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Hypoxia is a naturally occurring environmental challenge for embryonic reptiles, and this is the first study to investigate the impact of chronic hypoxia on the in ovo development of autonomic cardiovascular regulation and circulating catecholamine levels in a reptile. We measured heart rate (f(H)) and chorioallantoic arterial blood pressure (MAP) in normoxic ('N21') and hypoxic-incubated ('H10'; 10% O(2)) American alligator embryos (Alligator mississippiensis) at 70, 80 and 90% of development. Embryonic alligator responses to adrenergic blockade with propranolol and phentolamine were very similar to previously reported responses of embryonic chicken, and demonstrated that embryonic alligator has α and β-adrenergic tone over the final third of development. However, adrenergic tone originates entirely from circulating catecholamines and is not altered by chronic hypoxic incubation, as neither cholinergic blockade with atropine nor ganglionic blockade with hexamethonium altered baseline cardiovascular variables in N21 or H10 embryos. In addition, both atropine and hexamethonium injection did not alter the generally depressive effects of acute hypoxia - bradycardia and hypotension. However, H10 embryos showed significantly higher levels of noradrenaline and adrenaline at 70% of development, as well as higher noradrenaline at 80% of development, suggesting that circulating catecholamines reach maximal levels earlier in incubation for H10 embryos, compared to N21 embryos. Chronically elevated levels of catecholamines may alter the normal balance between α and β-adrenoreceptors in H10 alligator embryos, causing chronic bradycardia and hypotension of H10 embryos measured in normoxia., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Paramagnetic centers in the blood of patients with prostate adenocarcinoma have been studied prior to and after plastic orchectomy by EPR. It has been shown that significant alterations in blood paramagnetic centers occur after the surgery. These alterations point to an improvement of antioxidant properties of the blood. Specifically, the content of the Fe(3+)-transferrin complexes increased, and the number of inactivated adrenoreceptors, MetHb, and Mn(2+)-containing complexes decreased. It was found that, along with improvement of the antioxidant properties of the blood, a significant decrease in the intensity of lipid peroxidation in the blood of the patients occurs.

Objective: To investigate the effects of sympathetic neurotransmitters and adrenergic receptors on liver fibrosis in murine schistosomiasis., Methods: Mice were infestated with schistosoma by means of pasting cercariae on their abdomens. Thirty mice were randomly divided into a control group and a model group. Hematoxylin eosin and Van Gieson staining were used to view the histopathology of their livers. Immunofluorescence histochemistry and laser scanning confocal fluorescence microscopy were used to measure the a1A and beta2 adrenergic receptors in livers of the two groups of mice. High performance liquid chromatography-electrochemical detector (HPLC-ECD) was used to determine the concentration of norepinephrine (NE) and dopamine (DA) in the plasma of the mice., Results: Immunofluorescence histochemistry showed that a1A and beta2 receptors were present in hepatocytes and hepatic sinusoids of the livers of the mice of the two groups, but there were many more in the livers of the schistosoma infected mice (t=-2.888; t=-6.648) (P<0.05). The results of HPLC-ECD showed that the levels of NE and DA in the model group were higher than those of the control group (t=-3.372; t=-4.428) (P<0.05)., Conclusion: Sympathetic neurotransmitters and adrenergic receptors may participate in liver fibrogenesis in mice infected with schistosoma.

Aim: The purpose of this study was to evaluate the hypothesis that acute hyperglycaemia in hearts of rats without diabetes alters coronary vascular responses to nitric oxide (NO), adenosine (ADO) and phenylephrine (PHE)., Methods: Coronary function was studied in isolated, Langendorff-perfused, non-beating rat hearts that were perfused with an oxygenated Krebs-Henseleit solution containing 40 mM KCl to arrest the hearts. Changes in coronary vascular resistance were assessed by measuring changes in coronary perfusion pressure under constant flow conditions. Coronary responses to ADO, sodium nitroprusside (SNP), PHE and L-NAME (inhibitor of NO synthase) were studied either under normoglycaemic conditions (100 mg/dl d-glucose) or after 60 min of hyperglycaemic perfusion (500 mg/dl d-glucose). d-mannitol was used as a hyperosmotic control., Results: Hyperglycaemia did not alter vasodilator responses to ADO or SNP in the presence or absence of L-NAME. Furthermore, hyperglycaemia, compared with normoglycaemia, did not alter vasoconstrictor responses induced by L-NAME or PHE., Conclusions: Sixty minutes of exposure to 500 mg/dl of d-glucose in an isolated, non-beating, buffer-perfused rat heart did not significantly affect coronary vascular smooth muscle vasodilator responses to NO and ADO or alter alpha(1)-adrenoceptor-mediated vasoconstrictor responses to PHE. Furthermore, an unchanged vasoconstrictor response to L-NAME suggests that acute hyperglycaemia did not alter NO bioavailability.

The case study purpose was to investigate the oxidation-antioxidation process in the affected organism after traumatic shock and under the impact of Plapherone LB. A randomized experiment involved 94 patients who were shared between 2 groups: group 1--routine intensive therapy, group 2--it received additionally Plapherone LB (sublingually, 2 mg protein/day). Ten persons of the control group were investigated separately. It was found by the method of electron paramagnet resonance that the antixidant system became weaker (in patients with traumatic chock), the lipoid oxidants got more intensified, the activity of their oxidant enzymes went up and the concentration of free radical got to be higher. Finally, Plapherone LB was found to promote the optimization of such systemic changes, since it normalized the xanthine oxidase activity in experimental traumatic shock.

In this study, we examined whether the adrenergic volume response of teleost erythrocytes is related to cell maturity. Rainbow trout (Oncorhynchus mykiss) were made anaemic by reducing their haematocrit to approximately 50 % of the original value. After 3-4 weeks, small, young erythrocytes were seen in the circulation. By measuring the volume distribution of blood samples from anaemic fish before and after noradrenaline stimulation (10 min, 10(-5)mol l(-1) final concentration), we were able to show that the volume response of young, immature erythrocytes to catecholamine stimulation was greater than that of mature erythrocytes. In addition, the membrane fluidity, measured using the steady-state fluorescence polarisation method, was greater in anaemic fish after 24 days of recovery from bleeding than in control fish. Since blood from anaemic fish contained a large fraction of immature erythrocytes, this result indicates that the fluidity of the membrane of immature erythrocytes is greater than that of mature erythrocytes.

Serum catecholamine levels and myocardial and lymphocyte adrenergic receptor (AR) concentrations were measured in adult great danes affected by canine dilated cardiomyopathy (DCM) and compared to those of healthy animals. A non-homogeneous population of beta -AR, consisting of beta(1)-AR and beta(2)-AR, was observed in healthy (41 and 59%, respectively) and affected (17 and 83%, respectively) dog lymphocytes. Binding assays revealed that total beta -AR, beta(1)-AR and alpha(1)-AR were significantly downregulated (P<0.05;P<0.01;P<0. 001), both in lymphocyte and myocardial cell membranes of affected dogs. beta(2)-Adrenergic receptor concentrations were significantly reduced only in lymphocyte and right atrium cell membranes (P<0.05). Downregulation was not associated with alterations in receptor binding characteristics, as no significant differences in K(d)values were found. Mean plasma catecholamine levels were significantly higher (P<0.01) in DCM dogs (939+/-41) than in normal subjects (348+/-32), thus suggesting a sympathetic activation. The present study indicates a condition similar to that observed in human patients affected by DCM and that adrenergic receptors in canine lymphocytes reflect the fluctuation of adrenergic receptor concentrations in the myocardium., (Copyright 1999 Harcourt Publishers Ltd.)

Objective: The present study was undertaken to elucidate possible mechanisms underlying sex differences in cardiovascular measures or reactivity to challenge. Because there is vastly diverging literature on the issue, we tried to control for endocrine and psychological factors, which might contribute to some of the apparent discrepancies., Methods: Blood pressure, heart rate, adrenaline, and noradrenaline in women (N = 24) and men (N = 14) were examined during baseline and challenge (Stroop Test and Cold Face Test). Adrenoceptor density on lymphocytes (beta 2) and platelets (alpha 2) were determined to examine possible sex differences in underlying cardiovascular mechanisms. Gender effects were controlled by assessing gender role orientation and task appraisal. Women were tested during either the follicular (N = 12) or the luteal (N = 12) phase of the menstrual cycle (verified by estradiol, progesterone, and luteinizing hormone)., Results: Follicular and luteal phase women did not differ in any parameter except progesterone. We observed sex-related differences in absolute levels of physiological parameters, the male group having higher systolic blood pressure levels, higher adrenaline plasma concentrations, and significantly more alpha 2-adrenergic receptors. Both challenges elicited pronounced cardiovascular and endocrine responses. Men and women did not differ in response magnitude, in task appraisal, or gender role orientation., Conclusions: The assumption that female sex hormones reduce reactivity to challenge is not supported by our data. The frequently reported male/female differences in reactivity may be caused by an interaction of gender and task characteristics.

Plasma noradrenaline and platelet alpha 2-adrenoceptor density (sites/cell using 3H-rauwolscine with and without phentolamine) were correlated with withdrawal score in 23 hospitalized patients undergoing ethanol withdrawal. Control groups for plasma noradrenaline were 25 patients admitted to hospital for elective gastroscopy and 12 laboratory workers accustomed to venipuncture. Controls for platelet alpha 2-adrenoceptor measurements were a separate group of 31 normal subjects with a mean age close to that of the patients' withdrawing from ethanol. Plasma noradrenaline was significantly higher in the patients undergoing ethanol withdrawal than in patients admitted to hospital for elective endoscopy. Twelve laboratory controls had plasma noradrenaline levels significantly lower than either patient group. A significant though poor statistical correlation existed between ethanol withdrawal score and simultaneously determined plasma noradrenaline level. Platelet alpha 2-adrenoceptor sites/cell were reduced in ethanol withdrawal compared with the normal controls. Platelet alpha 2-adrenoceptor sites/cell increased over the first 24 hr of ethanol withdrawal but remained significantly lower than control values. The change in platelet adrenoceptors was accompanied by a fall in mean plasma noradrenaline. Thus, the stress of hospital admission itself is associated with an increase in plasma noradrenaline, but ethanol withdrawal enhances this increase, which is accompanied by and probably causes a reduction in platelet alpha 2-adrenoceptor numbers. These changes begin to return towards normal within 24 hr as the withdrawal reaction subsides.

beta-Adrenergic receptors are increased in some tissues of experimentally thyrotoxic animals but are reported to be unchanged in mononuclear leukocytes of spontaneously thyrotoxic humans. We examined the effects of triiodothyronine (100 mug/d for 7 d) and placebo on high-affinity mononuclear leukocyte beta-adrenergic receptors in 24 normal human subjects, using a double-blind design. beta-Adrenergic receptors were assessed by specific binding of the antagonist (-)[(3)H]dihydroalprenolol. Triiodothyronine administration resulted in objective evidence of moderate thyrotoxicosis and an increase in mean (-)[(3)H]dihydroalprenolol binding from 25+/-3 to 57+/-9 fmol/mg protein (P < 0.001). The latter was attributable, by Scatchard analysis, to an increase in beta-adrenergic receptor density (967 +/- 134 to 2250 +/- 387 sites per cell, P < 0.01); apparent dissociation constants did not change. Placebo administration had no effects. Marked inter- and intraindividual variation in mononuclear leukocyte beta-adrenergic receptor density was also noted. Because this was approximately threefold greater than analytical variation, it is largely attributable to biologic variation. Thus, we conclude: (a) The finding of a triiodothyronine-induced increase in mononuclear leukocyte beta-adrenergic receptor density in human mononuclear leukocytes, coupled with similar findings in tissues of experimentally thyrotoxic animals, provides support for the use of mononuclear leukocytes to assess receptor status in man. (b) There is considerable biologic variation in beta-adrenergic receptor density in man. (c) The findings of thyroid hormone-induced increments in beta-adrenergic receptor density provide a plausible mechanism for the putative enhanced responsiveness to endogenous catecholamines of patients with thyrotoxicosis.

Number and affinity of beta-adrenoceptors in human polymorphonucleates (PMN's) have been studied in patients with essential hypertension (n = 12) and in normal subjects of the same range of age and sex (n = 16). (-)Diidroalprenolol-H3 has been utilized as ligand. Membranes preparation was performed according to Galant (5). Number of beta-adrenoceptor is significantly decreased compared with controls (p less than 0.05), both with saturation curves and Scatchard analysis. Affinity of beta-adrenoceptors toward (-)diidroalprenolol-H3 is lightly increased but not significantly. These data could be explained on the basis of the desensitization occurring in hypertensive subjects by altered plasma catecholamines level, as in experimental in vitro systems.

The effects of acute release of endogenous catecholamines on both platelet alpha 2 and leukocyte beta adrenoreceptors and metabolic indices (glucose and free fatty acids) were investigated in dogs by means of a model of neurogenic hypertension following acute sinoaortic denervation (ASAD). Despite the marked increase in catecholamine levels (+4.2-fold for noradrenaline and 16.7-fold for adrenaline, for example, at minute 45 following ASAD) and in glucose plasma levels, and the significant decrease in free fatty acid plasma levels, no change in platelet alpha 2 or leukocyte beta adrenoreceptor binding sites (number as well as affinity) was observed during the whole experiment. It is suggested that the number of platelet alpha 2- and leukocyte beta-adrenoreceptors is not submitted to short-term regulation, at least by endogenous catecholamines in dogs.

Brief sonication of whole erythrocyte plasma membranes (ghosts) from toads at 4 degrees does not inactivate adenylate cyclase [ATP pyrophosphate-lyase (cyclizing); EC 4.6.1.1] or destroy the receptor binding properties of hydroxybenzylpindolol or insulin. The hormonal (but not the fluoride-induced) stimulation of this enzyme is, however, lost. Fractionation of the small, resealed membrane fragments (vesicles) on discontinuous sucrose gradients results in the separation of vesicle populations differing grossly in size and protein composition. In addition, the distribution of the beta-adrenergic receptor, an insulin binding site, and adenylate cyclase among these vesicles fractions differs. The pattern of distribution of these functional structures can be altered differentially by manipulations of the ghosts before sonication. For example, brief preincubation with isoproterenol leads to a change in the relative distribution of beta-receptor (but not adenylate cyclase) among the various vesicle fractions; this effect is not obtained with beta-receptor antagonists, which block the isoproterenol effect. Exposure of the ghosts to different temperatures, changes in the divalent cation composition of the medium, or the addition of ATP also leads to changes in the distribution of surface markers of the subsequently formed vesicles. The results indicate gross asymmetries in the distribution of protein components within the plane of the membrane and raise important questions regarding the manner whereby functionally related and coupled components, such as hormone receptors and adenylate cyclase, interact.

Cardiopulmonary bypass prolongs bleeding time and increases postoperative blood loss. During in vitro recirculation in an extracorporeal circuit containing a membrane oxygenator and primed with fresh heparinized human blood, we previously observed thrombocytopenia, impaired platelet aggregation, and depletion of granular contents, all of which were prevented with prostaglandin E1 (PGE1). To investigate these changes further, we studied the number and affinity of platelet alpha 2-adrenergic receptors by measuring the binding of 3H-yohimbine. Before recirculation, we found 235 +/- 28 alpha 2-adrenergic receptors per platelet, a Kd of 3.37 +/- 0.78 nmol/L, complete aggregation with 1.04 mumol/L epinephrine, and a platelet count of 281,000 +/- 33,000 microliters-1. After 2 minutes of recirculation, 9.44 mumol/L epinephrine was required to produce complete aggregation, and the platelet count was 104,000 +/- 22,000 microliters-1 (44% of control). The number of binding sites significantly decreased to 139 +/- 16 per platelet, but the affinity did not change (Kd = 3.78 +/- 0.44 nmol/L). After 2 hours of recirculation, the platelet count had increased to 123,000 +/- 21,000 microliters-1. However, epinephrine did not induce platelet aggregation even at 100 mumol/L. Moreover, alpha 2-adrenergic binding sites were not detectable, and affinity for yohimbine could not be calculated. Two minutes after PGE1 0.3 mumol/L was added to the circuit, platelet numbers, response to epinephrine, alpha 2-adrenergic binding sites per platelet, and affinity for yohimbine were not significantly different from control values. At 2 hours, the number of alpha 2-adrenergic sites was not significantly changed from control, but the affinity of yohimbine for platelets was significantly decreased 2.5-fold.(ABSTRACT TRUNCATED AT 250 WORDS)