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Effect of Pharmacological Intervention:

As Acetylcholine, Epinephrine, Atropine + Acetylcholine, and


Pilocarpine were applied to the frog heart in the order described by the
Heart Muscle Lab Manual LabTutor (Weixel, 2014), Acetylcholine and
Pilocarpine generally slowed the heart rate and Epinephrine and
Atropine + Acetylcholine increased the heart rate. With the application
of Acetylcholine, a heart rate of 55.2 BPM was recorded as dropping to
33.1 BPM. For Epinephrine, the heart rate increased from 33.3 BPM to
93.6 BPM. Administering Pilocarpine caused the heart rate to drop from
66.3 BMP to 41.8 BPM. Lastly, Atropine + Acetylcholine increased the
heart rate from 54.0 BPM to 150.2 BPM (Table 3, Figure 3). Using the
raw data (Table 4) to see if there was a difference between
heart rate before or after drug exposure, the absolute value of the
calculated t-value, 0.959207, is less than the two tailed t-critical value,
3.182446, therefore we would fail to reject the null hypothesis that there
are any differences between the two sets of data. Based on our prior
knowledge of the drugs’ effects on parasympathetic and sympathetic
control of the heart, we can assume that this counter evidence was due to
chance or error. In general, Acetylcholine produces parasympathetic
effects by binding to muscarinic cholinergic receptors, which activates
G- proteins and opens potassium channels (hyperpolarization), while
closing sodium and calcium channels. This caused the rate of action
potential firing to decrease, thus decreasing heart rate. Epinephrine is a
hormone secreted by the adrenal medulla together with norepinephrine,
and acts to increase both the strength of contraction of heart rate by
binding to beta-1 adrenergic receptors
(Silverthorn, 2012). In 1881, scientist Sydney Ringer first experimented
with Atropine and Pilocarpine to observe the effects on heart rate. Ringer
had discovered that Atropine increased heart rate, while Pilocarpine
decreased heart rate (Ringer, 1881). Atropine is an Ach antagonist,
which blocks the muscarinic Ach receptors and effects of Ach, thereby
increasing pupil size (dilation) and increasing heart rate (Animal
Physiology Lab Lecture Notes, 2014). Lastly, Pilocarpine is a
muscarinic receptor agonist that increases the activity of muscarinic
acetylcholine receptor, increasing the effects of acetylcholine in the
body. Since pilocarpine increases the activity of the parasympathetic
nervous system, it slows down the heart rate
(Silverthorn, 2014).