase heart rate and improve atrioventricular conduction it was found that in small doses, atropine actually has a paradoxical effect on the heart. Instead of increasing heart rate, it will instead decrease heart rate (Das, 1989). Hence, it is possible that not enough of the atropine was administered uniformly along the surface of the heart or at least along the pacemaker region to produce an effective increase in heart …show more content…

To improve this experiment, a better control for the experimental treatments needs to be established. Instead of comparing the experimental treatment against cold saline, a baseline period needs to be taken prior to the application of any experimental conditions. In addition, each experimental treatment should be conducted on a different frog of the same mass and health or at the very least on the same frog after ample recovery time has been given and the heart beat has stabilized instead of consecutive experimental treatments. Also, the temperature of the treatments and dosages of each neurotransmitters need to be standardized to prevent any discrepancies or

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