| Hepatocirrhosis is world disease, and it is frequently encountered disease inChina, too. For man, hepatocirrhosis is susceptible, according to Bei Jing You YiHospital ward patients' statistics, man is 76.5%, woman is 23.5%. Hepatocirrhosisis a multiple one after 40-year-old. Causes of diseases made hepatic cellsinflammation necrosis,regeneration, inducing hepatic extensive fiber connectivetissue hyperplasia,distruction of leaflet. Structure,false leaflet formation, fiberdisturbing hepatic cell regeneration to big and small node, then to hepatocirrhosis.Anatomy of hepatocirrhosis is not only extensive fiber but node regeneration.There are different about cirrhosis cause all over the world, in China, cirrhosiscause mainly are virus hepatitides (hepatitis),schistosomiasis,alcoholism, etc.Causes of kinds of cirrhosis all may induce inflammation necrosis. Only whenhepatic parenchymatous cell inflammation,necrosis, which are continous, willhepatocirrhosis happen. Hepatic cell inflammation,necrosis must relate to fiberregeneration, then to fibrosis. Indeed, hepatic fibrosis is a repair refection of bodyin impairment, in actue hepatic impairment, although hepatic impairment is heavy,the repair location don't leave any hepatic fibrosis, but, in chronic, fibrosishappened. According to pathological findings, there are 62.5% fibrosis inlow-grade chronic hepatitis B, and there are 100% fibrosis in moderate intensityand far advanced chronic hepatitides. Hepatic fibrosis are formed from liverfiber connective tissue far deposition, which comes from far fitogenesis and lowfiber degradation. dMain cells of cirrhosis is hepatic star cell (HSC) in last years.The effect of HSC on portal hypertensive has been more thought. After HSCactivation, smooth muscle actin in cells more express, which increase contractilityof HSC. Among factors of HSC contraction, ET-1 is the most important. High orlow of portal vein is related to its inhibition and flow. Contractition of HSCreguladtes portal vein inhibition and flow. Symptom of hepatocirrhosis are: loss ofappetite,loss of weight, weakness,abdominalgia and abdominal distention,special face without light,icterus,hydroperitoneum,edema,hepatomegaly,tenderness, etc. Exclude laboratory diagnosis, image examination is very good atcirrhosis. B-ultrasound examinating liver when it has or not fibrosis ,hepatocirrhosis, should think about below five indicators: hepatic parenchymaecho,hepatic surface,hepatic margin,hepatic vein,spleen area. These fiveindicators have well related to hepatic fibrosis pathological findings. When portalhypertensive portal vein true conjugate diameter>4mm, and following collateral,circulation, Often, spleen vein true conjugate diameter>10mm. Dopplerultrasound examination can quantitative analysis portal vein max flow speed,flow,these indicators are much higher than those of control people. Two importantfactors of portal hypertensive: (1) inhibiton in liver vessals is high. (2) flow ofpotal vein is large. Therapy hepatocirrhosis is extensive. First, depriving of kindsof cirrhosis causes. Far formed cirrhosis, (1) generous support therapy. (2)resisting fibrosis theraphy. (3) complication's theraphy. There are surgicaltheraphy about portal hypertensive, among lots of surgical diseases, portalhypertensive's theraphy may have the most ways, the most complicated operativemethods, the most different idea disease. As indicate that there arenot onetheraphy or operative method is the best and most received. The objective ofportal hypertensive is to control acute esophagus-fundus of stomach vein varicorupture hemorrhage. Internal medicine theoretical theraphical discipline mainlyare: a direct way of behind way supposition-vasodilator, a direct way of front waysupposition-vasoconstrictor,diuretic. The most using viscera vasodilator isvasopressin and its same structure drug,growth hormone release inhibitinghormone and its same structure drug,β-R inhibitor, but after input vasopressin,most patients have distinct side effects. Growth hormone release inhibitionhormone and its same structure drug affect flow of portal hypertensive, but, itsdiscipline is unknown, same writers found that this drug controlingesophagus-fundus of stomach vein varico rupture hemorrhage is not better thanthe control group. β-epinephrine receptor inhibitor may decrease viscera bloodflow, inducing hepatic encephalopathy vasodilator (nitroglycerin), discipline isthat decreasing of average artery pressure cause viscera vessals constractionreftectly. But when big dose, it will cause all body and viscera vessals dilatation.Our test mainly observe clinic and animal test to discuss effect of radix salviaemilliorrhize on hemodynamie of portal hypertensive. Clinic groups observe beforeand after injecting radix saliviae milliorrhize and radix saliviae milliorrhize drop,measuring portal vein true conjugate diameter,flow speed,flow, in order tounderstand radix salviae millorrhize's effect, animal group, at first made model ofcirrhosis rats, observe inject different concentration and different course oftreatment radix salivae, these indicators of cirrhosis-rat-models, and contrast everygroup rats' liver pathological findings. Result (T test) (1) Injecting radix salviae,after 2 weeks, it begins to affect, the effect can sustain 12 weeks, after 24 weeks, italmost hasnot effect. The effect between 2 weeks-4weeks is the most ddistinct. (2)After injecting radix salivae 1hour, it begins to decrease portal hemodynamic,2hour is the summit. after 24 hours, it almost hasnot effect. (3) Hemodynamic ofevery group indicated: compared with 0.9% natriichloridi control group, the bloodflow of vena portae,superior mesenteric artery,pressure of vena portae,averageartery pressure in radix salivae 3,10 and 15d groups were decreased gradientpressure of vena portan respectively decreased 0.902,1.452and 1.413 mmH2O,blood flow of vena portae respectively decreased 63.7 92.0 and 1010.9 ml·min-1.superior mesenteric artery flow decreased 15.2,44.8 and 52.1 ml·min-1, averageartery pressure decreased 11.43,16.5 and 17.00 mmH2O, 15d group is the mostdistinct, which indicate radix salviae may decrease portal hypertensive, and don'taffect body circulation. (4) Different concentration radix salviae had been injectedfor 15d, hemodynamic of rats have no change. Which indicate: efficient and thriftradix salviae concentration is 400mg/200ml-400mg/400ml. After injected themost radix salviae concentration (400mg/5ml), rats were alive, which indicate:radix salviae is a kind of low toxic drug. (5) Dfferent course of treatment of rats,pathological findings;as radix salivae course longer, the rate of hepatic cord andsinus hepaticws decreased, collagen fiber streak degradation, inflammation cellsinfiltration decreased, hepatic cell necrosis and fatty degeneration decreased, the10d group is distinct. Radix salviae's discipline maybe relate to below factors:cirrhosis, whole blood viscosity is distinctly higher than that of health people.Secondly, hepatic vein pressure has related to hepatic vein high shear rate andwhole blood viscosity. Radix salviae may inhibitd phosphodiesterase and decreaseblood high viscosity. Cirrhosis often have high endotoxemia, which can directlyinduce constraction portal vein, and may increase TXA2 in blood, increase portalvein inhibition, resulting to portal vein pressure increasing. Radix salviae maydispel endotoxemian and inhibit TXA2 forming. Through regularing abovehumoral factors, decreased portal vein inhibition, which may be discipline of radixsadlviae. Long course radix salviae still defense liver fibrosis. Radix salviae mayinhibit fibroblast in vitro cultivation, and active collagenase, to increase collagen'sabsorption,degradation. Radix salviae inhibiting HSC proliferation and action aremain discipline of resisting fibrosis. (1) Radix salviae may inhibit PDGF, soinhibibt HSC proliferation. (2) Radix salviae may inhibit TGF β1, so inhibitHSC action. (3) Radix salviae may increase collagen degradation, so to defenseliver fobrosis. (4) Improve sinus hepaticws capillary may be one of disciplines. (5)Radix salviae regular local RAS system to defense fibrosis and portalhypertensive which still study. Our test find a safe and efficient drug for cirrhosistheraphy.
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