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3. RESULTS
3.1 VERAPAMIL
3.1a VERAPAMIL MAP RECRUITMENT
A series of increasing stimuli were applied to the nerve beginning at 50mV until the maximum MAP was achieved. The control threshold occurred at 55mV and the maximum MAP amplitude of 35.6mV was first seen with a 90mV stimulation. After applying 0.5 mM Verapamil as indicated in section 2.3.2a, the nerve was again stimulated within the control range to observe changes. The results of this comparison are shown in Figure 7. Following treatment with Verapamil, the muscle did not begin to respond until a threshold between 90-100mV. The maximum MAP amplitude after treatment was 1.0mV which occurred at the highest stimulus given, 100mV.
3.1b VERAPAMIL FACILITATION
In order to observe facilitation, the nerve was stimulated with 5 supramaximal stimuli of 400mV in rapid succession as described in 2.3.1b. The control MAP amplitudes begin at 34.1mV and increase with each pulse. The fifth pulse caused a 54.3mV MAP. After treatment with Verapamil the MAPs did not increase each time. The values obtained from data in this portion are shown in Figure 8. After Verapamil the MAP amplitudes do not change significantly rather they range between the second pulse low of 0.9mV to the first pulse high of 1.8mV.
3.1c VERAPAMIL SYNAPTIC DELAY
The synaptic delay was calculated based on data recorded from the frog while the recording electrodes were placed in different positions as described in 2.3.1c. The control synaptic delay was 2.5ms while the delay after Verapamil increased to 3.1ms. The CAP conduction velocity was 43.5m/s before the treatment and 43.4m/s after treatment. The control conduction time of 0.90ms did not change post treatment. A summary of these calculations and other relevant data for the Verapamil trial is in Table 1. The method used to calculate conduction velocity and synaptic delay are as follows:
Conduction Velocity = distance traveled => 10 mm ¬ = 44.4mm/ms
time to travel distance 0.225ms
The typical CAP values resulting from this type of measurement are shown in Figure 4. Since the signal traveled 40mm between the B electrode and the G electrode (see Figure 1) where it was recorded, the total conduction time is:
Conduction Time = distance traveled (mm) => 40 (mm) = 0.90ms
conduction velocity (mm/ms) 44.4 (mm/ms)
The time between the beginning of the stimulus and the onset of the pulse is the MAP latency as measured in Figure 5. The CAP conduction time subtracted from the MAP latency will result in the synaptic delay. Synaptic delay = 3.40ms-0.90ms = 2.5ms. All reported values in sections 3.2c and 3.3c were also calculated in this manner.
3.2 CURARE
3.2a CURARE MAP RECRUITMENT
The effects of curare on threshold stimulus and MAP amplitude are shown in Figure 9. The preparation treated with 7.33μM curare as previously described reached threshold at the same stimulus amplitude as the control (55mV). The maximum MAP amplitude was much lower in the curare trial however, reaching only 9.0mV as opposed to the control’s 17.1mV. The maximum MAP was also reached with a significantly lower stimulus of 70mV, 20mV lower than what was required for the control.
3.2b CURARE FACILITATION
Figure 10 shows the effects that curare had on facilitation of MAPs arising from repetitive stimuli. Over the course of five 400mV stimulus pulses the control MAP amplitude increased by approximately 100% increasing from 16.7mV to 33.6mV. The curare treated preparation on the other hand showed only a roughly 20% increase in MAP amplitude as it ranged from 8.9mV to 10.7mV. In addition, the majority of facilitation for the drug test occurred within the first 3 pulses, whereas the control showed a fairly steady increase across all five pulses.
3.2c CURARE SYNAPTIC DELAY
The data obtained from the conduction velocity portion of the curare tests is recorded in Table 2 along with the maximum MAP amplitudes from MAP recruitment. The synaptic delay was calculated by moving the electrodes as described in section 2.3.1c. From this data it is clear that the drug treatment had no effect on the conduction velocity (45.5m/s), synaptic delay (2.1ms) or MAP latency (3.0ms). The conduction time for both was 0.90ms.
3.3 SUCCINYLCHOLINE
3.3a SUCCINYLCHOLINE MAP RECRUITMENT
Figure 11 shows the effects of succinylcholine (SCh) on the max MAP amplitude. The MAP threshold occurred with a stimulus of 85mV both in the control and after dripping 14 µM SCh on the muscle according to protocol (2.3.2a). The max MAP amplitude was found to be 3.1 when stimulated with a 100mV potential. After SCh treatment, the max MAP amplitude was found to be 2.0mV (1.1mV less than the control) when stimulated at 110mV.
3.3b SUCCINYLCHOLINE FACILITATION
Figure 12 shows the effects of SCh on facilitation of the MAP by applying a supramaximal stimulus of 400mV every 10ms. Prior to treatment with SCh, the control MAP amplitude began at 3.0mV and increased with each subsequent stimulus to reach a max amplitude of 19mV. After the administration of SCh, facilitation was still seen to occur as the MAP amplitudes increased after each pulse from 2.0mV to 12mV. The SCh treated muscle did not increase as steadily as the control since the MAP amplitude rate of increase was not as steep after the third pulse.
3.3c SUCCINYLCHOLINE SYNAPTIC DELAY
Table 3 shows the effects of SCh on conduction velocity of the nerve and synaptic delay when recorded as described in 2.3.1c. MAP latency measured in the control muscle was 3.1ms. Succinylcholine was seen to cause a 3.2% greater MAP latency (3.2 msec), but equivalent conduction velocity, and synaptic delay (47m/s and 2.3 ms respectively). The conduction time was 0.85 ms.
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