Remember the nitrate – nitrite – nitric oxide (NO) pathway? You get inorganic nitrates and nitrites from edible plants like spinach, beets and noni. Some of the ingested nitrate – quite a bit actually – gets served up by your salivary glands to those friendly bacteria that live on your tongue. They need nitrate to generate energy and drive metabolism. In the process, they convert nitrate into nitrite.
After swallowing the nitrite, it’s distributed widely throughout your body and stored by your cells for on-demand generation of NO.
NO is a “signaling molecule”, serving as a messenger to trigger a wide array of biologic events. For example, it may trigger relaxation of the smooth muscle in a blood vessel wall, causing that vessel to dilate. The result is an increase in blood flow to its territory. Perhaps no other organ is so critically dependent on NO’s role in turning on the spigot at a moment’s notice than your heart.
When it comes to heart health, NO does even more. It lowers blood pressure – even when taken in very small amounts. It also makes platelets less “sticky”, reducing their tendency to clot when a ruptured coronary plaque expels its angry contents. That may be just what’s needed to prevent a full on coronary occlusion and a fatal cardiac arrest.
When a coronary artery is suddenly blocked and the heart muscle supplied by that vessel becomes oxygen deprived, the conversion of nitrite to NO really ramps up. It’s easy to see how NO might play a special role in preventing or aborting a heart attack.
When a person in the throes of a heart attack arrives at the emergency room, an attempt will be made to open the blocked artery. This is usually achieved with a “clot busting” drug or even better, opening the vessel mechanically with a tiny balloon and a coronary stent.
Now it’s certainly better to open the vessel than to let the heart attack go to completion. It takes about 6 to 8 hours of no blood flow to irreversibly damage all the heart muscle in a coronary artery’s territory. So it seems obvious that restoring blood flow anytime during that interval will limit the amount of heart muscle that’s lost.
But there’s a problem. It’s called ischemia – reperfusion injury. And it means that additional damage will accrue when the blocked artery is opened.
Now you might wonder how this can happen. After all, restoring blood flow to oxygen-starved tissue should provide an immediate fix. The additional damage is due partly to a change in the function of endothelial nitric oxide synthase (eNOS), the enzyme that normally generates NO from the amino acid L-arginine.
When blood flow shuts down, BH4 (tetrahydrobiopterin) – an essential cofactor required for eNOS to generate NO – is consumed. When there’s no more BH4, eNOS turns into a free radical generator. And when oxygen is made available by restoring blood flow, the repurposed eNOS really goes to work. Predictably, the sudden explosion of free radicals damages otherwise viable tissue.
Whew, got that? If not, go back and read it again. It’ll come in handy in a minute and just might help with a future post or two.
A few years ago, researchers from the National Heart, Lung, and Blood Institute explored the impact of nitrite, and by extension NO, on heart muscle injury during a heart attack.1
They created an experimental model of heart attack with ischemia – reperfusion in three groups of dogs. All dogs had the left coronary artery tied off for 2 hours before blood flow was restored.
In the first (control) group, saline was infused during the last hour of the coronary occlusion. In group two, sodium nitrite was administered for the same interval. But in the third group, sodium nitrite was infused for only the final 5 minutes before blood flow was restored. Using a combination of techniques they were able to compare to the size of the territory at risk with the amount of heart damage that actually occurred.
Here’s what they found.
In the control group, a full 70% of the area at risk was irreversibly damaged. But in the two nitrite treated groups, the amount of tissue damage was much reduced. In group 2 dogs, the infarct size was only 23% of the area in jeopardy. But what was most surprising was what happened in group 3. These dogs received nitrite for only 5 minutes yet suffered only half the damage that occurred in controls.
Now that’s really amazing!
And it means the benefit of the infused nitrite had nothing to do with opening new channels from adjacent blood vessels or sparing the heart by lowering blood pressure and decreasing heart muscle oxygen requirements.
In their report, the researchers do propose some possible mechanisms to explain the results. More importantly, their findings suggest profound benefit from adding inorganic nitrite to the treatment regimen for heart attack.
A 5-minute infusion could easily be incorporated into current protocols. If more heart muscle is preserved, a marked decline in heart attack complications like heart failure and fatal cardiac arrest can be expected.
Now from where I sit, it seems better to have my heart nitrite loaded long before having a full-blown coronary thrombosis than waiting for the ambulance ride to the ER to get the good stuff on board.
That’s just one more reason to take a nitrate – nitrite supplement every day. And my favorite nitrate – nitrite supplements are – you guessed it – Kyäni Nitro Fx and Kyäni Nitro Xtreme!
By the way, two human clinical trials looking at the impact of nitrite infusion during a heart attack are now underway.2,3 Until they’re completed and their findings are reported, I’m banking on Nitro Xtreme.
How about you?
1. Gonzalez, FM, et al. Nitrite Anion Provides Potent Cytoprotective and Antiapoptotic Effects as Adjunctive Therapy to Reperfusion for Acute Myocardial Infarction. Circulation. 2008;117:2986-2994.
2. Nitrites in Acute Myocardial Infarction
3. Sodium Nitrite in Acute Myocardial Infarction
Disclaimer: These statements have not been evaluated by the Food and Drug Administration. Kyani Bytes is not intended to diagnose, treat, cure or prevent disease.