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To protect the ischemic brain tissue, nicardipine is not just talking.
Brain tissue ischemia can cause rapid transfer of calcium ions from extracellular to intracellular and directly activate the common pathway of cell death to cause cell death.
The increase in cellular calcium ion concentration can degrade phospholipids and release free fatty acids by activating membrane phospholipases.
Among them, prostaglandins and leukotrienes, which are further metabolized by arachidonic acid, can further damage cell membranes and lead to a vicious cycle.
Therefore, preventing calcium ions from entering cells is considered to be a method of treating cell damage caused by cerebral ischemia.
As a powerful dihydropyridine calcium channel blocker (CCB) that lowers blood pressure and can effectively prevent vasospasm in ischemic areas, nicardipine has been widely recognized by clinicians for many years of application experience.
As a CCB, can it reduce the influx of calcium ions to reduce the degree of cell damage in the cerebral ischemic area? As early as 1988, scientists from the New York University School of Medicine had already answered this question.
Let's take a look at this study.
This study included 21 male SD mice.
The ischemia model was constructed by surgically occluding the left middle cerebral artery.
The 21 SD rats were divided into 4 groups.
The first group of 7 mice was the experimental group.
The animals were given 1 mg/kg nicardipine hydrochloride physiological saline solution immediately after the left middle cerebral artery was blocked by intravenous infusion of 200 μl every 30 minutes.
Maintain for 4 hours.
The rats were sacrificed 6 hours later and the brain tissue calcium, sodium, potassium concentration and water content were analyzed; the second group of 6 mice served as the control group, and the animals were administrated with 200 μl of normal saline every 30 minutes within 4 hours after the ischemia model was established.
Drop once.
The rats were sacrificed 6 hours later, and the analysis items were the same as those in the first group; 5 mice in the third group were administered carbon-14 labeled nicardipine hydrochloride in the same manner as the first group after the model was established.
The rats were sacrificed 6 hours later and the brains were analyzed.
Within the drug distribution area; 3 mice in the fourth group did not undergo middle cerebral artery occlusion, but the content and method of analysis after administration and sacrifice were the same as those in the first group. The concentration of calcium, sodium, and potassium ions are measured by atomic absorption spectrometry, and the water content is quantified by measuring the difference between the wet weight of the brain tissue and the mass after drying.
Taking into account the individual differences between experimental animals, the changes in ions and water content of the left brain tissue of the same mouse were standardized by the untreated part of the right hemisphere.
In addition, the distribution of nicardipine was obtained from the third set of experimental results, and the units of tissue concentration and plasma concentration were ng/g and ng/ml, respectively.
Nicardipine can effectively reduce the cell damage in the hypoperfusion zone.
Table: Observing the changes of ions and water in the left cerebral hemisphere after the left middle cerebral artery occlusion.
It is not difficult to find that: After the ischemia model is established, intravenous nicardipine can significantly reduce Ion transfer in the infarct area, the changes of calcium, sodium and potassium ions in the infarct area in the nicardipine treatment group were significantly lower than those in the control group.
Since changes in tissue calcium, sodium, potassium ions and water reflect cell damage, it can be inferred that nicardipine has a protective effect on the infarct site.
In the exploration of the regional distribution of nicardipine, the experimental data showed that the uptake of nicardipine in the ischemic area was greater than the uptake of surrounding or normal cortical tissue, and the largest uptake occurred in the central area of the infarction, which indicated the ischemic area The limited blood flow can still allow the drug to reach the infarct site.
Scholars believe that the tissue protective effect of nicardipine is related to the hindrance of calcium ions from entering cells and the blocking of downstream arachidonic acid metabolic pathways.
TIME interactive time to avoid calcium overload and inhibit cell apoptosis.
Nicardipine effectively protects cells in hypoperfusion areas.
Ma Yawen, attending physician at the Department of Critical Care Medicine, Shengjing Hospital, China Medical University.
Nicardipine is a dihydropyridine calcium channel blocker , Has a good fat-soluble effect and low dissociation, can quickly distribute and dissolve in the ischemic cell membrane, reperfusion in the case of cerebral ischemia may damage the blood-brain barrier, nicardipine is beneficial to stabilize and repair blood The brain barrier promotes the metabolism of local parts of the brain.
The basic principle of nicardipine in the treatment of cerebral ischemia is to prevent myocardial and cerebral ischemia damage caused by reperfusion by reducing calcium overload in hypoperfused tissues, promote cell metabolism in ischemic tissues, and promote bcl-2 by dephosphorylation of phosphatase.
Quickly produce and promote the rise of bcl-2, and further inhibit cell apoptosis and protect brain cells. Depressing blood pressure, antispasmodic, and improving blood supply in ischemic areas.
Nicardipine has sufficient evidence.
Li Qingquan, Attending physician of neurosurgery at the Second Affiliated Hospital of Nanjing Medical University.
Nicardipine hydrochloride has a unique side chain structure-methylbenzylamino, which makes it possess The extremely strong lipid-water partition coefficient makes Nicardipine hydrochloride easier to penetrate the blood-brain barrier and enter the brain tissue than other drugs.
The unique side chain tertiary amino group of nicardipine hydrochloride easily binds to hydrogen ions and causes nicardipine hydrochloride to accumulate in the ischemic area, thereby improving the blood supply to the ischemic part of the brain tissue.
At the same time, the HINASH study proved that nicardipine hydrochloride has an antispasmodic effect and directly improves the prognosis of SAH patients.
Nicardipine hydrochloride injection is a dihydropyridine calcium antagonist, which reduces blood pressure only by dilating small and medium arteries, and it is not easy to cause excessive blood pressure, and it is safer to lower blood pressure.
Specific expansion of cerebrovascular, nicardipine provides more protection for ischemia-reperfusion injury, Gao Minnan, Sun Yat-sen University’s Sun Yat-sen Hospital, the chief physician of the Department of Cardiac Surgery Nicardipine has a specific expansion effect on cerebrovascular, increasing cerebral blood flow by relaxing vascular smooth muscle, It has a protective effect on ischemic and hypoxic brain tissue, and can prevent brain tissue damage caused by cerebral vasospasm during hypotension and postoperative period.
It has little effect on intracranial pressure.
Nicardipine has higher lipid solubility and lower negative logarithm of dissociation constant of acidic drugs, and is easily distributed on ischemic cell membranes.
It can improve tissue perfusion and metabolic disorders, inhibit calcium influx, reduce mitochondrial calcium overload, and restore The production of adenosine triphosphate reduces intracellular lactic acid poisoning and lowers intracellular pH, thereby reducing the occurrence of nerve cell apoptosis.
At the same time, it can also stabilize the blood-brain barrier and reduce local energy metabolism after ischemia, thereby protecting ischemic brain tissue and providing more protection for ischemia-reperfusion injury.
Sharing of clinical experience Zhang Xiangyang, Chief Physician of Beijing Tsinghua Chang Gung Memorial Hospital, has many indications and significant drug effects.
Nicardipine reduces blood pressure and protects target organs.
For patients with aortic dissection whose blood pressure control effect is not good, we can use β-blockers At the same time, nicardipine is used in combination to achieve the goal of rapid blood pressure reduction; for patients with hypertension caused by brain injury or cerebrovascular disease, nicardipine can also reduce blood pressure while maximizing protection of brain cells and brain function; in renal In the intervention of hypertension, nicardipine can effectively expand the arterioles in and out of the bulb, thereby improving refractory renal hypertension. Nicardipine has a moderate half-life and an ideal drug effect.
It is a commonly used antihypertensive drug in clinical practice.
Zhong Weixi, the attending physician in the emergency department of the Sixth People's Hospital of Shanghai Jiaotong University, was pumped to maintain after intravenous push.
Nicardipine usage is here.
Nicardipine is mostly used in clinical hypertensive emergencies.
The blood pressure drop can reach 30- after conventional 2mg intravenous push.
40mmHg.
Subsequently, we continue to pump 2-5mg/h, which can obtain a more effective and long-lasting antihypertensive effect, which is especially suitable for patients with subarachnoid hemorrhage.
Xuan Lizhen, the attending physician of the Department of Critical Care Medicine, Zhongshan Hospital, Fudan University, has a rapid blood pressure reduction and good curative effect.
Nicardipine is worthy of recommendation.
Clinically, patients with hypertension have a higher mortality rate and a more critical condition.
Intensified treatment is urgently needed.
Nicardipine can quickly and effectively lower blood pressure, it can take effect immediately, reach the peak blood concentration in 1 minute, and the 24-hour systolic blood pressure fluctuations are small.
It is recommended by domestic and foreign guidelines and is recommended for patients with hypertensive emergencies.
Brain tissue ischemia can cause rapid transfer of calcium ions from extracellular to intracellular and directly activate the common pathway of cell death to cause cell death.
The increase in cellular calcium ion concentration can degrade phospholipids and release free fatty acids by activating membrane phospholipases.
Among them, prostaglandins and leukotrienes, which are further metabolized by arachidonic acid, can further damage cell membranes and lead to a vicious cycle.
Therefore, preventing calcium ions from entering cells is considered to be a method of treating cell damage caused by cerebral ischemia.
As a powerful dihydropyridine calcium channel blocker (CCB) that lowers blood pressure and can effectively prevent vasospasm in ischemic areas, nicardipine has been widely recognized by clinicians for many years of application experience.
As a CCB, can it reduce the influx of calcium ions to reduce the degree of cell damage in the cerebral ischemic area? As early as 1988, scientists from the New York University School of Medicine had already answered this question.
Let's take a look at this study.
This study included 21 male SD mice.
The ischemia model was constructed by surgically occluding the left middle cerebral artery.
The 21 SD rats were divided into 4 groups.
The first group of 7 mice was the experimental group.
The animals were given 1 mg/kg nicardipine hydrochloride physiological saline solution immediately after the left middle cerebral artery was blocked by intravenous infusion of 200 μl every 30 minutes.
Maintain for 4 hours.
The rats were sacrificed 6 hours later and the brain tissue calcium, sodium, potassium concentration and water content were analyzed; the second group of 6 mice served as the control group, and the animals were administrated with 200 μl of normal saline every 30 minutes within 4 hours after the ischemia model was established.
Drop once.
The rats were sacrificed 6 hours later, and the analysis items were the same as those in the first group; 5 mice in the third group were administered carbon-14 labeled nicardipine hydrochloride in the same manner as the first group after the model was established.
The rats were sacrificed 6 hours later and the brains were analyzed.
Within the drug distribution area; 3 mice in the fourth group did not undergo middle cerebral artery occlusion, but the content and method of analysis after administration and sacrifice were the same as those in the first group. The concentration of calcium, sodium, and potassium ions are measured by atomic absorption spectrometry, and the water content is quantified by measuring the difference between the wet weight of the brain tissue and the mass after drying.
Taking into account the individual differences between experimental animals, the changes in ions and water content of the left brain tissue of the same mouse were standardized by the untreated part of the right hemisphere.
In addition, the distribution of nicardipine was obtained from the third set of experimental results, and the units of tissue concentration and plasma concentration were ng/g and ng/ml, respectively.
Nicardipine can effectively reduce the cell damage in the hypoperfusion zone.
Table: Observing the changes of ions and water in the left cerebral hemisphere after the left middle cerebral artery occlusion.
It is not difficult to find that: After the ischemia model is established, intravenous nicardipine can significantly reduce Ion transfer in the infarct area, the changes of calcium, sodium and potassium ions in the infarct area in the nicardipine treatment group were significantly lower than those in the control group.
Since changes in tissue calcium, sodium, potassium ions and water reflect cell damage, it can be inferred that nicardipine has a protective effect on the infarct site.
In the exploration of the regional distribution of nicardipine, the experimental data showed that the uptake of nicardipine in the ischemic area was greater than the uptake of surrounding or normal cortical tissue, and the largest uptake occurred in the central area of the infarction, which indicated the ischemic area The limited blood flow can still allow the drug to reach the infarct site.
Scholars believe that the tissue protective effect of nicardipine is related to the hindrance of calcium ions from entering cells and the blocking of downstream arachidonic acid metabolic pathways.
TIME interactive time to avoid calcium overload and inhibit cell apoptosis.
Nicardipine effectively protects cells in hypoperfusion areas.
Ma Yawen, attending physician at the Department of Critical Care Medicine, Shengjing Hospital, China Medical University.
Nicardipine is a dihydropyridine calcium channel blocker , Has a good fat-soluble effect and low dissociation, can quickly distribute and dissolve in the ischemic cell membrane, reperfusion in the case of cerebral ischemia may damage the blood-brain barrier, nicardipine is beneficial to stabilize and repair blood The brain barrier promotes the metabolism of local parts of the brain.
The basic principle of nicardipine in the treatment of cerebral ischemia is to prevent myocardial and cerebral ischemia damage caused by reperfusion by reducing calcium overload in hypoperfused tissues, promote cell metabolism in ischemic tissues, and promote bcl-2 by dephosphorylation of phosphatase.
Quickly produce and promote the rise of bcl-2, and further inhibit cell apoptosis and protect brain cells. Depressing blood pressure, antispasmodic, and improving blood supply in ischemic areas.
Nicardipine has sufficient evidence.
Li Qingquan, Attending physician of neurosurgery at the Second Affiliated Hospital of Nanjing Medical University.
Nicardipine hydrochloride has a unique side chain structure-methylbenzylamino, which makes it possess The extremely strong lipid-water partition coefficient makes Nicardipine hydrochloride easier to penetrate the blood-brain barrier and enter the brain tissue than other drugs.
The unique side chain tertiary amino group of nicardipine hydrochloride easily binds to hydrogen ions and causes nicardipine hydrochloride to accumulate in the ischemic area, thereby improving the blood supply to the ischemic part of the brain tissue.
At the same time, the HINASH study proved that nicardipine hydrochloride has an antispasmodic effect and directly improves the prognosis of SAH patients.
Nicardipine hydrochloride injection is a dihydropyridine calcium antagonist, which reduces blood pressure only by dilating small and medium arteries, and it is not easy to cause excessive blood pressure, and it is safer to lower blood pressure.
Specific expansion of cerebrovascular, nicardipine provides more protection for ischemia-reperfusion injury, Gao Minnan, Sun Yat-sen University’s Sun Yat-sen Hospital, the chief physician of the Department of Cardiac Surgery Nicardipine has a specific expansion effect on cerebrovascular, increasing cerebral blood flow by relaxing vascular smooth muscle, It has a protective effect on ischemic and hypoxic brain tissue, and can prevent brain tissue damage caused by cerebral vasospasm during hypotension and postoperative period.
It has little effect on intracranial pressure.
Nicardipine has higher lipid solubility and lower negative logarithm of dissociation constant of acidic drugs, and is easily distributed on ischemic cell membranes.
It can improve tissue perfusion and metabolic disorders, inhibit calcium influx, reduce mitochondrial calcium overload, and restore The production of adenosine triphosphate reduces intracellular lactic acid poisoning and lowers intracellular pH, thereby reducing the occurrence of nerve cell apoptosis.
At the same time, it can also stabilize the blood-brain barrier and reduce local energy metabolism after ischemia, thereby protecting ischemic brain tissue and providing more protection for ischemia-reperfusion injury.
Sharing of clinical experience Zhang Xiangyang, Chief Physician of Beijing Tsinghua Chang Gung Memorial Hospital, has many indications and significant drug effects.
Nicardipine reduces blood pressure and protects target organs.
For patients with aortic dissection whose blood pressure control effect is not good, we can use β-blockers At the same time, nicardipine is used in combination to achieve the goal of rapid blood pressure reduction; for patients with hypertension caused by brain injury or cerebrovascular disease, nicardipine can also reduce blood pressure while maximizing protection of brain cells and brain function; in renal In the intervention of hypertension, nicardipine can effectively expand the arterioles in and out of the bulb, thereby improving refractory renal hypertension. Nicardipine has a moderate half-life and an ideal drug effect.
It is a commonly used antihypertensive drug in clinical practice.
Zhong Weixi, the attending physician in the emergency department of the Sixth People's Hospital of Shanghai Jiaotong University, was pumped to maintain after intravenous push.
Nicardipine usage is here.
Nicardipine is mostly used in clinical hypertensive emergencies.
The blood pressure drop can reach 30- after conventional 2mg intravenous push.
40mmHg.
Subsequently, we continue to pump 2-5mg/h, which can obtain a more effective and long-lasting antihypertensive effect, which is especially suitable for patients with subarachnoid hemorrhage.
Xuan Lizhen, the attending physician of the Department of Critical Care Medicine, Zhongshan Hospital, Fudan University, has a rapid blood pressure reduction and good curative effect.
Nicardipine is worthy of recommendation.
Clinically, patients with hypertension have a higher mortality rate and a more critical condition.
Intensified treatment is urgently needed.
Nicardipine can quickly and effectively lower blood pressure, it can take effect immediately, reach the peak blood concentration in 1 minute, and the 24-hour systolic blood pressure fluctuations are small.
It is recommended by domestic and foreign guidelines and is recommended for patients with hypertensive emergencies.
