The study was carried out on 150 people who were divided into 3 groups: adults, nervous breakdown, and high blood pressure patients with relaxation training at the Hospital of Traditional Medicine. Following indicators: pressure, heart rhythm, and limb’s blood circulation at three points of time: before and after 30 minutes, and after 8 weeks of training. Result showed that: the traditional relaxation training decreased systolic and diastolic blood pressure, heart rhythm, extended RR and QT time, increased limb’s blood circulation (changes of the indicators still in permitted ranges)
Medicine, Traditional ; Splanchnic Circulation

Portal hypertension is responsible for most of the complications associated with liver cirrhosis, including variceal hemorrhage, ascites, and hepatic encephalopathy. It has become clear that a decrease in portal pressure can prevent or manage these serious complications. Until now, the pharmacotherapy of portal hypertension has focused on agents that reduce splanchnic blood flow, such as non-selective beta blockers and splanchnic vasoconstrictors. However, recent advances in the knowledge of the pathophysiology of portal hypertension have directed future treatment towards modulating the increased intrahepatic vascular resistance, in addition to managing the splanchnic circulation. Consequently, agents that modulate either the hyperdynamic circulation or angiogenesis are new therapeutic targets for managing portal hypertension. Several have been developed or are under investigation. To incorporate these pharmacologic approaches into clinical practice, data on patient-oriented outcomes are needed.
Ascites ; Hemorrhage ; Hepatic Encephalopathy ; Hypertension, Portal ; Liver Cirrhosis ; Portal Pressure ; Splanchnic Circulation ; Vascular Resistance ; Vasoconstrictor Agents

Portal hypertension (PHT) is associated with hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation. Increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation play a central role in the pathogenesis of PHT. PHT is also characterized by changes in vascular structure, termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the formation of new blood vessels, also occurs with PHT related in particular to the expansion of portosystemic collateral circulation. The complementary processes of vasoreactivity, vascular remodeling, and angiogenesis represent important targets for the treatment of portal hypertension. Systemic and splanchnic vasodilatation can induce hyperdynamic circulation which is related with multi-organ failure such as hepatorenal syndrome and cirrhotic cadiomyopathy.
Collateral Circulation/physiology ; Endothelial Cells/metabolism ; Hemodynamics ; Hepatic Stellate Cells/metabolism ; Hypertension, Portal/*etiology ; Liver Circulation/physiology ; Liver Cirrhosis/*etiology ; Splanchnic Circulation/physiology

OBJECTIVES: Hemodynamic measurements of chronic portal hypertension were done to study the mechanisms that maintain high portal pressure despite well developed collateral circulations. METHODS: A prehepatic portal hypertensive rat model was produced by partial portal vein ligation. Cardiac output, organ blood flow and porto-systemic shunt were measured by radioisotope labeled microsphere methods, and vascular resistance was calculated by standard equation. RESULTS: There was a significant reduction in the weight of the liver and increase in the weight of the spleen in the portal stenotic rats. Porto-systemic shunting, representing development of the collateral circulations, was 96.7+/-0.6% in the portal stenosis group compared with 0.9+/-0.2% in the control group (p<0.01). Portal pressure was significantly increased in the portal stenosis group compared with the control group(12.8+/-1.4 vs. 6.5+/-0.6mmHg; p<0.01). Mean arterial pressure was significantly decreased in portal stenosis group compared with control group(101.4+/-2.5 vs, 129.9+/-3.9mmHg; p<0.01). In the portal stenosis group, cardiac output(135.7+/-8.0 vs. 111.0+/-4.2ml/min; p<0.01) and splanchnic organ blood flow (28.97+/-2.03 vs. 17.90+/-1.27ml/min, p<0.01) were significantly increased, with concomitant decrease in total peripheral vascular resistance(58.0+/-3.3 vs. 88.2+/-4.8 dyne sec/cm5 X 105; p<0.01) and splanchnic vascular resistance(2.54+/-0.20 vs. 5.47+/-0.33 dyne sec/cm5 X 105; p<0.01), However, the portal venous resistance was not significantly different in both groups of rats (3.57+/-0.31 vs. 3.03+/-0.38 dyne sec/cm5 X 105; p>0.05). CONCLUSION: The hemodynamic results of this study indicate that hyperdynamic status of systemic and splanchnic circulation was present in chronic portal hypertension and that the primary factor contributing to the persistently elevated portal venous pressure was the markedly increased portal venous inflow.
Animals ; Arterial Pressure ; Cardiac Output ; Collateral Circulation ; Constriction, Pathologic ; Hemodynamics* ; Hypertension, Portal ; Ligation ; Liver ; Microspheres ; Models, Animal* ; Portal Pressure ; Portal Vein* ; Rats* ; Splanchnic Circulation ; Spleen ; Vascular Resistance

In cirrhotic patients undergoing liver transplantation, reperfusion of a liver graft typically increases portal venous blood flow (PVF) because of a decrease in resistance in the liver graft to the PVF and underlying hyperdynamic splanchnic circulation, which develops due to liver cirrhosis complicated by portal hypertension and persists even after successful liver transplantation. If the liver graft has enough capacity to accommodate the increased PVF, the shear stress inflicted on the sinusoidal endothelial cells of the graft promotes hepatic regeneration; otherwise, small-for-size syndrome (SFSS) develops, leading to poor graft function and graft failure. In particular, a partial graft transplanted to patients undergoing living donor liver transplantation has less capacity to accommodate the enhanced PVF than a whole liver graft. Thus, the clinical conditions that the partial graft encounters determine either hepatic regeneration or development of SFSS. Consistent with this, this review will discuss the two conflicting effects of portal hyperperfusion (hepatic regeneration vs. portal hyperperfusion injury) on the partial grafts in cirrhotic patients suffering from hyperdynamic splanchnic circulation, in addition to normal physiology and pathophysiology of hepatic hemodynamics.
Endothelial Cells ; Hemodynamics ; Humans ; Hypertension, Portal ; Liver Cirrhosis ; Liver Regeneration ; Liver Transplantation ; Liver* ; Living Donors ; Physiology ; Regeneration* ; Reperfusion ; Splanchnic Circulation* ; Transplants*

Renal dysfunction in patients with chronic liver disease encompasses a clinical spectrum of hyponatremia, ascites, and hepatorenal syndrome. Clinical observation has suggested that patients with cirrhosis have hyperdynamic circulation, and recent studies strongly suggest that peripheral arterial vasodilatation and subsequent development of hyperdynamic circulation are responsible for disturbances in renal function. Arterial vasodilatation predominantly occurs in the splanchnic vascular bed, and seems to precede an increase in blood flow in the splanchnic circulation. Nitric oxide plays a central role in progressive vasodilatation, as evidenced by in vivo and in vitro studies. Renal dysfunction negatively affects the prognosis of patients with cirrhosis, as hyponatremia, ascites, and azotemia are associated with increased rate of complications and mortality. Recent advances in understanding the pathophysiology of renal dysfunction have enabled clinicians to develop new diagnostic criteria and therapeutic recommendations. Hepatorenal syndrome is regarded as a potentially reversible disorder, as systemic vasoconstrictors with concomitant albumin administration are emerging as a promising management option, especially in terms of providing bridging therapy for patients awaiting liver transplantation.
Ascites ; Azotemia ; Fibrosis ; Hepatorenal Syndrome ; Humans ; Hyponatremia ; Liver ; Liver Cirrhosis ; Liver Diseases ; Liver Transplantation ; Nitric Oxide ; Prognosis ; Splanchnic Circulation ; Vasoconstrictor Agents ; Vasodilation

The purpose of the present study was to assess the correlation that likely exists among increased portal pressure (Pp), portal blood flow quantity (Qp) and ETA and ETB receptor mRNA expression in human cirrhosis. In situ hybridization and reverse-transcription polymerase chain reactions (RT-PCR) were performed to determined the expression of ETA and ETB receptor mRNA in liver tissues from traumatic subjects (n = 10) and cirrhotic patients (n = 15) in whom hepatic hemodynamic values were measured. The expression of the two transcripts was significantly higher in liver samples of cirrhotic patients than in those obtained from traumatic subjects. It has shown that ETA receptor mRNA predominantly located in hepatic stellate cells (HSCs) and vascular smooth muscle cells of intrahepatic arteries and portal veins, ETB receptor mRNA in HSCs, sinusoidal endothelial cells and Kuppfer cells. There was a highly significant direct relationship between ETA and ETB receptor mRNA and Pp and Qp in cirrhotic patients. It suggests that liver paracrine endothelin system may be overactivated in human cirrhosis accompanied with increased expression of ETA and ETB receptor mRNA which may play an important role in the pathogenesis and maintenance of splanchnic hyperdynamics.
Female ; Gene Expression ; Hemodynamics ; Humans ; Hypertension, Portal ; metabolism ; Liver Cirrhosis ; genetics ; metabolism ; Male ; Portal Vein ; physiopathology ; Receptors, Endothelin ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Splanchnic Circulation ; physiology

OBJECTIVETo study the regularity of splanchnic hemodynamic changes after orthotopic liver transplantation (OLT) for patients with portal hypertension. At the same time, effect of such changes on splenomegaly, hypersplenism, collateral circulation and the postoperative liver function was discussed.

METHODSBetween June 2002 and October 2005, 173 liver transplantations were performed. In 38 patients with portal hypertension undergoing OLT, the following parameters were measured before surgery and subsequently at 1, 3, 5, 7 days, 1, 6 months and 1, 2, 3 years after operation by using Color Doppler sonography: portal blood flow mean velocity (PBV), portal blood flow volume (PBF), hepatic artery resistance indexes (HA-RI) and spleen size. The same parameters were measured in 8 patients with acute liver failure and 20 healthy controls. Meanwhile to observe liver function and varicose vein of esophagus.

RESULTSIn cirrhotics, PBV and PBF increased immediately after transplantation [from (13.7 +/- 4.2) cm/s to (58.4 +/- 25.2) cm/s and from (958 +/- 445) ml/min to (3024 +/- 1207) ml/min respectively, P < 0.05]. HA-RI also augmented [from (0.65 +/- 0.11) to (0.74 +/- 0.12), P < 0.05]. PBV returned to normal values after 6 months, PBF returned to normal value after 2 years. Spleen size decreased significantly, but splenomegaly persisted after 3 years. In addition the esophagogastric varix ameliorated significantly.

CONCLUSIONSAbnormal splanchnic hemodynamic changes for patients with portal hypertension still will long-term exist after OLT, but does not effect recovery of hypersplenism, esophagogastric varix and liver function.

Adolescent ; Adult ; Aged ; Child ; Female ; Follow-Up Studies ; Hemodynamics ; Hepatic Artery ; physiopathology ; Humans ; Hypertension, Portal ; pathology ; physiopathology ; surgery ; Intraoperative Period ; Liver ; physiopathology ; Liver Transplantation ; Male ; Middle Aged ; Portal Vein ; physiopathology ; Splanchnic Circulation ; physiology ; Spleen ; pathology

The purpose of the present study was to assess the correlation that likely exists among increased portal pressure (Pp), portal blood flow quantity (Qp) and ETA and ETB receptor mRNA expression in human cirrhosis. In situ hybridization and reverse-transcription polymerase chain reactions (RT-PCR) were performed to determined the expression of ETA and ETB receptor mRNA in liver tissues from traumatic subjects (n = 10) and cirrhotic patients (n = 15) in whom hepatic hemodynamic values were measured. The expression of the two transcripts was significantly higher in liver samples of cirrhotic patients than in those obtained from traumatic subjects. It has shown that ETA receptor mRNA predominantly located in hepatic stellate cells (HSCs) and vascular smooth muscle cells of intrahepatic arteries and portal veins, ETB receptor mRNA in HSCs, sinusoidal endothelial cells and Kuppfer cells. There was a highly significant direct relationship between ETA and ETB receptor mRNA and Pp and Qp in cirrhotic patients. It suggests that liver paracrine endothelin system may be overactivated in human cirrhosis accompanied with increased expression of ETA and ETB receptor mRNA which may play an important role in the pathogenesis and maintenance of splanchnic hyperdynamics.
Gene Expression ; Hemodynamic Processes ; Hypertension, Portal/metabolism ; Liver Cirrhosis/genetics ; Liver Cirrhosis/*metabolism ; Portal Vein/*physiopathology ; Receptors, Endothelin/genetics ; Receptors, Endothelin/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; *Splanchnic Circulation/physiology

Acute Disease ; Animals ; Female ; Hypoxia ; physiopathology ; Male ; Microcirculation ; physiology ; Rats ; Splanchnic Circulation ; physiology ; Superoxide Dismutase ; blood