Does anyone know how vasodialators and vasoconstrictors would affect decompression?
Vasodialators, vasoconstrictors, and decompression
- Thread starter KellyAsh
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Excellent question, and I look forward to a medical response. I can say, as a migraine sufferer who takes vasoconstrictors to wrestle the migraines into submission, that I've never had an issue diving on days I'm medicated. I'm going out medicated again today, and if I've just been "lucky" and that luck changes, I'll come back and say so!
OP
No doctors have any input on this subject? Is anyone aware of any studies done on this subject?
Kelly, what kind of vasoconstrictors and vasodilators are you talking about?
OP
The idea was wrought from my past experience as a competitive powerlifter where they use an over the counter powdered drink containing a the vasodilator nitric oxide. I was also wondering about it's precursor, L-Arginine. These are the only ones I am aware of.
My train of thought was that the vasodilator might dilate the vessels, creating a more open passage through which the blood could flow around the bubbles, resulting in more efficient circulation and safer decomression. The antoginist in me took over and said, "What if bubble formation is more dependant on the surface area of the blood vessel than we realize?"; the greater surface area of a dilated vessel generating more bubbles? Might that complicate decompression by creating more bubbles in the blood stream over a shorter span of time, preventing the body from being allowed to sufficiently purge already accumilated N2 fast enough to prevent DCS?
Now, I know that we use compartment half times to determine the amount of N2 accumilation in our bodies and use that to determine an appropriate decompression schedule. However, the human body being what it is, as I know it, rarely ever has just one factor controlling any one phenomenon so I wonder if it possible that the surface are of the vessel affects the rate of bubble formation in any way and if so, just how much? Could using a vasodilator aid in decompression or is it more likely to be problematic?
Vica versa, how might a vasoconstriction, from whatever source, affect ones decompression?
You brought another question to mind, doc. Does the type of vasodilator/vasoconstrictor really matter? Do the various ones work in very different manners?
My train of thought was that the vasodilator might dilate the vessels, creating a more open passage through which the blood could flow around the bubbles, resulting in more efficient circulation and safer decomression. The antoginist in me took over and said, "What if bubble formation is more dependant on the surface area of the blood vessel than we realize?"; the greater surface area of a dilated vessel generating more bubbles? Might that complicate decompression by creating more bubbles in the blood stream over a shorter span of time, preventing the body from being allowed to sufficiently purge already accumilated N2 fast enough to prevent DCS?
Now, I know that we use compartment half times to determine the amount of N2 accumilation in our bodies and use that to determine an appropriate decompression schedule. However, the human body being what it is, as I know it, rarely ever has just one factor controlling any one phenomenon so I wonder if it possible that the surface are of the vessel affects the rate of bubble formation in any way and if so, just how much? Could using a vasodilator aid in decompression or is it more likely to be problematic?
Vica versa, how might a vasoconstriction, from whatever source, affect ones decompression?
You brought another question to mind, doc. Does the type of vasodilator/vasoconstrictor really matter? Do the various ones work in very different manners?
Kelly,
I don't think much work has been done on this. One consideration is that some vasodilators could increase cerebral blood flow and thus increase risk for CNS oxygen toxicity. I don't know how bioavailable ingested nitric oxide is so I can't comment specifically on that, but endogenous (manufactured by the body) nitric oxide is a powerful vasodilator that has been linked to O2 toxicity.
Re vasodilation and vasoconstriction: If a diver was vasodilated during the dive and vasoconstricted on decompression, it could impair off-gasing. This could happen if the diver performed heavy work on the bottom but was cold on ascent. On the other hand, if the diver was vasoconstricted on the dive and vasodilated on ascent, it could potentially improve off-gasing.
I've never heard of bubble formation being linked directly to vessel size. Maybe Dr. Powell can address that.
Re different types of vasodilators and vasoconstrictors: I wasn't sure if you were referring to a specific medication. If you were wondering what decompression benefits a beta blocker would have, for example, I'd have asked you why you were on a beta blocker in the first place.
Hope this helps provide some insight.
Best regards,
DDM
I don't think much work has been done on this. One consideration is that some vasodilators could increase cerebral blood flow and thus increase risk for CNS oxygen toxicity. I don't know how bioavailable ingested nitric oxide is so I can't comment specifically on that, but endogenous (manufactured by the body) nitric oxide is a powerful vasodilator that has been linked to O2 toxicity.
Re vasodilation and vasoconstriction: If a diver was vasodilated during the dive and vasoconstricted on decompression, it could impair off-gasing. This could happen if the diver performed heavy work on the bottom but was cold on ascent. On the other hand, if the diver was vasoconstricted on the dive and vasodilated on ascent, it could potentially improve off-gasing.
I've never heard of bubble formation being linked directly to vessel size. Maybe Dr. Powell can address that.
Re different types of vasodilators and vasoconstrictors: I wasn't sure if you were referring to a specific medication. If you were wondering what decompression benefits a beta blocker would have, for example, I'd have asked you why you were on a beta blocker in the first place.
Hope this helps provide some insight.
Best regards,
DDM
OP
Thanks. It gave me a direction to look. I was thinking about this as I learned about decompresson and offgasing and now I see a possibility to create longer, safer dive profiles. As far as the constriction during bottom time and dilation in deco, or vice versa, I was thinking about the feasability of supplementing with inhaled NO at the start of deco, according to permissible ppNO2 levels, but not constricting during bottom time; but since I'm brainstorming on this I should consider the constrction then dilation angle also. I found this on the AMAs site. I copied the pertinent paragraphs below all this: Inhaled Nitric Oxide . It looks like low doses (<1.4 ppNO2) of inhaled NO could increase offgasing and lower deco times but, like everything else, it works in gradients so an NO table would be required to manage it's use safely after testing proved it's safety and efficacy, of course. What that equates to in a cf/min rate, I dont know how to figure. Any insight on that?
[h=3]Toxicity and Side Effects of Inhaled NO[/h]Inhalation of low levels of NO appears to be safe. The major clinical toxicity is due to the formation of NO2 and methemoglobinemia. A review of the toxicology of inhaled NO has recently been published.67
[h=4]Nitrogen Dioxide and Methemoglobinemia[/h]Formation of NO2 during NO breathing is dependent on the NO concentration, inspiratory oxygen concentration (Fio2), and residence time of these gases.68 Increased airway reactivity has been reported in humans after exposures to as low as 1.5 ppm NO2.69 At higher inhaled NO2 doses, pulmonary edema is the major toxicological effect70 and can result in death.71 In a simulation using a model lung and commercially available ventilators, production of NO2 during NO inhalation at 20 ppm appears to be minimal (<0.7 ppm) even with an Fio2 of 95%.72
Inhaled NO can combine with Hb to form nitrosylhemoglobin, which is rapidly oxidized to metHb. The rates of uptake and release of NO from ferrous (Fe2+) Hb are 105- to 106-fold greater than those of oxygen. Tissue hypoxia can be produced at excessive circulating metHb concentrations.67 The enzyme metHb reductase rapidly converts metHb to Hb in the red blood cell.
Blood metHb concentrations and inspired NO2 concentrations are frequently monitored during clinical administration of inhaled NO. Significant methemoglobinemia or NO2 formation is uncommon in patients breathing NO at doses ≤80 ppm (see review by Steudel et al73).
[h=3]Toxicity and Side Effects of Inhaled NO[/h]Inhalation of low levels of NO appears to be safe. The major clinical toxicity is due to the formation of NO2 and methemoglobinemia. A review of the toxicology of inhaled NO has recently been published.67
[h=4]Nitrogen Dioxide and Methemoglobinemia[/h]Formation of NO2 during NO breathing is dependent on the NO concentration, inspiratory oxygen concentration (Fio2), and residence time of these gases.68 Increased airway reactivity has been reported in humans after exposures to as low as 1.5 ppm NO2.69 At higher inhaled NO2 doses, pulmonary edema is the major toxicological effect70 and can result in death.71 In a simulation using a model lung and commercially available ventilators, production of NO2 during NO inhalation at 20 ppm appears to be minimal (<0.7 ppm) even with an Fio2 of 95%.72
Inhaled NO can combine with Hb to form nitrosylhemoglobin, which is rapidly oxidized to metHb. The rates of uptake and release of NO from ferrous (Fe2+) Hb are 105- to 106-fold greater than those of oxygen. Tissue hypoxia can be produced at excessive circulating metHb concentrations.67 The enzyme metHb reductase rapidly converts metHb to Hb in the red blood cell.
Blood metHb concentrations and inspired NO2 concentrations are frequently monitored during clinical administration of inhaled NO. Significant methemoglobinemia or NO2 formation is uncommon in patients breathing NO at doses ≤80 ppm (see review by Steudel et al73).
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Weinberger B, Laskin DL, Heck DE, et al. The toxicology of inhaled nitric oxide. Toxicol Sci. 2001;59: 5–16.
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- ↵ Sokol GM, Van Meurs KP, Wright LL, et al. Nitrogen dioxide formation during inhaled nitric oxide therapy. Clin Chem. 1999;45: 382–387.
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- ↵ Frampton MW, Morrow PE, Cox C, et al. Effects of nitrogen dioxide exposure on pulmonary function and airway reactivity in normal humans. Am Rev Respir Dis. 1991;143: 522–527.
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Kelly,
That's an interesting idea and would make a great animal study. Inhaled nitric oxide does not typically affect cerebral blood flow but I'd want to see if it did anything under hyperoxic conditions.
Best,
DDM
That's an interesting idea and would make a great animal study. Inhaled nitric oxide does not typically affect cerebral blood flow but I'd want to see if it did anything under hyperoxic conditions.
Best,
DDM
OP
Thanks for your input Doc. Now I need to find a good dive testing facility to convince to test this theory, lol. Wish me luck.
Interesting thread. I'm trying to pin down one of our nitric oxide experts, Dr. Claude Piantadosi, but he warps in and out of here pretty quickly. I'll post again after I talk to him.
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