Lennox
No alarms, and no surprises...
- Jul 21, 2019
- 223
I suppose that, in the case of CTB'ing, the hypotension specifically will happen regardless of minimal impacts of antacids. Because the quantity taken to CTB (15~20g) is much much larger than the quantity administered in the study (0.3 mg kg-1 , which for a 70kg man would mean 21mg).It'll be interesting to see comment about this. Received wisdom has been that gastric acidity during the SN ingestion process is undesirable.
Anyway, does the hypotension thing really matter in the SN process ? The killing mechanism prevents the blood from transporting and releasing oxygen to the various organs of the body, including, crucially, the brain, and the increased heart rate plus hypotension (low BP) are really irrelevant to the oxygen exchange deficit.
Just a thought.
But the main point I was trying to get at is that, it doesn't seem to have been established that the interaction between PPIs and SN is necessarily different from the interaction between other types of antacids and SN. The paper doesn't seem to conclude that only the PPI class of antacids will cut down effects of SN, but only say that an acidic stomach seems to be important for the hypotension effect of SN. So, it seems to me any type of antacid could potentially play the same role here.
All that said, I haven't researched the issue further yet, I'm basing my conclusions off this paper alone.