CSPC OUYI Pharmaceutical Co., Ltd.

This product is a macrolide antibiotic, and its mechanism of action and antibacterial spectrum are similar to those of erythromycin, but it has a stronger antibacterial effect on Gram-positive bacteria, and is effective against Staphylococcus, hemolytic Streptococcus, Pneumococcus, Diphtheria Corynebacterium, Tetanus Corynebacterium, and Anthrax Corynebacterium. It also has antibacterial effects on Gram-negative bacteria such as gonococci and pertussis Bordetella. Some erythromycin-resistant Staphylococcus aureus are still sensitive to kitasamycin, and it is also quite active against Leptospira, Rickettsia, and Mycoplasma.

This product is a brain metabolism improving drug, a derivative of vitamin B6, which can promote glucose and amino acid metabolism in the brain, improve systemic assimilation, increase carotid blood flow, and enhance brain function. It also has a certain effect on the limbic system and reticular structure.

This product is a fluoroquinolone antibacterial drug with a broad-spectrum antibacterial effect, especially against aerobic Gram-negative bacteria. It acts on the A subunit of bacterial DNA helicase, inhibits DNA synthesis and replication, and causes bacterial death. It has effects on both Gram-positive and Gram-negative bacteria. Bacteria are not easy to develop resistance to this product, and there is no cross-resistance between similar drugs and antibiotics.

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 the 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. The effect of slowing heart rate is not obvious in people with normal heart rate, but it is obvious in people with sinus tachycardia. It acts on the hypothalamus to produce a sedative effect, but does not cause drowsiness and anesthesia. It does not change the electroencephalogram during sleep, and can relieve anxiety, tension and headaches in patients with hypertension.

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.

In the early stage after medication, diuresis and sodium excretion reduce the volume of plasma and extracellular fluid, blood volume and cardiac output, and thus blood pressure. When the drug is administered for a long time, blood volume and cardiac output can return to their original levels, but total peripheral vascular resistance decreases 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.