Final Drive Nitro

[Cori Lenon]

DoI use harnesses? Absolutely. Just at higher levels of training and very specific situations in which we want to build drive.

When drive has nowhere to go, you start having problems.

So there you have a dog in a harness that is possibly building up a bunch of drive. To get any kind of obedience, every single instance of pulling needs to be countered with something even more rewarding.

This, by the way, is a classic example of how drives can interact, which is something that your average positive trainer or positive adherent dispensing advice on Facebook simply does not understand. And there is always going to be some kind of fallout, the magnitude of which is going to depend on the specific dog and the drives in question.

Power: This pedal can be powered by a 9V battery or 9-18V 2.1mm center negative DC power source. Unplug the input jack to preserve battery. When a DC plug is inserted into the DC jack the battery is disconnected from the circuit.

Operation: Vol: raise or lower the output volume of the pedal. Sat: sets the amount of gain saturation going to the second gain stage. All the way counter clockwise is unity gain for the input signal. Gain: Raise or lower the amount of gain in the second stage- can go from clean to overdrive and distortion. Tone: raise or lower the amount of top end present in the output. Internal Voice trim pot: sets the voicing and feel of the pedal- CCW is darker, CW is brighter.

The Nitro Drive can do it all. The Gain knob sounds great across the entire range. Sat acts as "gain 1" and will saturate the second gain stage. It gives the pedal more grit, and really lets you feel the pedal's dynamic range.

Nitro Drive has a lot of volume on tap to really slam the front end of your amp or another drive pedal. It can be a boost with a little mid push, a light overdrive, tight distortion, or saturated without going mushy. It also takes boosts very well.

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Background: The role of nitric oxide (NO) production, at the brain-stem level, in ventilatory control and pain perception is poorly understood. Furthermore, it is not clear whether NO synthase (NOS) inhibition can affect morphine-induced ventilatory depression or analgesia. The central hypothesis of this investigation was that NO, at supraspinal sites, can influence ventilation and nociception and can modulate the ventilatory depressant and antinociceptive actions of morphine. Using drug delivery via the fourth cerebral ventricle, the authors examined the ventilatory and nociceptive effects of an NOS inhibitor and an NO donor in the presence or absence of morphine sulfate (MS).

Results: Nitro-L-arginine alone dose dependently and significantly reduced PaCO2 and increased the nociceptive threshold. S-nitroso-acetylpenicillamine alone did not change the ventilation or nociceptive threshold. Morphine sulfate elicited a marked increase in PaCO2, a decrease in ventilatory drive, and an increase in nociceptive threshold (P Conclusions: Endogenous NO, produced at supraspinal sites, acts as a ventilatory depressant and as a nociceptive mediator. When NOS is inhibited, the ventilatory depressant actions of morphine can be reduced and the antinociceptive actions of morphine can be potentiated. However, NOS inhibitor treatment is more effective in suppressing morphine-induced ventilatory depression when given before, rather than after, morphine administration. The specific mechanisms involved in these actions remain to be identified.

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