Dear All,
Few years ago, I proposed that ruminal acidosis was produced by the accumulation of dissolved carbon dioxide in the rumen a phenomenon known as CO2 holdup.
pH is not a cause of disease. The ionisation of water molecules measured by the pH sensor is a consequence of the increase in dissociated molecules or acids. The main acid in rumen is disolved carbon dioxide, a liquid, it does not increase the partial pressure of CO2 in the rumen (CO2 is a gas). The accumulation of dCO2 creates a large gradient of concentration that will lead to the increase in CO2 absorption and the development of metabolic acidosis.
Lactic acidosis is caused by the increase in blood bicarbonate, product of the dCO2 absorption (blood is dominated by bases, higher pH). Bicarbonate is highly toxic and the peripheral tissue will exchange HCO3- by lactate to improve oxygenation.
In this way, lactate increases in blood and bicarbonate is stored (temporarily) in the cells. The importance of this mechanism is that lactate will provide protons H3O+ for CO2 exchange in the lungs, as Bicarbonate is already high. This is my opinion, of course.
Ruminal acidosis is product of CO2 poisoning. dCO2 concentrations over 80 mmol/l will increase the risk of ruminal acidosis.
Article The role of dissolved carbon dioxide in both the decline in ...
What is your opinion?
I think it's worth looking at the gaseous portion of CO2 in addition to changes in pH of the ingesta. I'm a clinically oriented veterinarian. Ruminal bloat is externally visible in the paralumbar fossa. I propose that stretching of the ruminal wall is a problem on its own, as we see in horses with tympanic forms of colic. When the wall of a hollow viscus is distended by gas, its myoenteric activity is disturbed. So, aside from the biochemistry of ruminal acidosis, there is abnormal motility in the upper GI tract. It's also a source of pain, which separately intereferes with gut motility and biochemistry.
Many thanks for your reply. Yes indeed, the pCO2(%) will increase during bloat, however is the stable foam formed during bloat that impeded gas which will lead to tympanism.
foam formation is the counterpart to Co2 holdup in the liquid.
How to explain CO2 holdup?
A very simple example of CO2 holdup is to observe the evolution of CO2 bubbles on a glass of carbonated water. The CO2 gas bubbles are big and quickly leave the solution. If you add dishwasher soap to another similar glass of carbonated water and gently stir, you will see the change in behaviour of the CO2 bubbles: the bubbles become smaller and leave slowly the solution.
The addition of soap simulates the effect of feed components on the physicochemical properties of the rumen fluid. The CO2 gas volatility is reduced and because the CO2 formation in the rumen has not stopped, larger than expected dissolved CO2 concentrations can be found within the liquid. For instance, if we leave the glasses on a bench for a while, the carbonated glass without soap will go ‘flat’ sooner than the carbonated water glass with soap, the latter retains dCO2 for longer.
Now, please add salt(bicarbonate) to both glasses. You could also add citric acid, or any other substrate which enhances bubbles formation, i.e., a coin. The first glass without soap will “fizzles”, the addition of salt provides more substrate for bubbles formation (nucleation), but because there is no change in volatility, the CO2 gas escapes easily. Water behaves as an ideal solution, the equilibrium between gas and liquid is linear (Henry’s law).
The addition of salt to the second glass of carbonated water with soap will create stable foam. This is the behaviour on a non-ideal solution (Raoul’s Law). The CO2 cannot easily escape and the fast formation of bubbles will generate stable foam. This is the mechanism of bloat and abomasal dysplasia in ruminants. Once CO2 holdup is established and if the physicochemical properties of the fluid are disturbed; i.e., changes in temperature, ionic strength or acid addition in the abomasum, will lead to the fast release of the CO2 gas and tympanism (Waghorn 1991; Laporte-Uribe 2016).
If conditions remain constant and CO2 holdup is not disturbed, the large dCO2 gradient between the liquid and the blood for extended postprandial periods with the increase risk of CO2 poisoning or ruminal acidosis. Moreover, high dCO2 will also increase the osmotic pressure of the rumen fluid. Hyperosmolarity does explain the effect on motility and water secretion into de rumen during acidosis, as discussed elsewhere (i.e. Lodemann, U. and H. Martens. 2006).
I would like to expand a little my explanation in regards to the partial pressure of CO2 (ppCO2, %) vs the dissolved carbon dioxide (dCO2, mM) concentrations.
The intraruminal pressure is kept fairly constant due to eructation ~1 atm. If Co2 holdup develop the increase in ruminal dCO2 will not affect the intraruminal pressure (dCO2 is a liquid not a gas).
In fact, look at Graphic 2 in Laporte-Uribe (2016) were I used the information from Moate et al. (1997) from healthy and bloated cattle. I did include a explanation of this phenomenon, in a earlier document.
https://www.researchgate.net/project/Wireless-ruminal-sensor-to-improve-feed-conversion-efficiency/update/60d087ff6b95310001558b1d
As you can see, the ppCO2 might remain between 60 to 80% even during bloat, whereas ROE (an indirect method of measuring dCO2) can range from 0 to 120 mM (on that experiment). In fact, CO2 holdup can lead to ruminal dCO2 concentrations of 200 mM for extended postprandial periods with the increase risk of CO2 poisoning or ruminal acidosis.
Those concentrations can only be seeing if direct sampling methods of dCO2 monitoring are applied, such as the ATR sensor that I just described, indirect sampling methods will not work.
https://www.researchgate.net/publication/350373592_Apparatus_for_monitoring_nutrition_especially_fermentation_In_the_rumen_of_a_ruminant_PCTEP2020086850
Read my latest contribution to the topic.
Article CO2 holdup monitoring, ruminal acidosis might be caused by C...