Baxter Healthcare( Shanghai) Co., Ltd.

It produces direct pharmacological effects through hypertonic dehydration, eliminating cerebral edema and reducing intracranial pressure; it has an osmotic diuretic effect; it has a tissue dehydration effect, increasing plasma osmotic pressure to reduce tissue edema; it has a diuretic effect, increasing the osmotic concentration of the renal tubular fluid and reducing reabsorption.

Hypertonic dehydration produces direct pharmacological effects, eliminating brain edema, reducing brain water content, and lowering intracranial pressure; tissue dehydration and diuresis. 1g of mannitol can produce an osmotic concentration of 5.5mOsm, and injection of 100g of mannitol can transfer 2000ml of intracellular water to the extracellular space, and excrete 50g of urinary sodium.

Mannitol injection is a hypertonic preparation. It produces direct pharmacological effects through hypertonic dehydration, eliminates brain edema, reduces brain water content, and reduces intracranial pressure. 1g of mannitol can produce an osmotic concentration of 5.5mOsm. Injection of 100g of mannitol can transfer 2000ml of intracellular water to the extracellular space and excrete 50g of urinary sodium. Tissue dehydration effect: Increases plasma osmotic pressure, causing water in tissues (including eyes, brain, cerebrospinal fluid, etc.) to enter blood vessels, thereby reducing tissue edema, reducing intraocular pressure, intracranial pressure, and cerebrospinal fluid volume and pressure. Diuretic effect: Increases blood volume and promotes the secretion of prostaglandin I2, dilates renal blood vessels, increases renal blood flow, increases the osmotic concentration of renal tubular fluid, and reduces the reabsorption of water and Na, Cl-, K, Ca2, Mg2 and other solutes by the renal tubules.

The final metabolite is sodium bicarbonate, which can correct metabolic acidosis; when hyperkalemia is accompanied by acidosis, it can correct acidosis and allow potassium ions to enter the cells from the blood and extracellular fluid.

Under normal circumstances, human blood also contains a small amount of lactic acid, which is mainly produced by glucose or glycogenolysis, and comes from muscles, skin, brain and cells. After lactic acid is produced, it may be converted into glycogen or acetic acid, or enter the tricarboxylic acid cycle and be decomposed into water and carbon dioxide. Therefore, the final metabolite of sodium lactate is sodium bicarbonate, which can correct metabolic acidosis. When hyperkalemia is accompanied by acidosis, sodium lactate can correct acidosis and allow potassium ions to enter cells from blood and extracellular fluid. The main organs that degrade lactic acid are liver and kidney. When lactic acid metabolism in the body is abnormal or impaired, the therapeutic effect is poor.

When hyperkalemia is accompanied by acidosis, sodium lactate can cause potassium ions to enter cells from the blood and extracellular fluid.

Under normal circumstances, human blood also contains a small amount of lactic acid, which is mainly produced by glucose or glycogenolysis, and comes from muscles, skin, brain and cells. After lactic acid is produced, it may be converted into glycogen or acetic acid, or enter the tricarboxylic acid cycle and be decomposed into water and carbon dioxide. Therefore, the final metabolite of sodium lactate is sodium bicarbonate, which can correct metabolic acidosis. When hyperkalemia is accompanied by acidosis, sodium lactate can correct acidosis and allow potassium ions to enter cells from blood and extracellular fluid. The main organs that degrade lactic acid are liver and kidney. When lactic acid metabolism in the body is abnormal or impaired, the therapeutic effect is poor.

The final metabolite is sodium bicarbonate, which can correct metabolic acidosis; when hyperkalemia is accompanied by acidosis, it can correct acidosis and allow potassium ions to enter the cells from the blood and extracellular fluid.

Under normal circumstances, human blood also contains a small amount of lactic acid, which is mainly produced by glucose or glycogenolysis, and comes from muscles, skin, brain and cells. After lactic acid is produced, it may be converted into glycogen or acetic acid, or enter the tricarboxylic acid cycle and be decomposed into water and carbon dioxide. Therefore, the final metabolite of sodium lactate is sodium bicarbonate, which can correct metabolic acidosis. When hyperkalemia is accompanied by acidosis, sodium lactate can correct acidosis and allow potassium ions to enter cells from blood and extracellular fluid. The main organs that degrade lactic acid are liver and kidney. When lactic acid metabolism in the body is abnormal or impaired, the therapeutic effect is poor.

When hyperkalemia is accompanied by acidosis, sodium lactate can cause potassium ions to enter cells from the blood and extracellular fluid.

Under normal circumstances, human blood also contains a small amount of lactic acid, which is mainly produced by glucose or glycogenolysis, and comes from muscles, skin, brain and cells. After lactic acid is produced, it may be converted into glycogen or acetic acid, or enter the tricarboxylic acid cycle and be decomposed into water and carbon dioxide. Therefore, the final metabolite of sodium lactate is sodium bicarbonate, which can correct metabolic acidosis. When hyperkalemia is accompanied by acidosis, sodium lactate can correct acidosis and allow potassium ions to enter cells from blood and extracellular fluid. The main organs that degrade lactic acid are liver and kidney. When lactic acid metabolism in the body is abnormal or impaired, the therapeutic effect is poor.