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

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

Autologous red blood cells (RBC) labeled with fluorescence were immitted into microvessel of SD rat and observed under microscope. The movement of each individual labeled RBC was recorded by microscope video camera system. The recorded videotape is replayed to sample dark background fluorescent images through frame grabber. Sampled frame images were separated into odd and even field sequence images. Then these sequence images were analyzed to get the flow rate. The error between the actual flow velocity value and the flow velocity value of fluorescent globules in the chamber measured under the same system was below 7%. The upper limit was 9.6 mm/s. There are no obvious differences (P > 0.05). This system has been applied in the research of rat microcirculatory disturbance, and the temporal flow rate change in microvessel was obtained.
Animals ; Blood Flow Velocity ; physiology ; Image Processing, Computer-Assisted ; Microcirculation ; physiology ; Microscopy, Fluorescence ; Rats ; Rats, Sprague-Dawley ; Splanchnic Circulation ; physiology ; Videotape Recording

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*

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

OBJECTIVEBased on the observation that coagulation necrosis occurs in the majority of neonatal necrotizing enterocolitis (NEC) patients, it is clear that intestinal ischemia is a contributing factor to the pathogenesis of NEC. However, the published studies regarding the role of intestinal ischemia in NEC are controversial. The aim of this paper is to review the current studies regarding intestinal microcirculatory dysfunction and NEC, and try to elucidate the exact role of intestinal microcirculatory dysfunction in NEC.

DATA SOURCESThe studies cited in this review were mainly obtained from articles listed in Medline and PubMed. The search terms used were "intestinal microcirculatory dysfunction" and "neonatal necrotizing enterocolitis".

STUDY SELECTIONMainly original milestone articles and critical reviews written by major pioneer investigators in the field were selected.

RESULTSImmature regulatory control of mesentery circulation makes the neonatal intestinal microvasculature vulnerable. When neonates are subjected to stress, endothelial cell dysfunction occurs and results in vasoconstriction of arterioles, inflammatory cell infiltration and activation in venules, and endothelial barrier disruption in capillaries. The compromised vasculature increases circulation resistance and therefore decreases intestinal perfusion, and may eventually progress to intestinal necrosis.

CONCLUSIONIntestinal ischemia plays an important role through the whole course of NEC. New therapeutic agents targeting intestinal ischemia, like HB-EGF, are promising therapeutic agents for the treatment of NEC.

Endothelin-1 ; physiology ; Endothelium, Vascular ; physiopathology ; Enterocolitis, Necrotizing ; drug therapy ; etiology ; pathology ; Heparin-binding EGF-like Growth Factor ; Humans ; Infant, Newborn ; Intercellular Signaling Peptides and Proteins ; therapeutic use ; Intestines ; blood supply ; Ischemia ; complications ; Microcirculation ; physiology ; Nitric Oxide ; physiology ; Splanchnic Circulation

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