CT平扫对肠坏死诊断价值

目的:探讨CT平扫对肠坏死诊断价值,总结肠管坏死征象。方法:分析98例可疑肠坏死患者CT平扫图像,所有患者均经手术证实或未能及时治疗死亡患者CT平扫影像,总结、分析影像特点。结果:全部患者中40例患者存在肠坏死,肠壁厚度改变,包括29例肠壁增厚,8例肠壁菲薄,5例表现为肠壁密度减低,3例表现为肠壁密度增加,25例表现肠管扩张,8例表现肠管塌陷,36例肠管内积液,其中34例见气液平面,4例仅见积气,5例肠壁内见气泡影,38例见腹腔积液,10例见系膜水肿,2例见肠系膜血管密度增高,1例肠系膜静脉内气体,1例门静脉内气体,5例见腹腔游离气体。结论:多排螺旋CT平扫对肠坏死部位及范围的评价有较高的价值,同时CT平扫能明确病因,为及早治疗打下良好基础。     

Effect of endothelin-1 and vasoactive intestinal contractor on blood flow and output of vasoactive intestinal polypeptide in the feline colon

Injection of the structurally related peptides, endothelin-1 and vasoactive intestinal contractor (VIC), into a branch of the superior mesenteric artery in anesthetized cats caused dose-dependent reductions in blood flow in the portal vein and inferior mesenteric artery. The maximum effect occurred after 1 minute and was more prolonged in the portal vein. The effects of the two peptides were not significantly different. The colonic output of vasoactive intestinal polypeptide (VIP) into portal venous blood was decreased significantly by endothelin-1 and VIC, returning to baseline more rapidly than blood flow. When norepinephrine was injected to produce comparable reductions in blood flow, the output of VIP into portal venous blood was not altered significantly. These results suggest that inhibition of output of the vasodilator VIP contributes to the vasoconstrictor effects of endothelin-1 and VIC in the feline colonic vascular bed.     

Combined Hepatic Vein, Umbilicoportal Vein, and Superior Mesenteric Artery Catheterization in Portal Hypertension: Estimation of the Portal Fraction of Total Hepatic Blood Flow in Cirrhotic Patients

Hemodynamic data were obtained in 13 cirrhotic patients with severe portal hypertension, undergoing combined hepatic vein, umbilicoportal vein, and superior mesenteric artery catheterization. The relative clearance of indocyanine green, the portohepatic gradient (difference between the free portal venous pressure and the free hepatic venous pressure), and the estimated hepatic blood flow were measured. The portal fraction (PF) of total hepatic blood flow was calculated in all patients using indicator dilution curves obtained from the portal bifurcation, a right hepatic vein, and when possible a left hepatic vein (six cases) after injection of ⁵¹Cr-labeled red blood cells (⁵¹Cr RBC) into the superior mesenteric artery. Flows were overestimated because of loss of indicator through spontaneous portosystemic shunts; however, the ratio between hepatic and portal indicator dilution curves can be used to calculate the portal fraction of total hepatic blood flow since no extrahepatic shunts existed after the bifurcation of the portal vein (as shown on portography). In 10 patients, 15 series of curves were calculable and the PF varied between 30.1 and 100% (mean ± SE: 71.1 ± 6.2%). In the three other patients, only delayed activity from recirculation was detected from portal and hepatic vein samples and PF was 0%; in these three cases, portography and arteriography revealed spontaneous portacaval shunting with reverse and/or stagnant circulation in the portal vein. In the 13 patients, no correlation existed between PF and the relative clearance of indocyanine green or the portohepatic gradient, parameters generally used as indices of severity in cirrhosis. In 10 patients, no correlation was found between PF and the estimated hepatic blood flow.     

The effect of pancreatic and intestinal venous blood on hepatic atrophy and compensatory hyperplasia in the rat

Hepatotrophic effect of pancreatic and intestinal venous blood was studied in rats with mesocaval or distal splenocaval shunt following ligation of a branch of the portal vein supplying 70% of liver mass. Because 2/3 of liver mass was deprived of portal flow the nonligated liver lobes were not hypoperfused due to shunt procedure. During the first three postoperative days the DNA synthesis, mitotic index, and changes in relative weights were measured in both ligated (atrophied) and nonligated (compensatory hyperplasia) parts of the liver. It was found, that the restorative capacity of the liver existed in rats with selective portasystemic shunts. The stimulus to growth was greater in lobes supplied by intestinal venous blood compared to those perfused by pancreatic effluent. The increase in DNA synthesis occurred in lobes undergoing atrophy and the intensity of this response was also dependent on type of shunt since recirculation of intestinal blood by way of the hepatic artery inhibited atrophy to a greater extent than pancreatic venous effluent. Although the patency of arterial branches was confirmed the ligated lobes showed necrotic lesions. Systemic recirculation of intestinal venous blood far more inhibited necrosis than pancreatic venous blood.     

Effect of synthetic physalaemin on splanchnic circulation in dogs

Physalaemin has been reported as one of the most potent vasodilator and hypotensive peptides (1-4). In spite of these studies, however, the effect of the peptide on splanchnic circulation is not known precisely. In the present study, the effect of synthetic physalaemin on superior mesenteric arterial blood flow, portal venous blood flow and pancreatic capillary blood flow was investigated in dogs. Dose dependent increases of superior mesenteric arterial blood flow and portal venous blood flow were induced in response to physalaemin (0.1-10.0 ng/kg). Superior mesenteric arterial blood flow and portal venous blood flow attained maximal increases of 77 +/- 8.9% and 70 +/- 8.6%, respectively, at a dose of 5 ng/kg. Physalaemin caused a dose-related decrease in systemic arterial blood pressure. Pancreatic capillary blood flow did not show significant change with the administration of physalaemin. These data suggest that physalaemin may play some physiological roles in the regulation of splanchnic circulation.     

门静脉高压症脾切断流术后血栓形成的临床研究

目的:探讨门静脉高压症脾切断流术后门静脉系统血栓形成的相关原因。方法:回顾性分析2010年4月-2011年12月我科450例因肝硬化门静脉高压症行脾切断流术患者的临床资料,应用超声多普勒检测手术前后门静脉血流速度、门静脉直径及脾静脉、肠系膜上静脉、门静脉血栓情况,用Logistic回归分析术前肝功能Child-Pugh分级、门静脉直径、门静脉血流速度、脾脏的质量及术后血小板数量与门静脉系统血栓形成的关系。结果:术前门静脉系统有血栓患者75例,占16.7%。术后门静脉血栓再形成率52.9%。Logistic单因素分析提示门静脉系统血栓形成与门静脉内径、门静脉血流速度、脾脏质量、血清总胆红素、术后血小板数量有关。多因素分析发现门静脉系统血栓形成与门静脉内径、门静脉血流速度、脾脏质量有关,而与血清总胆红素、术后血小板数量无关。结论:肝硬化门静脉高压症脾切除术后门静脉系统血栓形成与门静脉内径、门静脉血流速度、脾脏质量有关。     

Splanchnic hemodynamic response to passive hyperventilation.

Two groups of anesthetized, splenectomized, and paralyzed dogs were hyperventilated (Vt 40 ml/kg). Normocapnia was maintained in one group (mean Paco2 37.6 mm"h'g, mean p"h '7.41) and respiratory alkalosis (mean Paco2 8 mmHg, mean pH 7.75) in the other. Splanchnic hemodynamic responses were similar in both groups. Average hepatic venous pressure increased from 3.2 to 6.4 mmHg in the normocapnic group and from 3.8 to 7.7 mmHg in the hypocapnic group. Average portal venous pressure increased from 10.7 to 12.0 mmHg and 10.8 to 12.7 mmHg in the normocapnic and hypocapnic groups, respectively. Mesenteric vascular resistance increased in 93 per cent of dogs. A decrease in functional intestinal capillary surface area during hyperventilation was indicated by a significant reduction in mesenteric Vo2 (from 15 to 11 ml/min, average 30 per cent), and a concomitant reduction in mesenteric O2 extraction ratio. Changes in mesenteric Vo2 were reflected in calculated splanchinic Vo2. Hepatic O2 uptake was essentially unchanged by tidal hyperventilation with or without hypocapnia.     

Characteristics of the microcirculation and blood rheology in arterial and venous forms of mesenteric vascular occlusion

The functional properties of microcirculation and rheology of blood were studied in dogs subjected to arterial and venous occlusion of mesenteric vessels (cranial mesenteric artery and cranial mesenteric vein). It was found that a local alterations of microvascular bed of intestinal wall are quite different in case of arterial or venous occlusion. The degree of hemorheological and microvascular deviations is higher in case of acute venous thrombosis than during the acute occlusion of cranial mesenteric artery.     

Angiostrongylus costaricensis: complete redescription of the migratory pathways based on experimental Sigmodon hispidus infection

Angiostrongylus costaricensis lives in the cecal and mesenteric arteries of its vertebrate hosts, and causes an inflammatory disease in humans. To investigate unknown aspects of the abdominal angiostrogyliasis pathogenesis, infected Sigmodon hispidus were sequentially studied in different times of infection. The study revealed that L3 goes alternatively through two migratory courses during its development into an adult worm: lymphatic/venous-arterial and venous portal pathways. The former is considered the principal one, because it is used by most of the larvae. Like other metastrongylides, A. costaricensis passes over the pulmonary circulation to migrate from the lymphatic system to the arterial circulation, where they circulate during some days before reaching their definitive habitat. The oviposition by mature females began on 15th day. Eggs and L1 were detected mainly in the intestine and stomach, surrounded by inflammatory reaction constituted by macrophages, monocytes, and eosinophils. They were also spread to the lungs, mesenteric lymph nodes, pancreas, spleen, and kidneys. The larvae (L1) exhibited the centripetal capacity to invade the lymphatic and venous vessels of the intestine and mesentery. Adult worms that developed in the venous intrahepatic pathway migrated downstream to reach the mesenteric veins and laid eggs that embolized in the portal hepatic vessels.     

Zinc transport by transferrin in rat portal blood plasma.

Zinc transport in mesenteric lymph and zinc distribution in portal plasma and venous plasma were examined in rats that had been given an oral dose of ⁶⁵Zn. Less than 1% of an oral dose of ⁶⁵Zn appeared in the mesenteric lymph over a period of 8 hr. In portal plasma, approximately 70% of the isotope recovered after gel-filtration chromatography was bound to a protein that was identified as transferrin on the basis of molecular weight and electrophoretic properties. In venous plasma, the major fraction of ⁶⁵Zn was bound to albumin while the remainder of the isotope was associated with higher molecular weight proteins including transferrin and α₂-macroglobulins. These results demonstrate that zinc is transported from the intestine to the liver via the portal blood, and the results demonstrate that zinc is transported in portal plasma bound to transferrin.     

Systemic and portal hemodynamic effects of anandamide

The endogenous cannabinoid anandamide causes hypotension and mesenteric arteriolar dilation. A detailed analysis of its effects on systemic and portal venous hemodynamics had not yet been performed. We assessed the effects of anandamide (0.4-10 mg/kg) on systemic and portal hemodynamics with and without prior treatment with various antagonists. The specific antagonists used included SR-141716A, N(omega)-nitro-L-arginine methyl ester, indomethacin, and nordihydroguaiaretic acid. Anandamide produced a dose-dependent decrease in mean arterial pressure due to a drop in systemic vascular resistance (SVR) that was accompanied by a compensatory rise in cardiac output. Anandamide also elicited an increase in both portal venous flow and pressure, along with a decline in mesenteric vascular resistance (MVR). Pretreatment with 3 mg/kg SR-141716A, a CB(1) antagonist, prevented the decline of SVR and MVR from the lower dose of anandamide. Antagonism of nitric oxide synthetase, cyclooxygenase, or 5-lipoxygenase did not prevent the systemic nor the portal hemodynamic effects of anandamide. Furthermore, the use of R-methanandamide, a stable analog of anandamide, produced similar hemodynamic effects on the mesenteric vasculature, thereby implying that the effects of anandamide are not related to its breakdown products. Anandamide produced profound, dose-dependent alterations in both the systemic and portal circulations that could be at least partially blocked by pretreatment with SR-141716A.     

Association between glutamine extraction and release of citrulline and glycine by the human small intestine

Although glutamine is an important fuel for the intestinal epithelium, the metabolic fate of glutamine extracted by the human intestine remains unclear. The aim of this study was to investigate the relationship between glutamine extraction and the release of other amino acids by the human intestine. In 21 patients undergoing major abdominal cancer surgery, differences in the plasma concentrations of 22 amino acids including glutamine across the superior or inferior mesenteric vein draining viscera were measured using a high-performance liquid chromatography. Arterial minus venous (A-V) or venous minus arterial (V-A) balances of the amino acids were calculated, and then the correlations between A-V differences of glutamine and V-A differences of amino acids released from the intestine were analyzed. Mean extraction rate of glutamine by the small intestine was 28.45%, approximately 3 times higher than 9.41% in the distal colon. Citrulline, proline, alanine, glycine, and arginine were released by the small intestine into the portal circulation. Positive correlations were found between glutamine uptake and the production of citrulline (r=0.814, P=0.0013) and glycine (r=0.734, P=0.0080). In conclusion, the synthesis of citrulline from glutamine by the small intestine is highly suspected, and the contribution of gut glutamine extraction to the release of glycine into the portal circulation is also supposed.     

双歧杆菌对门静脉血内毒素影响初步研究

本实验以大鼠为动物模型,探讨在肠道微生态失调的状态下,用大量双歧杆菌(Bifidobacteria)灌服,借以拮抗外源性需氧革兰氏阴性杆菌的生长繁殖,从而使肠源性内毒素自门静脉的吸收减少。对正常鼠、脱污染鼠、再污染鼠、治疗鼠和非治疗鼠,进行不同肠段的双歧杆菌、需氧革兰氏阴性杆菌的测定和门静脉血内毒素测定。结果表明:双歧杆菌对肠道需氧革兰氏阴性杆菌的生长繁殖,具有明显的生物拮抗作用,同时伴有相应的门静脉血内毒素水平的降低。     

Regulatory mechanisms in the luminal and portal release of vasoactive intestinal polypeptide during vagal nerve stimulation in the cat

The effect of vagal stimulation in chloralose-anesthetized cats on release of vasoactive intestinal polypeptide into the jejunal lumen and portal venous blood was tested simultaneously, and the effect of atropine and hexamethonium was investigated to elucidate the regulatory mechanisms involved in the release. Vagal stimulation caused a significant increase in vasoactive intestinal polypeptide concentrations in the luminal perfusates. A significant concomitant increase was seen in portal plasma. Gel filtration chromatography of luminal and portal samples demonstrated that the vasoactive intestinal polypeptide coeluted with synthetic porcine vasoactive intestinal polypeptide. Vasoactive intestinal polypeptide infusion at 80 and 160 pmol/kg.min produced portal plasma levels of at least 3000 pM but did not increase vasoactive intestinal polypeptide concentrations in the luminal perfusates. Thus, luminal vasoactive intestinal polypeptide originates from gastrointestinal tissue rather than by transduction from the circulation. Vagally induced release of vasoactive intestinal polypeptide into the lumen and portal plasma was not abolished by atropine but was totally suppressed by hexamethonium. The regulatory mechanisms controlling the parallel release of vasoactive intestinal polypeptide into both the jejunal lumen and portal circulation are identical and involve a non-muscarinic process which is under cholinoceptive, nicotinic control.     

Autophagy is decreased in mesenteric fat tissue but not in intestinal mucosae of patients with Crohn’s disease

Crohn??s disease (CD) is a chronic intestinal disease with a multifactorial etiology. Recently, a role for mesenteric fat has been proposed in CD pathophysiology, since fat hypertrophy is detected close to the affected intestinal area; however, there are few studies regarding autophagy and the hypertrophied mesenteric tissue in CD. To evaluate autophagy-related proteins in intestinal mucosae and mesenteric fat of patients with CD and controls, patients with ileocecal CD (CD Group) and with non-inflammatory disease (FC Group) selected for surgery were studied. Expression of LC3-II was determined by immunoblotting of protein extracts. In addition, beclin-1, LC3 and Atg16-L1 RNA levels were measured using RT-PCR. The expression of LC3-II was significantly lower in the mesenteric tissue and higher in intestinal mucosae of CD when compared to controls. However, mRNA expression of autophagy-related proteins was similar when comparing the mesenteric fat groups. These findings suggest a defect in autophagy activation in the mesenteric fat tissue of CD individuals, which could be involved in the maintenance of the inflammatory process.     

Ammonia absorption from the intestine in adult cockerels

Two ml of w mM ammonium acetate solution was introduced into 10 cm chicken intestinal sack having Meckel's diverticulum in the middle part. After the introduction, blood ammonia concentration in the mesenteric vein draining the sack reached a maximal increase within 5 min and returned to the initial level in 30 min. The difference of ammonia concentration between cardiac and mesenteric venous blood also showed a similar tendency. About 91% of the ammonia introduced into the intestinal lumen disappeared in 30 min. Amino acid metabolism in intestinal tissue appears to be affected by the introduction of ammonia into the intestinal lumen.     

HGF Gene Modification in Mesenchymal Stem Cells Reduces Radiation-Induced Intestinal Injury by Modulating Immunity

BackgroundEffective therapeutic strategies to address intestinal complications after radiation exposure are currently lacking. Mesenchymal stem cells (MSCs), which display the ability to repair the injured intestine, have been considered as delivery vehicles for repair genes. In this study, we evaluated the therapeutic effect of hepatocyte growth factor (HGF)-gene-modified MSCs on radiation-induced intestinal injury (RIII).MethodsFemale 6- to 8-week-old mice were radiated locally at the abdomen with a single 13-Gy dose of radiation and then treated with saline control, Ad-HGF or Ad-Null-modified MSCs therapy. The transient engraftment of human MSCs was detected via real-time PCR and immunostaining. The therapeutic effects of non- and HGF-modified MSCs were evaluated via FACS to determine the lymphocyte immunophenotypes; via ELISA to measure cytokine expression; via immunostaining to determine tight junction protein expression; via PCNA staining to examine intestinal epithelial cell proliferation; and via TUNEL staining to detect intestinal epithelial cell apoptosis.ResultsThe histopathological recovery of the radiation-injured intestine was significantly enhanced following non- or HGF-modified MSCs treatment. Importantly, the radiation-induced immunophenotypic disorders of the mesenteric lymph nodes and Peyer’s patches were attenuated in both MSCs-treated groups. Treatment with HGF-modified MSCs reduced the expression and secretion of inflammatory cytokines, including tumor necrosis factor alpha (TNF-α) and interferon-gamma (IFN-γ), increased the expression of the anti-inflammatory cytokine IL-10 and the tight junction protein ZO-1, and promoted the proliferation and reduced the apoptosis of intestinal epithelial cells.ConclusionsTreatment of RIII with HGF-gene-modified MSCs reduces local inflammation and promotes the recovery of small intestinal histopathology in a mouse model. These findings might provide an effective therapeutic strategy for RIII.     

Hemodynamic effects of Salvia miltiorrhiza on cirrhotic rats

Salvia miltiorrhiza (Sm) administration has been shown to reduce hepatic fibrosis in rats. We investigated the hemodynamic effects of Sm on bile duct ligated (BDL) rats. Hemodynamic, histological, and vascular contractile studies were conducted in rats 4 weeks after bile duct ligation. An aqueous extract of Sm (0.2 g twice per day) or vehicle was administered for 4 weeks to BDL rats. Sm treatment in BDL rats significantly reduced histological grades of fibrosis and ameliorated the portal hypertensive state (including portal venous pressure, superior mesenteric artery blood flow, cardiac index, and total peripheral resistance) as compared with vehicle treatment. Moreover, Sm treatment enhanced the vascular sensitivity of mesenteric arteries to phenylephrine in BDL rats. Sm treatment had no effect on plasma biochemical profiles of either BDL or normal rats. Our results suggest that 4-week Sm treatment ameliorates the portal hypertensive state in BDL rats.     

Impaired agonist-dependent myosin phosphorylation and decreased RhoA in rat portal hypertensive mesenteric vasculature

The purpose of the present study was to examine the effects of portal hypertension on agonist-induced myosin phosphorylation and RhoA expression in vascular smooth muscle. A possible link to cAMP-dependent events was also examined. Portal hypertension was produced by stenosis of the portal vein. Vessel segments were treated with or without 50 microM of the PKA inhibitor Rp-cAMPS for 30 min and subsequently stimulated with 10(-4) M phenylephrine. Myosin regulatory light-chain phosphorylation was detected by immunoblotting. Total RNA from first-order mesenteric arteries and portal veins was isolated and amplified by RT-PCR using RhoA and GAPDH primers. RhoA protein expression was also measured in first-order mesenteric arteries using Western blot analysis. Myosin phosphorylation in maximally stimulated first-order mesenteric arteries was significantly lower in portal hypertensive animals (19.9 +/- 2.86%) when compared with sham-operated control (43.8 +/- 3.53%). Inhibition of PKA selectively increased myosin phosphorylation to 34.7 +/- 4.18%. Rp-cAMPS did not affect the phosphorylation of the portal veins or superior mesenteric arteries. RhoA mRNA and membrane-associated RhoA protein expression in portal hypertensive first-order mesenteric arteries were significantly lower when compared with controls. Acute inhibition of PKA had no effect on RhoA mRNA expression. However, it restored membrane-associated RhoA protein expression in portal hypertensive vessels to control levels. The results suggest that reductions in membrane-associated RhoA expression, which appear to be regulated by cAMP-dependent events, lead to reduced myosin phosphorylation and may underlie the reduced vasoconstrictor effectiveness in the resistance vasculature of portal hypertensive intestine.     

iNOS expression in vascular resident macrophages contributes to circulatory dysfunction of splanchnic vascular smooth muscle contractions in portal hypertensive rats

Portal hypertension, a major complication of cirrhosis, is caused by both increased portal blood flow due to arterial vasodilation and augmented intrahepatic vascular resistance due to sinusoidal constriction. In this study, we examined the possible involvement of resident macrophages in the tone regulation of splanchnic blood vessels using bile duct ligated (BDL) portal hypertensive rats and an in vitro organ culture method. In BDL cirrhosis, the number of ED2-positive resident macrophages increased by two- to fourfold in the vascular walls of the mesenteric artery and extrahepatic portal vein compared with those in sham-operated rats. Many ED1-positive monocytes were also recruited into this area. The expression of inducible nitric oxide (NO) synthase (iNOS) mRNA was increased in the vascular tissues isolated from BDL rats, and accordingly, nitrate/nitrite production was increased. Immunohistochemistry revealed that iNOS was largely expressed in ED1-positive and ED2-positive cells. We further analyzed the effect of iNOS expression on vascular smooth muscle contraction using an in vitro organ culture system. iNOS mRNA expression and nitrate production significantly increased in vascular tissues (without endothelium) incubated with 1 μg/ml lipopolysaccharide (LPS) for 6 h. Immunohistochemistry indicated that iNOS was largely expressed in ED2-positive resident macrophages. α-Adrenergic-stimulated contractility of the mesenteric artery was greatly suppressed by LPS treatment and was restored by N(G)-nitro-L-arginine methyl ester (NO synthase inhibitor); in contrast, portal vein contractility was largely unaffected by LPS. Sodium nitroprusside (NO donor) and 8-bromo-cGMP showed greater contractile inhibition in the mesenteric artery than in the portal vein with decreasing myosin light chain phosphorylation. In the presence of an α-adrenergic agonist, the mesenteric artery cytosolic Ca(2+) level was greatly reduced by sodium nitroprusside; however, the portal vein Ca(2+) level was largely unaffected. These results suggest that the induction of iNOS in monocytes/macrophages contributes to a hypercirculatory state in the cirrhosis model rat in which the imbalance of the responsiveness of visceral vascular walls to NO (mesenteric artery > portal vein) may account for the increased portal venous flow in portal hypertension.