In the course of feeding cows, urea is often added as a protein supplement feed for ruminants, and the cost is low. However, if it is fed improperly, it will cause poisoning and it needs to attract the attention of a large number of farmers. First of all, the amount of urea is generally controlled below 1% of dry matter or below 3% of concentrate.
The use of urea is affected by many factors. Low protein diets and hunger can reduce cow's tolerance to urea. When urease-enriched feed and urea are fed at the same time, urease in the rumen can promote the decomposition of urea to produce more ammonia, which can easily cause cow poisoning.
35% of bacteria in the rumen of cows produce urease, and rumen bacteria can hydrolyze urea to CO2 and NH3 by urease. When the rumen pH is at 8, the activity of urease is the most vigorous, which can decompose a large amount of urea in a short time. Its decomposition products are then absorbed through the stomach wall and enter the liver where it is converted to urea by an ornithine cycle or combined with a-ketoglutarate to form glutamate and glutamine. The ammonia that enters the liver exceeds the detoxification capacity of the liver and enters the peripheral blood circulation along the portal vein. When the ammonia in the peripheral blood exceeds the normal level, symptoms of poisoning appear. Therefore, the severity of poisoning is closely related to the concentration of ammonia in the blood. Ammonia in the peripheral blood can directly act on the cardiovascular system, increasing capillary permeability and increasing body fluid loss, blood concentration, and death due to the toxic effects of blood nitrogen on the heart.
The symptoms of poisoning occur sooner or later with the amount of urea ingested. After eating intoxicated amount of urea, cows develop symptoms from 30 minutes to 60 minutes. At first, they showed depression and sluggishness. Then they showed anxiety and photosensitivity. They stopped twitching and rumination stopped. Drums, muscle twitching, unsteady gait, repeated The occurrence of ankylosing cramps, difficulty in breathing, rapid pulse, sweating, runny nose, late-stage sickness fell to the ground, and swim-like movements of the extremities, often due to suffocation.
There were no characteristic changes after dissection, and some showed only mild pulmonary edema, hyperemia and ecchymosis. The contents of the rumen have ammonia odor, mouth and nose filled with foamy liquids, and some can be seen systemic venous congestion, organ congestion, severe pulmonary edema, pleural effusion, pericardial accumulation of water, liver, kidney steatosis, and some endocardium And epicardial hemorrhage.
Urea poisoning without specific treatment, symptomatic treatment can be used. However, urea was stopped immediately after symptoms of poisoning were found, and gastric lavage or laxatives may be used at the beginning of the illness. Oral consumption of acetic acid in rumen content has a good effect. Oral antibiotics inhibit rumen bacteria and reduce ammonia production.
Strengthen the management of urea, regularly and quantitatively match feed additives, and do not dissolve urea in water to allow large amounts of cows to drink.
The use of urea is affected by many factors. Low protein diets and hunger can reduce cow's tolerance to urea. When urease-enriched feed and urea are fed at the same time, urease in the rumen can promote the decomposition of urea to produce more ammonia, which can easily cause cow poisoning.
35% of bacteria in the rumen of cows produce urease, and rumen bacteria can hydrolyze urea to CO2 and NH3 by urease. When the rumen pH is at 8, the activity of urease is the most vigorous, which can decompose a large amount of urea in a short time. Its decomposition products are then absorbed through the stomach wall and enter the liver where it is converted to urea by an ornithine cycle or combined with a-ketoglutarate to form glutamate and glutamine. The ammonia that enters the liver exceeds the detoxification capacity of the liver and enters the peripheral blood circulation along the portal vein. When the ammonia in the peripheral blood exceeds the normal level, symptoms of poisoning appear. Therefore, the severity of poisoning is closely related to the concentration of ammonia in the blood. Ammonia in the peripheral blood can directly act on the cardiovascular system, increasing capillary permeability and increasing body fluid loss, blood concentration, and death due to the toxic effects of blood nitrogen on the heart.
The symptoms of poisoning occur sooner or later with the amount of urea ingested. After eating intoxicated amount of urea, cows develop symptoms from 30 minutes to 60 minutes. At first, they showed depression and sluggishness. Then they showed anxiety and photosensitivity. They stopped twitching and rumination stopped. Drums, muscle twitching, unsteady gait, repeated The occurrence of ankylosing cramps, difficulty in breathing, rapid pulse, sweating, runny nose, late-stage sickness fell to the ground, and swim-like movements of the extremities, often due to suffocation.
There were no characteristic changes after dissection, and some showed only mild pulmonary edema, hyperemia and ecchymosis. The contents of the rumen have ammonia odor, mouth and nose filled with foamy liquids, and some can be seen systemic venous congestion, organ congestion, severe pulmonary edema, pleural effusion, pericardial accumulation of water, liver, kidney steatosis, and some endocardium And epicardial hemorrhage.
Urea poisoning without specific treatment, symptomatic treatment can be used. However, urea was stopped immediately after symptoms of poisoning were found, and gastric lavage or laxatives may be used at the beginning of the illness. Oral consumption of acetic acid in rumen content has a good effect. Oral antibiotics inhibit rumen bacteria and reduce ammonia production.
Strengthen the management of urea, regularly and quantitatively match feed additives, and do not dissolve urea in water to allow large amounts of cows to drink.
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