It has a direct relaxing effect on vascular smooth muscle, reducing external resistance and lowering blood pressure. It has an antispasmodic effect on gastrointestinal smooth muscle.

The mechanism of inhibiting the central nervous system has not been clearly elucidated, but it may be due to indirectly reducing the irritability of the brainstem reticular activating system. In addition, it also has an anti-motion sickness effect.

This product is a compound antihypertensive drug. Dibazole has a direct relaxing effect on vascular smooth muscle, which reduces external resistance and lowers blood pressure. It has an antispasmodic effect on gastrointestinal smooth muscle. Reserpine achieves antihypertensive, heart rate slowing and central nervous system inhibition by depleting norepinephrine in peripheral sympathetic nerve endings, and depleting catecholamines and 5-hydroxytryptamine storage in the heart, brain and other tissues. The antihypertensive effect is mainly achieved by reducing cardiac output and peripheral resistance, and partially inhibiting cardiovascular reflexes. The effect of slowing the heart rate is not obvious for people with normal heart rate, but it is obvious for those with sinus tachycardia. Reserpine acts on the hypothalamus to produce a sedative effect, but it does not cause drowsiness and anesthetic effects, does not change the electroencephalogram during sleep, and can relieve anxiety, tension and headaches in hypertensive patients. In the early stage after the administration of hydrochlorothiazide, the volume of plasma and extracellular fluid is reduced, blood volume and cardiac output are reduced through diuresis and sodium excretion, thus reducing blood pressure; when the drug is administered for a long time, blood volume and cardiac output can return to their original levels, but the total peripheral vascular resistance is reduced and blood pressure can still be reduced. Guanidine sulfate selectively acts on the adrenergic nerve endings after the sympathetic nerves, causing the norepinephrine stored in the nerve endings to be slowly replaced by this product and released. The norepinephrine that should be in the nerve endings and tissues is depleted and missing. This product can also prevent the normal release of norepinephrine during nerve stimulation, weaken the vasoconstriction effect, especially when the sympathetic nerves are sluggish in response when the body position changes, and the excitement that should be reduced, thereby lowering blood pressure. The mechanism by which promethazine hydrochloride inhibits the central nervous system has not yet been clearly elucidated, but it may be due to indirectly reducing the irritability of the brainstem reticular activation system. In addition, it also has an anti-motion sickness effect. The mechanism of action of chlordiazepoxide is related to its selective action on the limbic system of the brain, binding to the central benzodiazepine receptors to promote the release of r-aminobutyric acid and promote synaptic conduction function. This product also has central muscle relaxant and anticonvulsant effects. It has antianxiety effects at low doses. As the dose increases, it can show sedation, hypnosis, and memory impairment. Potassium chloride and calcium lactate in the compound are used to supplement potassium and calcium. Magnesium trisilicate has a mild laxative effect. Non-clinical acute toxicity test: LD50 = 10.525g/kg. (Feiller correction) 95% confidence limit = 9.5731-11.592g/kg.

It selectively acts on the postganglionic adrenergic nerve endings of the sympathetic nerves, causing the norepinephrine stored in the nerve endings to be slowly replaced by this product and released. This causes the necessary norepinephrine in the nerve endings and tissues to be depleted and lost. It can also prevent the normal release of norepinephrine during nerve stimulation, weakening the vasoconstriction effect, especially when the body position changes, the sympathetic nerves react slowly, and the necessary excitement is weakened, thereby lowering blood pressure.

This product is a compound antihypertensive drug. Dibazole has a direct relaxing effect on vascular smooth muscle, which reduces external resistance and lowers blood pressure. It has an antispasmodic effect on gastrointestinal smooth muscle. Reserpine achieves antihypertensive, heart rate slowing and central nervous system inhibition by depleting norepinephrine in peripheral sympathetic nerve endings, and depleting catecholamines and 5-hydroxytryptamine storage in the heart, brain and other tissues. The antihypertensive effect is mainly achieved by reducing cardiac output and peripheral resistance, and partially inhibiting cardiovascular reflexes. The effect of slowing the heart rate is not obvious for people with normal heart rate, but it is obvious for those with sinus tachycardia. Reserpine acts on the hypothalamus to produce a sedative effect, but it does not cause drowsiness and anesthetic effects, does not change the electroencephalogram during sleep, and can relieve anxiety, tension and headaches in hypertensive patients. In the early stage after the administration of hydrochlorothiazide, the volume of plasma and extracellular fluid is reduced, blood volume and cardiac output are reduced through diuresis and sodium excretion, thus reducing blood pressure; when the drug is administered for a long time, blood volume and cardiac output can return to their original levels, but the total peripheral vascular resistance is reduced and blood pressure can still be reduced. Guanidine sulfate selectively acts on the adrenergic nerve endings after the sympathetic nerves, causing the norepinephrine stored in the nerve endings to be slowly replaced by this product and released. The norepinephrine that should be in the nerve endings and tissues is depleted and missing. This product can also prevent the normal release of norepinephrine during nerve stimulation, weaken the vasoconstriction effect, especially when the sympathetic nerves are sluggish in response when the body position changes, and the excitement that should be reduced, thereby lowering blood pressure. The mechanism by which promethazine hydrochloride inhibits the central nervous system has not yet been clearly elucidated, but it may be due to indirectly reducing the irritability of the brainstem reticular activation system. In addition, it also has an anti-motion sickness effect. The mechanism of action of chlordiazepoxide is related to its selective action on the limbic system of the brain, binding to the central benzodiazepine receptors to promote the release of r-aminobutyric acid and promote synaptic conduction function. This product also has central muscle relaxant and anticonvulsant effects. It has antianxiety effects at low doses. As the dose increases, it can show sedation, hypnosis, and memory impairment. Potassium chloride and calcium lactate in the compound are used to supplement potassium and calcium. Magnesium trisilicate has a mild laxative effect. Non-clinical acute toxicity test: LD50 = 10.525g/kg. (Feiller correction) 95% confidence limit = 9.5731-11.592g/kg.

Supplement potassium.

By depleting norepinephrine in peripheral sympathetic nerve endings, the catecholamine and 5-hydroxytryptamine storage in the heart, brain and other tissues are depleted to achieve the effects of anti-hypertension, slowing heart rate and inhibiting the central nervous system. The antihypertensive effect is mainly achieved by reducing cardiac output and peripheral resistance, and partially inhibiting cardiovascular reflexes. It can relieve anxiety, tension and headaches in hypertensive patients.

The mechanism of action is related to its selective action on the limbic system of the brain, binding to the central benzodiazepine receptors to promote the release of r-aminobutyric acid and promote synaptic conduction function. It also has central muscle relaxant and anticonvulsant effects, antianxiety effects at low doses, and sedation, hypnosis, and memory impairment as the dose increases.

By excreting sodium through diuresis, the volume of plasma and extracellular fluid is reduced, blood volume and cardiac output are reduced, and thus blood pressure is lowered; when the drug is administered for a long time, total peripheral vascular resistance is reduced and blood pressure can still be lowered.

Supplement calcium.

This product is a compound antihypertensive drug. Dibazole has a direct relaxing effect on vascular smooth muscle, which reduces external resistance and lowers blood pressure. It has an antispasmodic effect on gastrointestinal smooth muscle. Reserpine achieves antihypertensive, heart rate slowing and central nervous system inhibition by depleting norepinephrine in peripheral sympathetic nerve endings, and depleting catecholamines and 5-hydroxytryptamine storage in the heart, brain and other tissues. The antihypertensive effect is mainly achieved by reducing cardiac output and peripheral resistance, and partially inhibiting cardiovascular reflexes. The effect of slowing the heart rate is not obvious for people with normal heart rate, but it is obvious for those with sinus tachycardia. Reserpine acts on the hypothalamus to produce a sedative effect, but it does not cause drowsiness and anesthetic effects, does not change the electroencephalogram during sleep, and can relieve anxiety, tension and headaches in hypertensive patients. In the early stage after the administration of hydrochlorothiazide, the volume of plasma and extracellular fluid is reduced, blood volume and cardiac output are reduced through diuresis and sodium excretion, thus reducing blood pressure; when the drug is administered for a long time, blood volume and cardiac output can return to their original levels, but the total peripheral vascular resistance is reduced and blood pressure can still be reduced. Guanidine sulfate selectively acts on the adrenergic nerve endings after the sympathetic nerves, causing the norepinephrine stored in the nerve endings to be slowly replaced by this product and released. The norepinephrine that should be in the nerve endings and tissues is depleted and missing. This product can also prevent the normal release of norepinephrine during nerve stimulation, weaken the vasoconstriction effect, especially when the sympathetic nerves are sluggish in response when the body position changes, and the excitement that should be reduced, thereby lowering blood pressure. The mechanism by which promethazine hydrochloride inhibits the central nervous system has not yet been clearly elucidated, but it may be due to indirectly reducing the irritability of the brainstem reticular activation system. In addition, it also has an anti-motion sickness effect. The mechanism of action of chlordiazepoxide is related to its selective action on the limbic system of the brain, binding to the central benzodiazepine receptors to promote the release of r-aminobutyric acid and promote synaptic conduction function. This product also has central muscle relaxant and anticonvulsant effects. It has antianxiety effects at low doses. As the dose increases, it can show sedation, hypnosis, and memory impairment. Potassium chloride and calcium lactate in the compound are used to supplement potassium and calcium. Magnesium trisilicate has a mild laxative effect. Non-clinical acute toxicity test: LD50 = 10.525g/kg. (Feiller correction) 95% confidence limit = 9.5731-11.592g/kg.

Has a mild laxative effect.

Counteracts the decrease in peripheral leukocytes in mice caused by common anti-tumor drugs and 60Co-Y-ray irradiation; improves immune function; increases the percentage of peritoneal macrophages and hemolysis value in mice; increases the hemoglobin and red blood cell count in bleeding mice; reduces the wet weight of tumors in S180 mice

Counteracts the decrease in peripheral leukocytes in mice caused by common anti-tumor drugs and 60Co-Y-ray irradiation; improves immune function; increases the percentage of peritoneal macrophages and hemolysis value in mice; increases the hemoglobin and red blood cell count in bleeding mice; reduces the wet weight of tumors in S180 mice

Counteracts the decrease in peripheral leukocytes in mice caused by common anti-tumor drugs and 60Co-Y-ray irradiation; improves immune function; increases the percentage of peritoneal macrophages and hemolysis value in mice; increases the hemoglobin and red blood cell count in bleeding mice; reduces the wet weight of tumors in S180 mice

Counteracts the decrease in peripheral leukocytes in mice caused by common anti-tumor drugs and 60Co-Y-ray irradiation; improves immune function; increases the percentage of peritoneal macrophages and hemolysis value in mice; increases the hemoglobin and red blood cell count in bleeding mice; reduces the wet weight of tumors in S180 mice

Counteracts the decrease in peripheral leukocytes in mice caused by common anti-tumor drugs and 60Co-Y-ray irradiation; improves immune function; increases the percentage of peritoneal macrophages and hemolysis value in mice; increases the hemoglobin and red blood cell count in bleeding mice; reduces the wet weight of tumors in S180 mice

Counteracts the decrease in peripheral leukocytes in mice caused by common anti-tumor drugs and 60Co-Y-ray irradiation; improves immune function; increases the percentage of peritoneal macrophages and hemolysis value in mice; increases the hemoglobin and red blood cell count in bleeding mice; reduces the wet weight of tumors in S180 mice

Counteracts the decrease in peripheral leukocytes in mice caused by common anti-tumor drugs and 60Co-Y-ray irradiation; improves immune function; increases the percentage of peritoneal macrophages and hemolysis value in mice; increases the hemoglobin and red blood cell count in bleeding mice; reduces the wet weight of tumors in S180 mice