Post-lymphangiographic computed tomography in chylothorax after esophagogastrectomy: a case report.

Chylothorax is a rare complication of thoracic surgery. Lymphangiography has long been considered to be the standard of reference for diagnosis and post-treatment evaluation while the role of post-lymangiographic CT is debated. We report a case of chylothorax in a 68-year-old male following esophagogastrectomy for which conservative treatment and thoracic duct ligation failed. Lymphangiography performed after these attempts revealed persistent thoracic duct leakage into the right pleural space. Subsequent non-contrast CT and reformatted images clearly depicted the sources of leakage, and this documentation targeted direct percutaneous treatment. Unfortunately, the lack of access precluded the planned percutaneous CT-guided embolization of the thoracic duct. Nevertheless, this case suggests that post- lymphangiographic CT can serve as a value-added modality in the evaluation and potential treatment of chylothorax.

Lymphadenectomy in colorectal cancer liver metastases resection: incidence of hilar lymph nodes micrometastasis.

BACKGROUND: Liver resection is considered the best treatment for metastatic colorectal cancer. Several prognostic factors have been investigated, and many studies have shown that hepatic hilum lymph nodes involvement has a negative impact on prognosis. The present study evaluated the frequency of microscopic involvement of hilar lymph nodes, through systematic lymphadenectomy and analysis of micrometastases in patients undergoing hepatectomy due to colorectal metastasis. METHODS: A total of 28 patients underwent hepatic resection with hilar lymphadenectomy. Lymph nodes considered negative by conventional hematoxylin and eosin (H&E) staining were analyzed by serial sectioning with 100-microm intervals and immunohistochemistry (IHC) with anti-human pancytokeratin antibody AE1/AE3. RESULTS: In average, 6.18 lymph nodes were dissected per patient. No morbidity or mortality was associated to lymphadenectomy. In two patients, conventional H&E analysis showed presence of microscopic lymph node metastasis. IHC analysis allowed the identification of three other patients with lymph node micrometastases. The overall frequency of microscopic metastases, including micrometastasis, was 18%. CONCLUSIONS: Systematic lymphadenectomy allowed the detection of microscopic lymph node metastases, resulting in more accurate staging of extrahepatic disease. The inclusion of IHC increased the detection of lymph node micrometastasis.

Medial septal area vasopressin receptor subtypes in the regulation of urine and sodium excretion in rats.

The present study aimed to determine the effects of selective antagonists of V(1a), V(2), and V(1a)/V(2) (Conivaptan; Astellas Pharma Inc., Tokyo, Japan) arginine vasopressin (AVP) receptors on the flow of urine and sodium excretion induced by AVP, by means of microinjections into the medial septal area (MSA) of the rat brain. Male Holtzman rats had a guide cannula implanted into the dorsal surface of the MSA. Intravenous infusion of hypotonic saline was used to promote urinary flow, which was collected for 4 h. Pretreatment with the V(1a) antagonist decreased, and the V(2) antagonist and Conivaptan (a V(1a)/V(2) antagonist) increased, the urinary flow induced by AVP. Administration of AVP increased sodium excretion. Pretreatment with V(2) or V(1a) antagonists decreased, and Conivaptan abolished, the sodium excretion induced by AVP. These results indicate that the V(1a) and V(2) receptors of the MSA are important in the central regulation of urine and sodium excretion.

Smoking increases salivary arginase activity in patients with dental implants.

It is believed that an increased arginase activity may lead to less nitric oxide production, which consequently increases the susceptibility to bacterial infection. Considering the hypothesis that smoking may alter the arginase activity and that smoking is considered a risk factor to dental implant survival, the present study aimed at evaluating the effect of smoking on the salivary arginase activity of patients with dental implants. Salivary samples of 41 subjects were collected: ten non-smoking and with no dental implants (group A), ten non-smoking subjects with dental implants (group B), ten smoking subjects with implants (group C), and 11 smoking subjects with no dental implants (group D). The levels of salivary arginase activity were determined by the measurement of L-ornithine and expressed as mIU/mg of protein. A significant increase in the salivary arginase activity was verified in groups C (64.26 +/- 16.95) and D (49.55 +/- 10.01) compared to groups A (10.04 +/- 1.95, p = 0.00001 and p = 0.0110, groups C and D, respectively) and B (11.77 +/- 1.45, p = 0.00001 and p = 0.0147, groups C and D, respectively). No significant difference was found between groups C and D (p = 0.32). Within the limits of the present study, it can be concluded that salivary arginase activity is increased in smoking subjects with dental implants in contrast to non-smoking subjects with dental implants, therefore suggesting a possible mechanism by which cigarette smoking may lead to implant failure. The analysis of salivary arginase activity may represent an important tool to prevent implant failure in the near future.

Pediatric liver transplantation: comparison between results from deceased and living related transplantation.

Timely access to a living donor has reduced pretransplant mortality in pediatric liver transplantation. We hypothesized that this strategy may provide better posttransplant outcomes, due to shorter waiting times on the transplant list. A extensive search in the medical literature from the last 10 years showed clear evidence of the benefits of living donors, namely, decreased dropout rates as well as the chance to transplant the patients in better clinical situation. However, a negative impact was related to the higher morbidity rates when compared to whole grafts from deceased donors.

Periodontal therapy reduces arginase activity in saliva of patients with chronic periodontitis.

This present study evaluated the salivary arginase activity (SAA) in patients with chronic periodontitis and the effect of periodontal therapy on the activity of such enzyme. Thirty-six patients (mean age, 45.97 +/- 14.52), 18 chronic periodontitis subjects (test group), and 18 periodontally healthy individuals (control group) participated in the study. Clinical periodontal examinations included measurements of probing pocket depth (PD), clinical attachment level (CAL), plaque (PI), and gingival (GI) indexes. The test group received periodontal therapy according to individual needs. The saliva sample was collected from all study population at baseline (both groups) and 30 days after periodontal therapy (test group). SAA was determined by measuring the L: -ornithine formation from L-arginine and was expressed as mU/ml. The results showed that the mean values of SAA were statistically different between control and test groups. SAA was about 2.5 times higher in test than control groups. Thirty days after periodontal therapy, enzyme levels were 1.56 times lower than before periodontal therapy. We concluded that SAA is increased in chronic periodontitis subjects when compared to periodontally healthy individuals and that periodontal therapy significantly reduced SAA levels. It was suggested that in the near future, SAA may be used as a salivary marker of periodontal status.

Solitary fibrous tumor of the liver: report of a rare case and review of the literature.

Solitary fibrous tumor of the liver is extremely rare, with only 38 cases reported in the literature. We present one case of a SFT originating from the caudate lobe of the liver, treated by surgical resection and review the previous reported cases.

Evaluation of molecular markers in hepatic metastasis of colorectal adenocarcinoma.

BACKGROUND/AIMS: There were 49 patients studied, coming from The Liver Unit at the "Hospital das Clinicas da Faculdade de Medicina da USP (N=41) and from "Prof. Dr. Angelita Habr-Gama and Joaquim Gama-Rodrigues Surgery Institute", SP (N=8); all of which had hepatic metastasis of colorectal adenocarcinoma, with no evidence of concurrent metastasis in any other organs and were submitted to surgical treatment, during the period of 1992 to 2002, with the aim of analyzing the immunoexpression of the p53, ki-67, p16 and molecular markers in order to relate the disease-free period with the prognosis. METHODOLOGY: The patient's clinical data were analyzed retrospectively for verification of information such as age, gender, size of the hepatic metastasis and/or the largest lesion, number of satellite nodules resected and compromised, margin of resection free from neoplasia. RESULTS: The immunoexpression of the p53 was associated with the shortest period of life free from disease (p = 0.04). The proliferation marker ki-67 was not associated with the reduction of the disease-free interval and survival; the immunoexpression of the proliferation marker p16 was not associated with the reduction of disease-free period and survival, however, it was associated with hepatic metastasis synchronism. In patients who received postoperative systemic chemotherapy with 5-FU and leucovorin, the immunoexpression on the hepatic metastasis was not associated with a longer disease-free interval. CONCLUSIONS: Molcular markers may be useful to evaluate hepatic metastasis of colorectal Adenocarcinoma.

Pseudoaneurysm of cystic artery after laparoscopic cholecystectomy.

BACKGROUND: The formation of a pseudoaneurysm of the cystic artery is a rare occurrence after laparoscopic cholecystectomy. CASE OUTLINE: Seven weeks after laparoscopic cholecystectomy, a 31-year-old woman presented with a picture of obstructive jaundice. The diagnosis of cystic artery aneurysm was verified by arteriography, CT and MRCP. At laparotomy the pseudoaneurysm was found to be compressing the common bile duct. It was successfully managed by ligation of the right hepatic artery. DISCUSSION: Although this complication is rare, the surgeon must have a high index of suspicion to make the diagnosis.

The main hepatic anatomic variations for the purpose of split-liver transplantation.

BACKGROUND/AIMS: Variant hepatic anatomy must be recognized and appropriately managed during split-liver transplantation to ensure complete vascular and biliary supply to both grafts. The aim of this study was to demonstrate the importance of an assessment of the hepatic anatomical structures for the purpose of split-liver transplantation. MATERIAL AND METHODS: Human cadaveric livers (n = 60) were obtained during routine autopsies. The cadavers and the livers had to comply with the following requirements: (1) minimum age 18 years, (2) no liver pathology expected from medical history, and (3) no liver pathology noted at autopsy. Resections were carried out en bloc with liver, celiac trunk, left gastric artery, lesser omentum, superior mesenteric artery, and head of the pancreas. The main anatomical structures of the liver as hepatic artery, portal vein, biliary tree, and hepatic veins were dissected and correlated hepatic segments for the application of liver splitting. RESULTS: The right the median, and the left hepatic veins were unique, with in 59 (98.3%), 53 (88.3%) and 46 (76.3%) cases, respectively. The portal vein trunk divided into right and left branches in 59 (98.3%) cases. A median branch appeared in 9 (15.2%) cases and no bifurcation of the portal vein occurred in 1 (1.6%) case. The right and left hepatic ducts were multiple in 47 (78.3%) and 57 (95%) cases, respectively, however, the median, hepatic duct was unique in 16 (26.6%) cases. Examining the intrahepatic distribution of the right hepatic duct, we found 4 branches in 28 (59%) cases (segments V, VI, VII, and VIII) 2 branches in 11 (23%) cases, (segments V and VI) and 2 branches in 8 (17%) cases (segments VII and VIII). Fifty-seven cadavers had multiple left hepatic ducts. The intrahepatic dissection showed that the distribution of the major branches were toward hepatic segments II and III. Three separate branches of the left hepatic duct were found in 11 (19%) cases (segments II, III, and IV). Two intrahepatic ducts coming from hepatic segments V and VI drained separately into the left intrahepatic biliary tree in 1 (2%) case. The arterial supply of the liver was by right and left hepatic artery with only 9 (15%) cases there being median hepatic artery. The right hepatic artery, coming from the superior mesenteric artery, was present in 15 (25%) cases and a left hepatic artery originating from the left gastric artery in only 2 (3.3%) cases. The left hepatic artery had 2 exceptional origins, in 1 (1.6%) case coming directly from the abdominal aorta and in the other from the superior mesenteric artery. The right and left hepatic artery was accessory, in 11 (18.3%) and 2 (3.3%) cases, respectively. The right hepatic artery was dominant in 4 (6.6%) cases. The median hepatic artery was directed to segment IV in 6 (10%) cases and to segment II and III in 3 (4.9%) cases. CONCLUSION: The study showed that the technique of controlled liver splitting for transplantation in 2 recipients is an acceptable method to increase the number of liver allografts. The anatomical and technical details of the splitting procedure are critical for the success of this technique. Good graft function and avoidance of complications depend on each graft having an intact arterial and portal blood supply as well as biliary and venous drainage from all retained liver segments. The absence of a bifurcation of the portal vein is a rare anomaly and would certainly contraindicate a partition.

Impact of steatotic grafts on initial function and prognosis after liver transplantation.

Steatotic grafts are considered a risk factor for dysfunction or even primary nonfunction of liver transplants; grafts with more than 50% fatty infiltration are routinely discarded. This retrospective study evaluated the impact of macrovesicular and microvesicular steatosis on postoperative initial liver function and prognosis by comparing outcomes to nonsteatotic grafts in 48 liver transplantation patients. Fifteen grafts had macrovesicular steatosis, 13 (27.09%) up to 50% fatty infiltration (MG2), and 2 (4.16%) more than 50% (MG3). Thirty-three (69.75%) grafts had no macrovesicular steatosis (MG1). Initial liver function was adequate in 26 (78.78%), 10 (76.93), and 2 (100%) patients, respectively, in subgroups MG1, MG2, and MG3 (P =.892). Thirty-day survival rates were 90.90%, 100%, and 100%, respectively, in subgroups MG1, MG2, and MG3 (P =.606). Twenty-six grafts showed microvesicular steatosis: 18 (37.50%) showed less than 50% fatty infiltration (mG2), and 8 (16.67%) more than 50% (mG3). Twenty-two (45.83%) grafts had no microvesicular steatosis (mG1). Initial liver function was adequate in 16 (72.72%), 16 (88.88%), and 6 (75%) patients, respectively, in subgroups mG1, mG2, and mG3 (P =.547). Thirty-day survival rates were 90.90%, 100%, and 87.5% respectively, in subgroups mG1, mG2, and mG3 (P =.380). In conclusion, macrovesicular and microvesicular steatotic liver grafts displayed adequate initial function, did not compromise survival, and thus should not be routinely discarded.

Effects of angiotensin and vasopressin V(1) receptors on water and sodium intake induced by injection of vasopressin into lateral septal area.

The specific arginine(8)-vasopressin (AVP) V(1) receptors antagonist (AAVP) was injected (20, 40 and 80 nmol) into the lateral septal area (LSA) to determine the effects of selective septal V(1) receptor on water and 3% sodium intake in rats. Was also observed the effects of losartan and CGP42112A (select ligands of the AT(1) and AT(2) ANG II receptors, respectively) injected into LSA prior AVP on the same appetites. Twenty-four hours before the experiments, the rats were deprived of water. The volume of drug solution injected was 0.5 microl. Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Injection of AVP reduced the water and sodium ingestion vs. control (0.15 M saline). Pre-treatment with AAVP (40, 80 and 160 nmol) did not alter the decrease in the water ingestion induced by AVP, whereas AAVP abolished the action of AVP-induced sodium intake. Losartan (40, 80 and 160 nmol) did not alter the effect of AVP on water and sodium intake, whereas CGP42112A (20, 40 and 60 nmol) at the first 30 min increased water ingestion. Losartan and CGP42112A together increased the actions of AVP, showing more pronounced effects than when the two antagonists were injected alone. The results showed that AVP inhibited the appetites and these effects were increased by the AAVP. The involvement of angiotensinergic receptors in the effects of AVP is also suggested.

Interaction between paraventricular nucleus and septal area in the control of physiological responses induced by angiotensin II.

We determined the effects of losartan (40 nmol) and PD 123319 (40 nmol) (both non-peptides and selective antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar1, Ala8] angiotensin II (ANG II) (40 nmol) (a non-selective peptide antagonist of angiotensin receptors) injected into the paraventricular nucleus (PVN) on the water and salt appetite, diuresis and natriuresis and mean arterial pressure (MAP) induced by administration of 10 nmol of ANG II into the medial septal area (MSA) of male Holtzman rats weighing 250-300 g. The volume of drug solution injected was 0.5 micro l over a period of 10-15 s. The responses were measured over a period of 120 min. ANG II alone injected into the MSA induced an increase in all the above parameters (8.1 +/- 1.2, 1.8 +/- 0.3, and 17.1 +/- 1.0 ml, 217 +/- 25 micro Eq/120 min, and 24 +/- 4 mmHg, respectively, N = 10-12) compared with vehicle-treated rats (1.4 +/- 0.2, 0.6 +/- 0.1, and 9.3 +/- 0.5 ml, 47 +/- 5 micro Eq/120 min, and 4.1 +/- 0.8 mmHg, respectively, N = 10-14). Pretreatment with losartan and [Sar1, Ala8] ANG II completely abolished the water and sodium intake, and the pressor increase (0.5 +/- 0.2, 1.1 +/- 0.2, 0.5 +/- 0.2, and 0.8 +/- 0.2 ml, and 1.2 +/- 3.9, 31 +/- 4.6 mmHg, respectively, N = 9-12), whereas losartan blunted the urinary and sodium excretion induced by ANG II (13.9 +/- 1.0 ml and 187 +/- 10 micro Eq/120 min, respectively, N = 9). Pretreatment with PD 123319 and [Sar1, Ala8] ANG II blocked the urinary and sodium excretion (10.7 +/- 0.8, 9.8 +/- 0.7 ml, and 67 +/- 13 and 57 +/- 17 micro Eq/120 min, respectively, N = 9), whereas pretreatment with PD 123319 partially blocked the water and sodium intake, and the MAP induced by ANG II administration (2.3 +/- 0.3, 1.1 +/- 0.1 ml, and 12 +/- 3 mmHg, respectively, N = 9-10). These results suggest the angiotensinergic effect of the MSA on the AT1 and AT2 receptors of the PVN in terms of water and sodium homeostasis and MAP modulation.

Interaction between paraventricular nucleus and septal area in the control of physiological responses induced by angiotensin II

We determined the effects of losartan (40 nmol) and PD 123319 (40 nmol) (both non-peptides and selective antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar¹, Ala8] angiotensin II (ANG II) (40 nmol) (a non-selective peptide antagonist of angiotensin receptors) injected into the paraventricular nucleus (PVN) on the water and salt appetite, diuresis and natriuresis and mean arterial pressure (MAP) induced by administration of 10 nmol of ANG II into the medial septal area (MSA) of male Holtzman rats weighing 250-300 g. The volume of drug solution injected was 0.5 æl over a period of 10-15 s. The responses were measured over a period of 120 min. ANG II alone injected into the MSA induced an increase in all the above parameters (8.1 ± 1.2, 1.8 ± 0.3, and 17.1 ± 1.0 ml, 217 ± 25 æEq/120 min, and 24 ± 4 mmHg, respectively, N = 10-12) compared with vehicle-treated rats (1.4 ± 0.2, 0.6 ± 0.1, and 9.3 ± 0.5 ml, 47 ± 5 æEq/120 min, and 4.1 ± 0.8 mmHg, respectively, N = 10-14). Pretreatment with losartan and [Sar¹, Ala8] ANG II completely abolished the water and sodium intake, and the pressor increase (0.5 ± 0.2, 1.1 ± 0.2, 0.5 ± 0.2, and 0.8 ± 0.2 ml, and 1.2 ± 3.9, 31 ± 4.6 mmHg, respectively, N = 9-12), whereas losartan blunted the urinary and sodium excretion induced by ANG II (13.9 ± 1.0 ml and 187 ± 10 æEq/120 min, respectively, N = 9). Pretreatment with PD 123319 and [Sar¹, Ala8] ANG II blocked the urinary and sodium excretion (10.7 ± 0.8, 9.8 ± 0.7 ml, and 67 ± 13 and 57 ± 17 æEq/120 min, respectively, N = 9), whereas pretreatment with PD 123319 partially blocked the water and sodium intake, and the MAP induced by ANG II administration (2.3 ± 0.3, 1.1 ± 0.1 ml, and 12 ± 3 mmHg, respectively, N = 9-10). These results suggest the angiotensinergic effect of the MSA on the AT1 and AT2 receptors of the PVN in terms of water and sodium homeostasis and MAP modulation

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II.

We investigated the role of alpha-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na+, K+ and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/ micro l) increased water intake (12.5 +/- 1.7 ml/120 min). Clonidine (20 nmol/ micro l) injected into the MSA reduced the ANGII-induced water intake (2.9 +/- 0.5 ml/120 min). Pretreatment with 80 nmol/ micro l yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 +/- 0.4 and 3.1 +/- 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGII-induced water intake (0.2 +/- 0.1 and 0.2 +/- 0.1 ml/120 min, respectively). ANGII reduced Na+ (23 +/- 7 micro Eq/120 min), K+ (27 +/- 3 micro Eq/120 min) and urine volume (4.3 +/- 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of alpha1- and alpha2-antagonists decreased ANGII-induced water intake, and abolished the Na+, K+ and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal alpha1- and alpha2-adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII.

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

We investigated the role of alpha-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na+, K+ and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/æl) increased water intake (12.5 ± 1.7 ml/120 min). Clonidine (20 nmol/æl) injected into the MSA reduced the ANGII-induced water intake (2.9 ± 0.5 ml/120 min). Pretreatment with 80 nmol/æl yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 ± 0.4 and 3.1 ± 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGII-induced water intake (0.2 ± 0.1 and 0.2 ± 0.1 ml/120 min, respectively). ANGII reduced Na+ (23 ± 7 æEq/120 min), K+ (27 ± 3 æEq/120 min) and urine volume (4.3 ± 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of alpha1- and alpha2-antagonists decreased ANGII-induced water intake, and abolished the Na+, K+ and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal alpha1- and alpha2-adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII

[Hepatosplenic schistosomiasis portal hypertension: effect of esophagogastric devascularization with splenectomy on the diameter and mean flow velocity in the portal system (ultra-sonographic Doppler]. / Hipertensão portal por esquistossomose mansônica hepatoesplênica: efeito da desconexão ázigo-portal com esplenectomia no diâmetro e na velocidade média de fluxo do sistema portal (estudo ultra-sonográfico com Doppler).

BACKGROUND: Esophagogastric devascularization with splenectomy has been used for the treatment of upper digestive bleeding due to esophagic varices in hepatoportal mansoni's schistosomic portal hypertension. Nevertheless, early portal thrombosis has hampered this surgical technique (13.3% and 53.2%), compromising the good results on the hemorrhagic side. Supposing that portal circulatory changes, due to the surgical treatment, may play an important role in this kind of complication, our objective was to identify the hemodynamic facilitating factors. Portal hemodynamic aspects, identified by ultra-sonographic Doppler study, from two groups of patients: non-operated upon and splenectomized with esophagogastric devascularization in late post-operatory phase (in excess of 6 moths), with portal hypertension due to mansoni hepatoesplenic portal hypertension and in similar clinical conditions, were compared. METHOD: Fifty eight ambulatorial patients were studied, all had portal hypertension caused by mansoni's hepatosplenic schistosomiasis and previous bouts of digestive bleeding. They were divided in two groups: A--29 followed clinically/endoscopically, and group B--29 previously submitted to esophagogastric devascularization with splenectomy. In all was measured the diameter and mean flow velocity in the portal vein and its right and left branches by ultra-sonographic Doppler study. The results were submitted to statistical analysis for inter- and intra-group comparison. RESULTS: Group A (non-operated): the portal vein diameter was greater than the right and left branches (10.6 +/- 2.9, 8.0 +/- 1.8, 9.1 +/- 2.6 cm), the mean flow velocities in the portal vein and its branches were similar (15.62 +/- 6.17, 14.92 +/- 5.33, 16.12 +/- 4.18 cm/seg). Group B (operated): the diameter and mean flow velocity in all vessels were reduced (8.8 +/- 1.7, 5.2 +/- 1.2, 7.5 +/- 2.2 cm/12.53 +/- 2.60, 8.86 +/- 1.75, 9.69 +/- 3.75 cm/seg). CONCLUSIONS: After esophagogastric devascularization with splenectomy, there was a reduction of the diameter and mean flow velocity in the portal vein, its right and left branches.

Role of the alpha(1)- and alpha(2)-adrenoceptors of the paraventricular nucleus on the water and salt intake, renal excretion, and arterial pressure induced by angiotensin II injection into the medial septal area.

In this study we investigated the influence of alpha-adrenergic antagonists injections into the paraventricular nucleus (PVN) of the hypothalamus on the thirst and salt appetite, diuresis, natriuresis, and pressor effects of angiotensin II (ANG II) stimulation of medial septal area (MSA). ANG II injection into the MSA induced water and sodium intake, diuresis, natriuresis, and pressor responses. The previous injection of prazosin (an alpha(1)-adrenergic antagonist) into the PVN abolished, whereas previous administration of yohimbine (an alpha(2)-adrenergic antagonist) into the PVN increased the water and sodium intake, urinary, natriuretic, and pressor responses induced by ANG II injected into the MSA. Previous injection of a nonselective alpha-adrenergic antagonist, regitin, into the PVN blocked the urinary excretion, and reduced the water and sodium intake, sodium intake, and pressor responses induced by ANG II injected into the MSA. The present results suggest that alpha-adrenergic pathways involving the PVN are important for the water and sodium excretion, urine and sodium excretion, and pressor responses, induced by angiotensinergic activation of the MSA.

[Doppler ultrasonography evaluation of paraumbilical vein and portal hypertension]. / Evaluation par échographie-Doppler de la veine para-ombilicale dans l'hypertension portale.

UNLABELLED: Portal hypertension is associated to the development of portosystemic collateral veins, particularly the paraumbilical vein. PURPOSE: To evaluate the biometric and hemodynamic characteristics of the portal vessels related to the presence of a patent paraumbilical vein, in the setting of portal hypertension secondary to hepatosplenic schistosomiasis. METHODS: 75 patients with portal hypertension secondary to hepatosplenic schistosomiasis were evaluated by Doppler US. The patients were studied based on the presence (group B) or not (Group A) of a patent paraumbilical vein. The diameter and blood flow velocity of the portal vessels and of the paraumbilical vein were recorded. RESULTS: The paraumbilical vein was detected in 17.33% of patients. The results showed an increase of the diameter of the main and left portal vessels whenever a patent paraumbilical vein was present (portal vein: A = 1.14 +/- 0.29 cm/B = 1.33 +/- 0.16 cm; left branch: A = 0.95 +/- 0.25 cm/B = 1.30 +/- 0.24 cm). The mean blood flow velocity was also increased in the portal trunk (A = 15.96 +/- 6.17 cm/sec/B = 19.82 +/- 6.26 cm/sec) and in the left portal branch (A = 14.77 +/- 4.29 cm/sec/B = 19.92 +/- 6.88 cm/sec). CONCLUSION: The presence of a patent paraumbilical vein is related to significant biometric and hemodynamic variations in the portal venous system, in the setting of portal hypertension secondary to hepatosplenic schistosomiasis.

[Patent paraumbilical vein: hemodynamic importance in Mansoni's hepatosplenic portal hypertension (Study with ultrasonography Doppler]. / Veia paraumbilical pérvia: importância hemodinâmica na hipertensão portal por esquistossomose mansônica hepatoesplênica. (Estudo com ultra-sonografia Doppler).

BACKGROUND: The hemodynamical effect of the collateral portosystemic circulation upon the portal system has not yet been fully understood. The US-Doppler made possible the non-invasive study of the portal system by evaluating the parameters: flow direction, diameter and flow velocity in it's vessels. AIMS: To study the paraumbilical vein as a collateral portosystemic pathway and identify patterns for appraising its hemodynamic importance to the portal system. METHOD: US-Doppler study of the portal system of 24 patients with Mansoni's hepatosplenic schistosomic portal hypertension, previous esophagic variceal bleeding and patent paraumbilical vein with hepatofugal flow. The diameter and the mean flow velocity were measured in the paraumbilical vein and so were the mean flow velocity in the portal vein, right and left portal branches. The Pearson test (linear correlation) was applied to the portal vein's mean flow velocity and the paraumbilical vein's diameter and mean flow velocity. The patients were divided in four groups: D1-paraumbilical vein with diameter < 0.68 cm (n = 14), D2-paraumbilical vein with diameter > or = 0.68 cm (n = 10), V1-paraumbilical vein with mean flow velocity < 18.41 cm/seg (n = 13) and V2-paraumbilical vein with mean flow velocity > or = 18.41 cm/seg (n = 11). The mean flow velocity in the portal vein, right and left portal branches of the four groups were compared. RESULTS: The paraumbilical vein diameter was 0.68 +/- 0.33 cm (range: 0.15-1.30 cm) and the mean flow velocity was 18.41 +/- 11.51 cm/seg (range: 5.73-38.20 cm/seg). The linear correlation between the portal vein's mean flow velocity/paraumbilical vein diameter and the paraumbilical vein's mean flow velocity showed r = 0.504 and r = 0.735, respectively. In the group D2 there was an increase in the mean flow velocity in the portal vein (17.80 +/- 3.42/22.30 +/- 7.67 cm/seg) and in the left portal branch (16.00 +/- 4.73/22.40 +/- 7.90 cm/seg). In the group V2 there was an increase in the mean flow velocity in the portal vein (16.31 +/- 3.49/21.96 +/- 5.89 cm/seg) and in the left portal branch (14.22 +/- 4.41/21.94 +/- 7.20 cm/seg). There was no change in the right portal branch (13.67 +/- 5.74/15.43 +/- 3.43 cm/seg). CONCLUSIONS: In portal hypertension due to hepatosplenic schistosomiasis, the patent paraumbilical vein, with hepatofugal flow, diameter > or = 0.68 cm and mean flow velocity > or = 18.41 cm/seg causes an increase of the mean flow velocity in the portal vein and left portal branch. The best US-Doppler parameter to appraise the paraumbilical vein influence upon the portal system is the mean flow velocity. The correlation between the increase in portal vein's mean flow velocity is stronger with the paraumbilical vein's mean flow velocity than with its diameter. The increase in the portal vein's and left portal branch's mean flow velocity may be understood as the paraumbilical vein's hemodynamic influence upon the portal system. An active portosystemic collateral pathway increases the mean flow velocity in the vein's segment proximal to its point of origin.