Modulation of norepinephrine release by galanin in rat medulla oblongata.

Galanin, a 29-amino acid peptide, is widely distributed in both the central and peripheral nervous systems and is colocalized with catecholamines, although its physiological significance remains to be elucidated. In the present study we investigated the regulatory mechanisms of galanin on norepinephrine release in rat medulla oblongata. In slices of medulla oblongata of Sprague-Dawley rats, galanin inhibited the stimulation-evoked [3H]norepinephrine release in a concentration-dependent manner (fractional release ratio during electrical stimulation: control 0.937 +/- 0.043, mean +/- SEM, n = 6; galanin 1 x 10(-7) M 0.501 +/- 0.037, n = 6, p less than 0.05; and galanin 1 x 10(-6) M 0.299 +/- 0.018 n = 6, p less than 0.05). Galanin potentiated inhibition of [3H]norepinephrine release by the alpha 2-agonists (UK 14,304 and clonidine). The blockade of alpha 2-adrenergic receptors by RX 781094 diminished the inhibition of norepinephrine release by galanin. Pretreatment of pertussis toxin, which interferes with the coupling of inhibitory guanosine triphosphate-binding proteins to adenylate cyclase, significantly attenuated the suppressive effects of galanin on norepinephrine release. In slices of medulla oblongata obtained from spontaneously hypertensive rats (SHR), the inhibitory effect of galanin on norepinephrine release was significantly less than in those from age-matched Wistar-Kyoto rats. These results show that galanin might inhibit the stimulation-evoked norepinephrine release in rat medulla oblongata, at least partially mediated by alpha 2-adrenergic receptors and the pertussis toxin-sensitive guanosine triphosphate-binding proteins. Moreover, less suppression of norepinephrine release by galanin in SHR suggests that galanin might be involved in the regulation of central sympathetic nervous activity in hypertension.     

Alterations in catecholamine release in the central nervous system of spontaneously hypertensive rats.

The aim of the present study was to investigate alterations in catecholamine release in the central nervous system of spontaneously hypertensive rats. Slices of hypothalamus, medulla oblongata and striatum were prepared from spontaneously hypertensive rats (SHR: 9-10 weeks old) and age-matched Wistar Kyoto rats (WKY). The slices were incubated with (3H)norepinephrine (NE) or (3H)dopamine (DA), superfused with Krebs-solution in vitro, and the release of the catecholamines was compared between the two strains. The basal release of hypothalamic (3H)NE did not differ between SHR and WKY slices. However, stimulation (1 Hz)-evoked (3H)NE release was significantly greater in SHR than in WKY (percent fractional release of total tissue NE: WKY 0.494 +/- 0.019%, n = 6, SHR 0.730 +/- 0.053%, n = 6, p less than 0.05). The stimulation-evoked (3H)NE release from the medulla oblongata did not differ significantly between SHR and WKY slices. Finally stimulation-evoked release of striatal (3H)DA was significantly depressed in SHR (percent fractional release of total tissue DA: WKY 2.048 +/- 0.24%, n = 6, SHR 1.460 +/- 0.068%, n = 6, p less than 0.05). These results indicate that the release of hypothalamic NE and striatal DA are altered in SHR. It is suggested that enhanced hypothalamic noradrenergic activity and reduced striatal dopaminergic activity can increase sympathetic outflow to the periphery, which may play a role in the pathogenesis of this form of hypertension.     

Effect of emotional stress on catecholamine and dopa levels in some central nervous regions and in the heart of experimental animals]

The paper presents the results of examining the levels of dopamine, norepinephrine, epinephrine and precursors of their DOPA biosynthesis in the hypothalamus, hypophysis, medulla oblongata, adrenals and heart in miniature pigs exposed to acute stress. The acute emotional stress was shown to be characterized by a significant increase in the activity of the brain hypothalamic region, adrenals, peripheral portion of the sympathoadrenal system, as evidenced by higher norepinephrine release and hence lower neurotransmitter levels in the above structures. This resulted in abnormal physiological norepinephrine/epinephrine ratios in the central nervous system and heart, predisposing to myocardial metabolic and electric instability.     

Decreased hypothalamic and medullary GABA turnover in spontaneously hypertensive rats.

OBJECTIVE: The aim was to assess whether Gamma-aminobutyric acid (GABA) neurone activities in the central nervous system, especially in the hypothalamus and medulla oblangata, are altered in hypertension. METHODS: Central GABA content and turnover rate were measured in spontaneously hypertensive rats (SHR) and their normotensive Wistar Kyoto controls (WKY). GABA content was determined with high performance liquid chromatography, and in vivo GABA turnover rates were estimated by GABA accumulation after injection of amino-oxyacetic acid, a selective inhibitor of GABA degrading system. Two groups of nine week old male rats (32 SHR and 32 WKY) were used. RESULTS: GABA concentrations in cerebrospinal fluid were lower in SHR than in WKY. Since hypothalamus and medulla oblongata are the possible active sites of this system, basal GABA contents and in vivo GABA turnover rates were measured in hypothalamus and medulla oblongata. Basal GABA content in the medulla oblongata and hypothalamus was almost equal in SHR and WKY. On the other hand, GABA turnover rates were significantly lower in SHR than in WKY in both the hypothalamus and the medulla. CONCLUSIONS: Since it is known that GABA is an inhibitory neurotransmitter in the central nervous system and that it controls autonomic and cardiovascular activities, the findings suggest that the decreased hypothalamic and medullary GABAergic activities may permit sympathetic hyperactivity to contribute to the increase in blood pressure in SHR.     

Oxyntomodulin and glicentin: brain-gut peptides in the rat

Glucagon-like materials and glucagon have been identified by immunoassay and immunocytochemistry in the mammalian central nervous system. However, the molecular forms relevant to brain glucagon-like immunoreactivity (GLI) have not been precisely defined. In the rat small intestine, more than 90% of GLI is constituted by two peptides: oxyntomodulin (OXM) and glicentin. This work was initiated to characterize and determine the concentrations of these two peptides and glucagon in the rat central nervous system and to compare their relative proportions with those found in the gut. Different regions from the adult rat brain were analyzed by HPLC in association with RIA, using a central glucagon antiserum and an antibody directed toward the C-terminal end of OXM and glicentin. The elution profiles of hypothalamus extracts were constituted by two main peaks, both detected by the two antibodies used and displaying the same retention times as glicentin and OXM, respectively. A third small peak, which coeluted with glucagon, was constantly recorded with the central glucagon antiserum. The percentages of glicentin, OXM, and glucagon in 10 hypothalami were 37 +/- 1%, 55 +/- 1%, and 8 +/- 2%, respectively (n = 8). This distribution was quite similar to that in small intestinal extracts (38 +/- 1%, 59 +/- 1%, and 1.3 +/- 0.1%, respectively; n = 7); however, the peptide concentrations were almost 50-fold greater in intestine than in hypothalamus. In the medulla oblongata, the same peptide ratio was observed, with 10-fold lower concentrations compared to those in hypothalamus. In olfactory bulb, cerebellum, and cortex the concentrations were close the the detection limit, whereas they could be not detected in the pituitary. The combination of HPLC and specific RIAs allowed us to unambiguously characterize OXM and glicentin as the major components of GLI in the rat hypothalamus and medulla oblongata. The same proportion of these two peptides in the central nervous system and the gut indicates that a similar posttranslational processing exists in these rat tissues, another example of the brain-gut axis.     

A modified canine model of portal hypertension with hypersplenism

Objective. The aim of this study was to develop and describe an experimental canine model of portal hypertension with hypersplenism. Material and methods. Twenty-five dogs were used randomly divided into three groups: group I (control group, n = 5), group II (PVS, n = 10) and group III (PVS + SVS, n = 10). Portal vein stenosis (PVS) was performed in dogs of group II; in group III dogs the model was first prepared by PVS and additional splenic vein stenosis 3 weeks later (PVS + SVS). Portal vein pressure (PVP), length of spleen and fluctuation of hematocyte counts were measured and recorded at the appointed times. Surgery permitted visual verification of portosystemic collateral circulation. Histopathological variation of the spleen and condition of the bone marrow hyperplasia were examined to confirm the development of hypersplenism. Result. Both group II and group III developed prehepatic portal hypertension; group III also presented satisfactory hypersplenism compared to the control group and group II, as documented at surgery and by hematologic and pathologic examination. Conclusions. Based on this study, the modified model of portal hypertension (by PVS + SVS) appears appropriate when studying the relationship between hypersplenism and hemodynamics in portal hypertension. It is also likely to be useful in studying the influence of diseased spleen in the treatment of portal hypertension.     

Progressive hepatocytic fatty infiltration in rats with prehepatic portal hypertension

BACKGROUND/AIMS: Homogenous evolution, with a narrow range of portal hypertension, degree of portosystemic shunt and hepatic atrophy has been described in the experimental model of prehepatic portal hypertension in the rat. However the great differences observed in the rats' liver weight could be attributed to a pathological alteration of the liver. Based on this, we performed an evolutive histological study of the liver. This study shows the existence of a progressive hepatocytic fatty infiltration. METHODOLOGY: Male Wistar rats with portal hypertension induced by triple stenosing ligation of the portal vein at 1 month (group II, n=4) and at 1 year (group IV, n=10) of postoperative evolution were used. The portal pressure, body, liver and splenic weights, types of collateral circulation and degree of mesenteric venous congestion were studied. The intracytoplasmatic lipid microvacuoles were quantified in hepatocytes with an image analyzer (software MIP/CID, Spain). The results were compared with those obtained in control rats with the same evolutive periods (Groups I and III). RESULTS: The hepatic fatty infiltration in Group II (TPVS 1 month) (30.12+/-53.92 micron2) is similar to that presented by Group III (Control 1 year) (16.52+/-45.20 micron2), while there is an increase (p<0.001) in Group IV (triple portal vein stenosis 1 year) (182.03+/-371.42 micron2) in relation to the other groups studied. The progressive hepatic fatty infiltration in triple portal vein stenosis rats is associated with a decrease of portal pressure and of the incidence of liver hepatic atrophy, portosystemic collateral circulation and mesenteric venous congestion. CONCLUSIONS: TPVS produces progressive hepatocytic fatty infiltration in the rat so that this prehepatic portal hypertension experimental model could also be considered as a hepatic steatosis model.     

Duplex sonography study in schistosomiasis portal hypertension: characterization of patients with and without a history of variceal bleeding

BACKGROUND: Presinusoidal portal hypertension with frequent episodes of upper gastrointestinal variceal bleeding are hallmarks of hepatosplenic Mansons schistosomiasis; a clinical form that affects about 5% of Brazilians who are infected by Schistosoma mansoni. AIMS: To evaluate duplex sonography findings in patients with hepatosplenic Mansons schistosomiasis with and without upper gastrointestinal variceal hemorrhage. METHODS: A cross-sectional study was performed whereby 27 consecutive patients with hepatosplenic Mansons schistosomiasis were divided into two groups: group I (six men and six women; mean age 48.7 years) with a past history of bleeding and group II (four men and eight women; mean age 44.7 years) without a past history of upper gastrointestinal bleeding, underwent duplex sonography examination. All patients underwent the same upper gastrointestinal endoscopy and laboratory examinations. Those with signs of mixed chronic liver disease or portal vein thrombosis (three cases) were excluded. RESULTS: Group I showed significantly higher mean portal vein flow velocity than group II (26.36 cm/s vs 17.15 cm/sec). Although, as a whole it was not significant in all forms of collateral vessels (83% vs 100%), there was a significantly higher frequency of splenorenal collateral circulation type in group II compared with group I (17% vs 67%). The congestion index of the portal vein was significantly lower in group I than in group II (0.057 cm vs 0.073 cm/sec). CONCLUSION: Our duplex sonography findings in hepatosplenic Mansons schistosomiasis support the idea that schistosomotic portal hypertension is strongly influenced by overflow status, and that collateral circulation seems to play an important role in hemodynamic behavior.     

Effects of angiotensin-converting enzyme inhibitors and sclerotherapy on portal hemodynamics in patients with portal hypertension

BACKGROUND/AIMS: Since pharmacotherapy of portal hypertension has always been a subject of wide interest, we decided to study the effects of different angiotensin-converting enzyme inhibitors and endoscopic sclerotherapy on portal hemodynamics in patients with portal hypertension and bleeding esophageal varices. METHODOLOGY: The study included 72 patients with portal hypertension divided into 6 equal groups. Endoscopic sclerotherapy was done to all patients every 2 weeks for 3 months. In addition, the first 5 groups of patients were maintained on angiotensin-converting enzyme inhibitors for 3 months as follows: group I on perindopril, II on ramipril, III on fosinopril, IV on lisinopril and V on captopril. Portal hemodynamics were determined before and after therapy (using an ultrasonic duplex system). New Doppler portal indices were derived and portal vein kinetic pressure was estimated for the first time by using data derived from the ultrasonic duplex system. RESULTS: 1) Short-term endoscopic sclerotherapy alone resulted in significant elevation of portal vein kinetic pressure, wall stress index and flow volume (P < 0.01) and non-significant increase in the total portal circulation resistance index (P > 0.05) and significantly decreased portal vein compliance and distensibility indices (P < 0.05); 2) Angiotensin-converting enzyme inhibitors reduced the maximum and average portal velocities, the portal flow volume, total portal circulation resistance index and increased portal vein compliance and distensibility indices, hence they reduced the portal vein kinetic pressure significantly in group IV (P < 0.05 for the flow volume and P < 0.01 for other indices); 3) The only side effect encountered was allergic cough (in 8.33% of patients). No effects were noticed on the pulse, systolic, diastolic or mean blood pressures or Child-Pugh Score of liver disease. CONCLUSIONS: 1) Angiotensin-converting enzyme inhibitors when added to endoscopic sclerotherapy can ameliorate the effects of the latter on portal hemodynamics in patients with portal hypertension; 2) Portal vein kinetic pressure, total portal circulation resistance index, portal vein wall stress index, compliance and distensibility indices are new Doppler portal indices that proved to be of value in the follow-up of patients with portal hypertension under sclerotherapy alone or in conjunction with pharmacotherapy; 3) Angiotensin-converting enzyme inhibitors are safe drugs that can be used for portal decompression with endoscopic sclerotherapy. Their use as sole portal anti-hypertensive agents still awaits further studies.     

Altered alpha adrenergic vasoresponsiveness in a non-cirrhotic portal hypertension model of E. coli injection

BACKGROUND AND AIM: Portal hypertension is associated with decreased vascular responsiveness to vasoconstrictors, which may contribute to the hyperdynamic circulation in cirrhosis. Animal models of cirrhosis and portal vein ligation have helped in our understanding of portal hypertension. The etiopathogenesis of non-cirrhotic portal fibrosis (NCPF), a common cause of portal hypertension, is still poorly understood. The aim of this study was to investigate the pathophysiology of NCPF in a rabbit model. METHODS: An indwelling cannula was inserted into the gastrosplenic vein of rabbits. Animals were randomly injected with saline (Group I, n = 13) or lipopolysaccharide (Group II, n = 13) from heat killed Escherichia coli at 0, 1, 2, 7, 14 and 28 days. Portal pressure was measured at 3 months and vasoresponsiveness studied in isolated aortic rings in intact and in endothelium-denuded tissues from both groups. RESULTS: In all group II compared with group I animals, the splenic weight (0.89 +/- 0.16 vs 0.62 +/- 0.1 g, P < 0.05) and the portal pressure (14.99 +/- 0.56 vs 7.04 +/- 0.42 mmHg, P < 0.05) were higher at 3 months. The group II animals showed reduced responsiveness to phenylephrine showing maximal contraction of 1.25 +/- 0.08 at 10(-4) mol/L as compared to 2.85 +/- 0.33 g tension in Group I (P < 0.05). Endothelium denudation of aortic rings had no effect on reduced reactivity in Group II animals. Acetylcholine induced an increase in vasorelaxation at lower concentrations in preconstricted aortic rings in Group II compared to Group I animals, but this decreased in higher concentrations. Nifedipine produced comparable vasodilatation in preconstricted rings in both the groups of animals. CONCLUSIONS: Repeated injection of lipopolysaccharide into the gastrosplenic vein leads to the development of portal hypertension. This non-cirrhotic model of portal hypertension is characterized by generalized arterial hyporeactivity to vasoconstrictors akin to other models of portal hypertension.     

Nephrectomy-induced alterations in the synthesis of catecholamines in the sympathetic nervous system and central nervous system

Reduction in renal function is a key factor to the development of salt-dependent hypertension; however, the mechanism is obscure. To examine the role of the sympathetic nervous system (SNS) and central catecholaminergic neurons in this predisposition to the development of hypertension, the activity of tyrosine hydroxylase (TH) was determined in SNS and in several brain regions. In another group of unilaterally nephrectomized rabbits, cardiovascular responsiveness to norepinephrine was determined. A unilateral nephrectomy increased the activity of TH in the midmedulla, a brain region important in the baroreflex regulation of blood pressure, and in the adrenal gland, the major source of circulating catecholamines. The activity of TH was decreased in the pons-upper medulla region. No alterations were found in the proximal and distal mesenteric arteries, lower medulla, midbrain or hypothalamus. No alteration in blood pressure or cardiovascular responsiveness to norepinephrine was found. This study indicates that a unilateral nephrectomy produces long-lasting effects on central catecholaminergic neurons and the sympathetic nervous system without an effect on blood pressure or cardiovascular responsiveness.     

Hepatic dysfunction in patients with extrahepatic portal venous obstruction

Background: Extrahepatic portal venous obstruction (EHPVO) developing due to thrombotic occlusion of the portal vein in children is generally considered a benign disease. Whether hepatic dysfunction develops in these patients in the absence of a gastrointestinal bleed has not been well studied. Materials and methods: Forty‐three patients with EHPVO who had not bled in the last 3 months were studied. Patients were divided into those with (group I) or without ascites (group II). Matched cirrhotic patients with ascites (group III) served as controls. Clinical, biochemical, ultrasonographic, and histopathological evaluation was carried out. Portal biliopathy was assessed in five patients in group I and in 12 patients in group II by cholangiography. Results: Of 43 EHPVO patients, ascites was seen in nine (21%) patients (group I). Thirty‐four patients had no ascites (group II). Serum ALT (54±24 vs. 34±10 IU/l, P<0.01), albumin (3.2±0.3 vs. 3.7±0.4 g/dl, P<0.01), and prothrombin time difference (9.0±4.5 vs. 2.4±1.9 s, P<0.05) were deranged in patients in group I compared with group II. Patients in group I were 4 years older, and the duration of portal hypertension was longer than in group II (11.5 vs. 5.6 year, P<0.05). Portal biliopathy changes were significantly more severe in group I than in group II patients. Ascites was high gradient in all the patients in group I and the serum‐ascitic albumin gradient was comparable between groups I and III. None of the EHPVO patients, but four cirrhotic patients, developed spontaneous bacterial peritonitis during a follow‐up of 11±4 months. Conclusions: Hepatic dysfunction in the form of ascites and deranged liver functions is not uncommon in patients with EHPVO, more so in patients with prolonged portal hypertension. Based on our data it would be worthwhile to study whether prolonged portal vein thrombosis in EHPVO patients could lead to progressive liver disease.     

肾上腺髓质素在中枢神经系统内的分布

目的研究肾上腺髓质素（ＡｄＭ）在中枢神经系统内的分布。方法应用免疫组织化学（ＡＢＣ法）和反转录－聚合酶链式反应（ＲＴ－ＰＣＲ）方法，观察免疫活性的ＡｄＭ及其ＡｄＭｍＲＮＡ在大鼠和人脑内的分布。结果在所检查的大鼠每一个脑区，包括大脑皮层、室旁组织、下丘脑、中脑、延髓和小脑均发现有免疫活性的ＡｄＭ及ＡｄＭｍＲＮＡ存在，应用半定量ＲＴ－ＰＣＲ分析方法发现，在大鼠的室旁组织和延髓中，ＡｄＭｍＲＮＡ表达水平较高。在人脑也发现有ＡｄＭｍＲＮＡ表达。结论在大鼠和人的中枢神经系统中存在肾上腺髓质素，它可能作为一种神经递质、神经调质或神经激素发挥生物学作用。     

Neuropeptide Y and galanin enhance the inhibitory effects of clonidine on norepinephrine release from medulla oblongata of rats.

The medulla oblongata is thought to play an important role in the central regulation of blood pressure. Neuropeptide Y (NPY) and galanin (Gal) coexist with norepinephrine (NE) and may have a functional interaction in this region. The aim of the present study was to investigate whether NPY and Gal could modulate the presynaptic neuronal mechanisms, especially the alpha-adrenoceptor function, inhibiting NE release in medulla oblongata. In slices of rat medulla oblongata, clonidine, an alpha-adrenoceptor agonist, inhibited the NE release elicited by electrical stimulation in a concentration-dependent manner. A combination of clonidine and low concentration of NPY (1 X 10(-9) mol/L) resulted in an increase in the inhibitory action of clonidine on stimulation-evoked NE release. The inhibitory action of clonidine was also potentiated by Gal (1 X 10(-8) mol/L). These results indicate the existence of the presynaptic NPY- and Gal-receptors on noradrenergic nerve terminals, which may enhance the presynaptic alpha-adrenoceptor function to inhibit NE release. This suggests a possible involvement of NPY and Gal in the regulation of sympathetic nerve activity in medulla oblongata.     

Echo-Doppler evaluation of acute flow changes in portal hypertensive patients: flow velocity as a reliable parameter

In order to evaluate the behavior of the portal vein cross-sectional area during changes in portal flow, two groups of subjects were analyzed in two blinded cross-over studies using echo-Doppler flowmetry. The first group (I) consisted of 21 patients with cirrhosis and 16 controls. They received a standardized meal which is known to increase portal flow. The second group (II) consisted of 31 patients with cirrhosis who received a dose of propranolol which is known to decrease portal flow. In Group I, 30 min after the meal, the portal vein blood velocity increased by 35 +/- 6% (p less than 0.01) in cirrhotic patients and by 55 +/- 5% (p less than 0.01), in normal subjects. The portal vein cross-sectional area increased significantly in normal subjects (22 +/- 2%, p less than 0.01) but not in cirrhotic patients (4 +/- 2%, n.s.). In Group II, 2 h after propranolol, there was a significant decrease in portal blood velocity (-14 +/- 2%), whereas the portal vein cross-sectional area did not show any significant changes. These data demonstrate that, in portal hypersensitive patients, the portal area measured by echo-Doppler flowmetry can be assumed to be constant and hence its calculation to estimate changes in portal blood flow can be omitted. Therefore, the use of blood velocity alone is suggested to monitor acute changes in flow in portal hypertension using Doppler flowmetry. The elimination of the portal vein cross-sectional area measurement simplifies the quantitative calculation of portal hemodynamics and increases the reliability of the technique by avoiding a source of error.     

Relationship between encephalopathy and portal vein-vena cava shunt： Value of computed tomography during arterial portography

AIM: TO assess the value of computed tomography during arterial portography (CTAP) in portal vein-vena cava shunt,and analysis of the episode risk in encephalopathy.METHODS: Twenty-nine patients with portal-systemic encephalopathy due to portal hypertension were classified by West Haven method into grade Ⅰ(29 cases), gradeⅡ(16 cases), grade Ⅲ(10 cases), grade Ⅳ( 4 cases). All the patients were scanned by spiraI-CT. Plane scans, artery phase and portal vein phase enhancement scans were performed, and the source images were thinly reconstructed to 1.25 mm. We reconstructed the celiac trunk, portal vein,inferior vena cava and their branches and subjected them to three-dimensional vessel analysis by volume rendering(VR) technique and multiplanar volume reconstruction (MPVR) technique. The blood vessel reconstruction technique was used to evaluate the scope and extent of portal vein-vena cava shunt, portal vein emboli and the fistula of hepatic artery- portal vein. The relationship between the episode risk of portal-systemic encephalopathy and the scope and extent of portal vein-vena cava shunt,portal vein emboli and fistula of hepatic artery- portal vein was studied.RESULTS: The three-dimensional vessel reconstruction technique of spiraI-CT could display celiac trunk, portal vein,inferior vena cava and their branches at any planes and angles and the scope and extent of portal vein-vena cavashunt, portal vein emboli and the fistula of hepatic artery- portal vein. In twenty-nine patients with portal-systemicencephalopathy, grade Ⅰ accounted for 89.7% esophageal varices, 86.2% paragastric varices; grade Ⅱ accounted for 68.75% cirsomphalos, 56.25% paraesophageal varices,62.5% retroperitoneal varices and 81.25% dilated azygos vein; grade Ⅲ accounted for 80% cirsomphalos, 60%paraesophageal varices, 70% retroperitoneal varices, 90% dilated azygos vein, and part of the patients in grades Ⅱand Ⅲ had portal vein emboli and fistula of hepatic arteryportal vein; grade Ⅳ accounted for 75% dilated left renal vein, 50% paragallbladder varices, all the patients had fistula of hepatic artery- portal vein.CONCLUSION: The three-dimensional vessel reconstruction technique of spiraI-CT can clearly display celiac trunk, portal vein, inferior vena cava and their branches at any planes and angles and the scope and extent of portal vein-vena cava shunt. The technique is valuable for evaluating the episode risk in portal-systemic encephalopathy.     

Prehepatic portal hypertension produces increased mast cell density in the small bowel and in mesenteric lymph nodes in the rat

BACKGROUND: Because most of the characteristics of the portal hypertensive enteropathy can be explained on the basis of increased levels of mast cell mediators, the purpose of the present paper was to study mast cell splanchnic infiltration. METHODS: Duodenum, jejunum, ileum and mesenteric lymph node complex infiltration by mast cells was assayed by a stereological technique in control rats (group I; n = 5) and in an experimental model of portal hypertension (the portal vein-stenosed rat, group II; n = 5) at 6 weeks after operation. RESULTS: Intestinal and mesenteric lymph node complex infiltration by mast cells increased in the animals with partial portal vein ligation. The mast cell density progressively increased distally along the small bowel. The mast cell increase in the mesenteric lymph node complex in portal vein-stenosed rats was greater than in the duodenum (P = 0.001), jejunum (P = 0.006) and ileum. CONCLUSION: The rise of mast cells density in the small bowel and mesenteric lymph node complex in rats with partial portal vein ligation suggests that these cells are involved in the etiopathogenesis of experimental portal prehepatic hypertensive enteropathy.     

大剂量雌二醇对大鼠血浆和组织中P物质和锌离子含量的影响

采用放射免疫和原子吸收方法．检测雌二醇诱发高血压过程中大鼠血浆和部分组织中P物质和微量元素锌含量的改变。结果表明雌二醇诱发高血压大鼠下丘脑、延脑中P物质含量显著升高．脑垂体、肾上腺和血浆中P物质含量显著降低（P＜0.05～0.01）。延脑、肾上腺和血浆中锌离子升高，肾脏锌离子显著降低（P＜0．05～0．01）。提示P物质参与雌二醇诱发高血压过程；雌二醇可能通过影响心血管中枢、肾上腺、肾脏及血浆中依赖于锌离子的酶的活性而使血压升高。     

Norepinephrine release and reuptake by hypothalamic synaptosomes of spontaneously hypertensive rats

We compared the overflow of endogenous norepinephrine during electrical field stimulation, the norepinephrine content, and the rate of initial neuronal uptake of [3H]norepinephrine in synaptosomes isolated from hypothalamus and brainstem of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats at 7 and 13 weeks of age. The synaptosomes of two rats, a SHR and a WKY rat control, were simultaneously processed and subjected to the same electrical field stimulation. The overflow of endogenous norepinephrine during electrical stimulation (2 Hz, 2 minutes) in the hypothalamic synaptosomes of 7-week-old SHR was significantly greater, whereas the overflow of 13-week-old SHR was equivalent to the age-matched WKY rat. The norepinephrine content of synaptosomes was about the same in SHR and age-matched controls. There was also significantly enhanced [3H]norepinephrine uptake in the hypothalamic synaptosomes of young SHR, but neither the hypothalamic nor the brainstem samples of 13-week-old SHR showed any significant difference in their rate of [3H]norepinephrine uptake. These data are similar to those we observed (unpublished observations) in perfused mesenteric artery system in which norepinephrine release was significantly elevated during periarterial nerve stimulation only in young SHR. Thus, these results suggest that a parallel enhancement of norepinephrine release in hypothalamus with that of peripheral nervous system may play an important role during development of hypertension in young SHR.     

NaCl does not affect hypothalamic noradrenergic input in deoxycorticosterone acetate/NaCl and Dahl salt-sensitive rats

Previous studies from our laboratories demonstrated that dietary NaCl supplementation in NaCl-sensitive spontaneously hypertensive rats elevates blood pressure, increases peripheral sympathetic nervous system activity, and depresses endogenous norepinephrine stores and turnover in the anterior hypothalamus. These findings suggest that reduced noradrenergic input to sympathoinhibitory neurons in anterior hypothalamus contributes to NaCl-sensitive hypertension in spontaneously hypertensive rats. The current study tested the hypothesis that dietary NaCl supplementation depresses endogenous norepinephrine stores and turnover in anterior hypothalamus of two other NaCl-sensitive models of hypertension, the Dahl salt-sensitive rat and the deoxycorticosterone acetate/NaCl hypertensive rat, thus increasing blood pressure by reducing noradrenergic input to the anterior hypothalamus. Dahl salt-sensitive rats were fed a high (8%) NaCl diet, and deoxycorticosterone acetate/NaCl rats rats drank 1% NaCl solution ad libitum for 2 or 4 weeks. Age-matched Dahl salt-sensitive rats fed a basal 1% NaCl diet and uninephrectomized Sprague-Dawley rats drinking tap water were controls. Regional brain catecholamines were determined by high-performance liquid chromatography with electrochemical detection. Norepinephrine turnover in hypothalamus (anterior, posterior, and ventral regions) and brain stem (pons and medulla) was assessed using the dopamine beta-hydroxylase inhibitor 1-cyclohexyl-2-mercapto-imidazole. High NaCl treatment caused significant elevations in blood pressure in Dahl salt-sensitive and deoxycorticosterone acetate/NaCl rats, but endogenous norepinephrine levels and turnover rates were not significantly different in anterior hypothalamus or any other brain region studied between the NaCl-supplemented and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)