Sympathetic Nervous System Lab Report

Background
The stress response in the body triggered by the sympathetic nervous system (SNS) contains two different chemicals – neurotransmitters and hormones. Neurotransmitters, specifically norepinephrine (NE), are released into the postganglionic synapses of the sympathetic nervous system (SNS) during flight or fight response. NE carries out its effects on a target cell by binding to and activating adrenergic receptors. NE is usually eliminated through the reuptake into presynaptic cells and enzymes in the synapse, but can also spillover into the bloodstream acting as a hormone. Spillover is often caused when the body is under stressful conditions, like extreme blood loss in this simulation and decides to send neuron signals to the SNS to
initiate fight or flight response leading to an increase in heart rate and the adrenal gland to release NE as a hormone in the bloodstream. Blood loss (hemorrhaging) can often lead to an increase in arterial blood pressure or decrease in cardiac output. In extreme cases of severe hemorrhaging, the blood pressure could decrease causing the blood vessels to constrict. In this simulation, the effects of NE on heart rate after hemorrhaging will be tested. Hypothesis
An increase of NE as a hormone in the bloodstream from spillover is the primary cause of an increase in heartrate proceeding hemorrhage.
Experimental Design and Methods
Go to www.justphysiology.com and Log in. Open the “Fight or Flight II” lab. Make graphs of Blood Volume vs. Time, Heart Rate vs. Norepinephrine, and Sympathetic Nerve Activity vs. Time. Set the simulation time to 5 minutes and let run. Turn HEMORRHAGE ON, set type: CONSTANT and HEMORRHAGE RATE to 100 mL/min, and let the simulation run for 15 minutes. Turn the NOREPINPHRINE PUMP ON and set RATE at 4000 pG/mL to get norepinephrine to spillover into the bloodstream. Let simulation run for 5 minutes. Watch the relation between the graphs.

Results
During hemorrhaging, the heart rate begins to increase above 90 beats per minute (Fig. 2). This increase in heart rate is caused by a loss of over 1000 mL of blood from the normal blood volume of about 5600 mL (Fig. 1). At this point, the body is trying to compensate for the amount of blood being lost by increasing neuron signals in the SNS (Fig. 3). The neurons are sending signals (Fig. 6) to specific tissues associated with the fight or flight response (adrenal medulla, muscles, and glands) to decrease the amount of blood being lost, which explains the slow decrease in blood volume after the hemorrhage (Fig. 4). An influx of NE at 4000 pG/mL after hemorrhaging caused the heart rate to increase above 180 beats per minute, which in turn, caused the patient to not respond
(Fig. 5).

Conclusion
According to the simulation, an increase in NE as a hormone after hemorrhaging is the primarily cause of an increase in heart rate.
During a hemorrhage, heart rate and blood pressure increases to coincide for the excessive blood loss. After a hemorrhage has stopped, the body is still experiencing stress due to the decrease in blood volume, which activates the stimulation of sympathetic nerves and the influx of NE as a hormone into the bloodstream. Since the heart rate increased in this simulation, it can be concluded that NE properly bonded to and activated adrenergic receptors in order to carry out its effects. This simulation helps with understanding patients who experience hemorrhaging and have dramatic effects afterwards. If a doctor were to treat a patient after hemorrhaging, a drug that deactivates NE should be administrated to maintain homeostatic conditions and keep the patient
alive.