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.

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.

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.

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.

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.

Evidence for a role of prolactin in prostate and seminal vesicle growth in immature male rats.

To determine if prolactin secreted endogenously by anterior pituitary grafts could augment male accessory organ weights, single anterior pituitary grafts were placed under the kidney capsule of male rats, whereas control animals received a graft of muscle. Three weeks after transplantation, the animals were sacrificed by decapitation and a significant increase in plasma prolactin was observed, which was accompanied by a highly significant increase in the weights of seminal vesicles, ventral and dorsal prostates, and adrenals. To determine the importance of testicular steroids in the response, animals were castrated. The increases in prolactin, seminal vesicle and ventral and dorsal prostate weights still occurred whether or not a small dose of testosterone replacement therapy was employed. In the presence of the pituitary graft, adrenal weight usually increased in these animals as well. To rule out a requirement for adrenal steroids in the response, adrenalectomized-castrate animals were also studied, and the increases in prolactin and prostate weights still occurred although there was no significant increase in the size of the seminal vesicles. To rule out the participation of other pituitary hormones, pituitary grafts were also placed in hypophysectomized animals, and in these animals, there was also a significant increase in prolactin, accessory sex organ and testicular weights, but the adrenals did not increase in size. The grafts failed to alter gonadotropin titers in any experiment. It is concluded that single anterior pituitary grafts are capable of secreting sufficient prolactin to increase the size of the sex accessories and sometimes the testes and adrenals of the rat. Furthermore, the effects on the male sex accessory organs were demonstrable in the absence of testicular or both testicular and adrenal steroids. The data suggest that prolactin may play a physiological role in the growth of the testes, adrenals and sex accessories.

Imidazoline receptors of the paraventricular nucleus on the pressor response induced by stimulation of the subfornical organ.

In the present experiments we investigated a possible involvement of imidazoline receptors of the paraventricular nucleus (PVN) of the hypothalamus on the pressor effects of the angiotensin II (ANG II) injected into the subfornical organ (SFO), in male Holtzman rats (250-300 g) with a cannula implanted into the third ventricle (3rdV), PVN and SFO. At first we tested the participation of alpha 2 and imidazoline agonist and antagonist compounds on the pressor effect of ANG II injected into the 3rdV. Based on the results we may conclude that clonidine associated with rilmenidine was able to block the hypertensive response to ANG II. The ANG II (20 pmol) injected into SFO induced a robust increase in blood pressure (37 +/- 2 mmHg). Isotonic saline (0.15 M) NaCl did not produce any change in blood pressure (5 +/- 2 mmHg). The injection of rilmenidine (30 micrograms/kg/1 microL), an imidazoline agonist agent injected into PVN before ANG II injection into SFO, blocked the pressor effect of ANG II (5 +/- 2 mmHg). Also, the injection of idazoxan (60 micrograms/kg/microL) before rilmenidine blocked the inhibitory effect of rilmenidine on blood pressure (39 +/- 4 mmHg). The injection of clonidine (20 nmol/microL) prior to ANG II into the 3rdV produced a decreased in arterial blood pressure (37 +/- 2 mmHg) to (15 +/- 4 mmHg). The injection of yohimbine (80 nmol/microL) prior to clonidine blocked the effect of clonidine on the effect of ANG II (27 +/- 2 mmHg). The injection of rilmenidine prior to ANG II also induced a decrease in arterial blood pressure (10 +/- 3 mmHg). The injection of idazoxan prior to rilmenidine also blocked the inhibitory effect of rilmenidine (24 +/- 3 mmHg). In summary, the present study demonstrated that rilmenidine decreases the hypertensive effect of ANG II, with more potency than clonidine, even when injected into 3rdV or PVN. This study established that the PVN interacts with SFO by imidazoline receptors in order to control the arterial blood pressure.

Ibotenate lesion of the medial hypothalamus alters the salt intake and pressor responses to activation of the median preoptic nucleus in rats.

We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and pressor responses induced by the concomitant angiotensinergic, alpha 2 and beta adrenergic activation of the MnPO, whereas alpha 1 activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.

Renal effects of angiotensin II receptor subtype 1 and 2-selective ligands injected into the paraventricular nucleus of conscious rats.

We determined the effects of losartan and CGP42112A (selective ligands of the AT1 and AT2 angiotensin receptors, respectively) and salarasin (a relatively nonselective angiotensin receptor antagonist) on urinary volume and urinary sodium and potassium excretion induced by administration of angiotensin II (ANG II) into the paraventricular nucleus (PVN) of conscious rats. Both the AT1 and AT2 ligands and salarasin administered in the presence of ANG II elicited a concentration-dependent inhibition of urine excretion, but losartan inhibited only 75% of this response. The IC50 for salarasin, CGP42112A, and losartan was 0.01, 0.05, and 6 nM, respectively. Previous treatment with saralasin, CGP42112A and losartan competitively antagonized the natriuretic responses to PVN administration of ANG II, and the IC50 values were 0.09, 0.48, and 10 nM, respectively. The maximum response to losartan was 65% of that obtained with saralasin. Pretreatment with saralasin, losartan, and CGP42112A injected into the PVN caused shifts to the right of the concentration-response curves, but the losartan concentrations were disproportionately greater compared with salarasin or CGP42112A. The IC50 values were 0.06, 0.5, and 7.0 for salarasin, CGP42112A, and losartan, respectively. These results suggest that both AT1 and AT2 receptor subtypes in the PVN are involved in ANG II-related urine, sodium, and potassium excretion, and that the inhibitory responses to AT2 blockade are predominant.

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.

Effects of subtypes alpha- and beta-adrenoceptors of the lateral hypothalamus on the water and sodium intake induced by angiotensin II injected into the subfornical organ.

The present experiments were conducted to investigate the role of the alpha(1A)-, alpha(1B), beta(1)- and beta(2)-adrenoceptors of the lateral hypothalamus (LH) on the water and salt intake responses elicited by subfornical organ (SFO) injection of angiotensin II (ANG II) in rats. 5-methylurapidil (an alpha(1A)-adrenergic antagonist), cyclazosin (an alpha(1B)-adrenergic antagonist) and ICI-118,551 (a beta(2)-adrenergic antagonist) injected into the LH produced a dose-dependent reduction, whereas efaroxan (an alpha(2)-antagonist) increased the water intake induced by administration of ANG II into the SFO. These data show that injection of 5-methylurapidil into the LH prior to ANG II into the SFO increased the water and sodium intake induced by the injection of ANG II. The present data also show that atenolol (a beta(1)-adrenergic antagonist), ICI-118,551, cyclazosin, or efaroxan injected into the LH reduced in a dose-dependent manner the water and sodium intake to angiotensinergic activation of SFO. Thus, the alpha(1)- and beta-adrenoceptors of the LH are possibly involved with central mechanisms dependent on ANG II and SFO that control water and sodium intake.

Role of adrenergic pathways of the medial preoptic area in ANGII-induced water intake and renal excretion in rats.

In this study, we investigated the participation of adrenergic neurotransmission in angiotensin II- (ANGII)-induced water intake and urinary electrolyte excretion by means of injection of the alpha 1-, alpha 2-, and beta-adrenoceptor antagonists and ANGII into the medial preoptic area (MPOA) in rats. Prazosin (an alpha 1-adrenergic antagonist) antagonized the water ingestion, Na+, K+ and urine excretion induced by ANGII, whereas yohimbine (an alpha 2-adrenergic antagonist) enhanced the Na+, K+ and urine excretion induced by ANGII. Propranolol (a nonselective beta-adrenoceptor blocker) antagonized the water ingestion and enhanced the Na+, and urine excretion induced by ANGII. Previous treatment with prazosin reduced the pressor responses to ANGII, whereas yohimbine had opposite effects. Previous injection of propranolol produced no effects in the pressor responses to ANGII. These results suggest that the adrenergic neurotransmission in the MPOA may actively participate in ANGII-induced dipsogenesis, natriuresis, kaliuresis and diuresis in a process that involves alpha 1-, alpha 2-, and beta-adrenoceptors.

Lesion of the anteroventral third ventricle region impairs the recovery of arterial pressure induced by hypertonic saline in rats submitted to hemorrhagic shock.

The effect of intravenous infusion of hypertonic saline (HS, 7.5% NaCl) on the recovery of mean arterial pressure (MAP) after hemorrhage was studied in sham-operated rats and in rats with electrolytic lesion of the anteroventral third ventricle (AV3V) region (4 h, 4 and 20 days). Rats anesthetized with thiopental sodium were bled (about 2.8 ml/100 g) until the MAP was stabilized at the level of 60 mmHg for 30 min. In sham-lesioned rats, MAP increased to 90 mmHg and became stable near this level after intravenous infusion of 7.5% NaCl (4 ml/kg b.wt.). In AV3V-lesioned rats, the same infusion induced a smaller increase in MAP (80 mmHg) and the MAP returned to pre-infusion levels within 30 min. These results show that the AV3V region plays an important role in the recovery of arterial pressure induced by hypertonic saline in rats submitted to hemorrhagic shock.

AV3V lesion suppresses the pressor, dipsogenic and natriuretic responses to cholinergic activation of the septal area in rats.

In the present study we investigated the effect of anteroventral third ventricle (AV3V) lesion on pressor, dipsogenic, natriuretic and kaliuretic responses induced by the injection of carbachol (a cholinergic agonist) into the medial septal area (MSA) of rats. Male rats with sham or AV3V lesion and a stainless-steel cannula implanted into the MSA were used. Carbachol (2 nmol) injected into the MSA in sham lesion rats produced pressor (43 +/- 2 mmHg), dipsogenic (9.6 +/- 1.2 ml/h), natriuretic (531 +/- 82 microEq/120 min) and kaliuretic (164 +/- 14 microEq/120 min) responses. In AV3V-lesioned rats (1-5 days and 14-18 days), the pressor (11 +/- 2 and 14 +/- 2 mmHg, respectively), dipsogenic (1.9 +/- 0.7 and 1.4 +/- 0.6 ml/h), natriuretic (21 +/- 5 and 159 +/- 44 microEq/120 min) and kaliuretic (124 +/- 14 and 86 +/- 13 microEq/120 min) responses induced by carbachol injection into the MSA were reduced. These results show that the AV3V region is essential for the pressor, dipsogenic, natriuretic and kaliuretic responses induced by cholinergic activation of the MSA in rats.

Role of the alpha 1-, and alpha 2- and beta-adrenoceptors of the median preoptic area on the water intake, renal excretion, and arterial pressure induced by ANG II.

The present experiments were conducted to investigate the role of the alpha 1-, alpha 2- and beta-adrenergic receptors of the median preoptic area (MnPO) on the water intake and urinary electrolyte excretion, elicited by central injections of angiotensin II (ANG II). Prazosin (an alpha 1-adrenergic receptor antagonist) and yohimbine (an alpha 2-adrenergic receptor antagonist) antagonized the water ingestion, Na+, K+, and urine excretion induced by ANG II. Administration of propranolol, a beta-adrenergic receptor antagonist increased the Na+, K+, and urine excretion induced by ANG II. Previous treatment with prazosin and yohimbine reduced the pressor responses to ANG II. These results suggest that the adrenergic neurotransmission in the MnPO may actively participate in ANG II-induced dipsogenesis, natriuresis, kaliuresis, diuresis and pressor responses in a process that involves alpha 1-, alpha 2-, and beta-adrenoceptors.

Clonidine and phenylephrine injected into the lateral hypothalamus inhibits water intake in rats.

It has been demonstrated that peripheral or intracerebroventricular (i.c.v.) administration of the alpha 2-adrenoceptor agonist, clonidine, blocks the water intake induced by several dipsogenic stimuli in rats. In the present investigation we studied the effect of the injection of clonidine, phenylephrine, prazosin or yohimbine into the lateral hypothalamic area (LHA) on the water intake induced by water deprivation or central angiotensin II (AII) in rats. Rats with chronic cannulas implanted into the lateral ventricle and LHA were used. Injection of clonidine or phenylephrine into the LHA reduced the water intake produced by both water deprivation and i.c.v. injection of AII. Previous injection of the alpha 1- or alpha 2-adrenoceptor antagonists, prazosin or yohimbine, into the LHA reduced the antidipsogenic effect of clonidine or phenylephrine injected into the same area. These results suggest that the alpha 1- and alpha 2-adrenergic receptors of the hypothalamus are part of the central inhibitory system for the thirst produced by dehydration or central AII.

Role of the alpha 1- and alpha 2-adrenoceptors of the lateral hypothalamus in the dipsogenic response to central angiotensin II in rats.

The present experiments were conducted to investigate the role of the alpha 1- and alpha 2-adrenergic receptors of the lateral hypothalamus (LH) on the drinking response elicited by intracerebroventricular (i.c.v.) injections of carbachol and angiotensin II (AII) in rats. Clonidine (an alpha 2-adrenergic agonist) injected into the LH produced a dose-dependent reduction of the drinking responses elicited by i.c.v. administration of carbachol and AII. The alpha 1-adrenergic agonist phenylephrine injected into the LH reduced the dipsogenic response to i.c.v. AII, but not to carbachol. Injection of yohimbine (an alpha 2-adrenergic antagonist) and prazosin (an alpha 1-adrenergic antagonist) into the LH also reduced the water intake produced by i.c.v. injection of AII. Previous injection of alpha 1- or alpha 2-adrenergic antagonists into the LH increased the antidipsogenic effect of clonidine or phenylephrine injected into the same area on the water intake induced by i.c.v. AII. These results show that the alpha 1- and alpha 2-adrenergic receptors of the LH are involved in the control of drinking responses elicited by i.c.v. injection of AII in rats. They also show that clonidine, but not phenylephrine, suppresses the drinking induced by i.c.v. carbachol. The data suggest that the discharge of central alpha-adrenergic receptors has a dual (inhibitory and excitatory) effect on water intake induced by central AII.

Lesion of the anteroventral third ventricle region abolishes the beneficial effects of hypertonic saline on hemorrhagic shock in rats.

The effect of intravenous infusion of hypertonic saline (HS, 7.5% NaCl) on the recovery of mean arterial pressure (MAP) during hemorrhage was studied in sham-operated rats and in rats with electrolytic lesion in the anteroventral third ventricle (AV3V) region. After intravenous infusion of 7.5% NaCl (4 ml/kg b.wt.), MAP increased from about 60 to 90 mmHg in sham rats and became stable at this level during all the time of observation (30 min). In AV3V-lesioned rats, after the same infusion, the MAP increased to 80 mmHg, but returned to the pre-infusion levels within 30 min. These results show that the integrity of the AV3V region is important for the beneficial effect of HS during hemorrhagic shock in rats. The AV3V lesion disrupts neural pathways involved in the maintenance of fluid balance and these changes probably abolish the effect of hypertonic saline.

Role of alpha 1 and alpha 2-adrenoceptors of the lateral hypothalamic area on urinary excretion caused by centrally administered angiotensin II.

To determine whether central alpha 1 and alpha 2-adrenergic mechanisms are involved in urinary sodium and potassium excretion and urine volume induced by angiotensin II (ANGII), these renal parameters were measured in volume-expanded Holtzman rats with cannulas implanted into lateral ventricle (LV) and lateral hypothalamus (LH). The injection of ANGII into LV in rats with volume expansion reduced the sodium, potassium and urine excretion in comparison to the control injections of isotonic saline, whereas prazosin (alpha 1 antagonist) potentiated these effects. Clonidine (alpha 2 agonist) and yohimbine (alpha 2 antagonist) injected into LH previous to injection of ANGII into LV also abolished the inhibitory effect of ANGII. These results suggest that the discharge of central alpha-adrenergic receptors has dual inhibitory and excitatory effect on antinatriuretic, antikaliuretic and antidiuretic effect induced by central ANGII in volume-expanded rats.