Panax notoginseng dissipates blood stasis, reduces swelling and relieves pain, PNS and other active ingredients have a wide range of pharmacological activities on the cardiovascular system. Effects on the heart PNS is injected into anesthetized cats or large veins to significantly reduce the left ventricular pressure (LVP) and the maximum rate of rise of left ventricular pressure (dp/dtmax), and significantly prolong the time to reach the peak value (t-dp/dtmax) , the heart rate slowed down, the total peripheral vascular resistance and blood pressure decreased significantly, but the cardiac output (CO), cardiac index, and cardiac index did not decrease or increased.
The above shows that PNS has the functions of reducing myocardial contractility, slowing heart rate, expanding external blood vessels, and reducing peripheral resistance. Remove Rg1 and Rb1 from the PNS, and inject the remaining part (RX) into rats intravenously, and the effect on hemodynamics is similar to the above. PNS can antagonize the CaC12-induced increase in the contraction force and contraction frequency of guinea pig isolated myocardium, and shorten the plateau period of the action potential, indicating that it has a calcium channel blocking effect.
Effects on vascular blood pressure Panax notoginseng and PNS have blood pressure-lowering effects on dogs, cats, rabbits, spontaneously hypertensive rats and other animals, especially in reducing diastolic blood pressure. PNS has a selective expansion effect on blood vessels in different parts, and has a weak expansion effect on canine arteries, such as thoracic aorta and pulmonary artery, but has a strong expansion effect on small arteries and veins such as renal arteries, mesenteric arteries, portal veins, and inferior vena cava, and can significantly Reduce coronary resistance (CR) and increase coronary blood flow (CBF). The effect of PNS is stronger than that of monomer, and the effect of Rbl is greater than that of Rg1. The vasodilator and blood pressure lowering effects of Panax notoginseng are mainly related to blocking Ca++ inflow. PNS can specifically block the receptor-dependent calcium channel (ROC) on vascular smooth muscle, reduce the influx of Ca++, and can also significantly reduce the influx of Ca++ caused by norepinephrine.
Anti-myocardial ischemia Sanqi, Panax notoginseng total flavonoids and Panax notoginseng root extract can resist the increase of T wave caused by acute myocardial ischemia in rabbits caused by pituitary hormone. For dogs with experimental acute myocardial infarction, Panax notoginseng injection can significantly reduce the deviation of ST segment of electrocardiogram and the appearance of pathological Q wave. In the experiment of acute myocardial ischemia induced by coronary artery ligation in rabbits, PNS was injected intravenously for 5 minutes before ligation and reperfusion, which can significantly improve ischemic ECG and reduce the size of myocardial infarction. For myocardial ischemia caused by reperfusion after coronary artery ligation in rats, PNS can reduce the size of infarction in a dose-dependent manner, and inhibit the further increase of creatine phosphokinase (CPK) in serum.
The mechanism of PNS anti-myocardial ischemia is as follows: ① dilate coronary artery, promote the formation of collateral circulation in experimental myocardial infarction area, increase coronary blood flow, improve myocardial blood oxygen supply; ② inhibit myocardial contractility, slow down heart rate, reduce peripheral 3) Anti-lipid peroxidation, increase the activity of superoxide dismutase (SOD) and reduce the production of malondialdehyde (MDA); Survival time under hypoxic conditions.
Anti-cerebral ischemia PNS intravenous injection can significantly expand the pial microvessels of anesthetized mice, accelerate blood flow velocity, and increase local blood flow. Incomplete cerebral ischemia caused by rapid bloodletting of the bilateral common carotid and femoral arteries in rabbits, intravenous injection of PNS can significantly relieve the low level of brain waves caused by ischemia, and significantly reduce the water, sodium, and calcium levels in the cerebral cortex. content and the activity of CPK and LDH in cerebral venous blood, and reduce the damage of cerebral cortex tissue structure. The anti-ischemic effect of notoginseng is not only related to the expansion of cerebral blood vessels and the increase of local blood flow, but also to delaying the decomposition of ATP in ischemic tissue, improving energy metabolism, inhibiting lipid peroxidation, increasing the activity of SOD in brain tissue, and eliminating Oxygen free radicals, etc. are related.
Antiarrhythmic PNS can significantly improve the sinus rhythm recovery rate, shorten the time required to restore sinus rhythm, and prolong the duration of sinus rhythm for dog arrhythmias caused by ouabain and ouabain K; The arrhythmia induced by acetidine can significantly prolong the latent period of arrhythmia and shorten the duration of arrhythmia; the rat tachycardia induced by BaC12 can restore sinus rhythm; Tremor, can significantly reduce its incidence. Notoginseng glycosides (PDS) and notoginseng triol glycosides (PTS) have obvious antagonism effects on rat arrhythmia induced by aconitine and BaC12, and on rat coronary arrhythmia induced by ligation of rats. IqS can also shorten the duration of epinephrine-induced arrhythmia in rabbits, and reduce the arrhythmia induced by myocardial ischemia-reperfusion in rats.
The antiarrhythmic mechanism of PNS, PTS, PDS includes:
Reduce self-discipline; slow down conduction; prolong action potential duration (APD) and effective refractory period (ERP), eliminate reentry excitation; block slow calcium channels, so that the peak value of slow inward current (Isi) is significantly reduced.
The electrophysiological characteristics of PTS are similar to that of amiodarone, and it is mainly antiarrhythmic by prolonging APD and ERP and blocking the impulse conduction of premature beats.
Intraperitoneal injection of anti-atherosclerotic PNS for 8 weeks can significantly inhibit the formation of experimental atherosclerotic rabbit arterial intima plaques, the mechanism may be that PNS increases the content of prostaglandin I2 in the arterial wall and reduces the content of thromboxane A2 in platelets. Thereby correcting the imbalance between prostaglandin I2-thromboxane A2 and stabilizing the intravascular environment. The methanol extract of notoginseng can inhibit the increase of β-lipoprotein, total lipid, phospholipid and free fatty acid in male rats fed with high cholesterol food, and the relationship is dose-effect.