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PubMed1986

Demonstration that corticotropin-releasing factor binding to rat peripheral tissues is modulated by glucocorticoid treatment in vivo and in vitro.

In a recent study we reported the presence of specific binding sites for corticotropin-releasing factor (CRF) in peripheral tissues of the rat (Endocrinology, 116, 2151, 1985). The objective of this study was to determine if CRF binding to peripheral tissues was modified following adrenalectomy and glucocorticoid replacement therapy. Adult male rats were adrenalectomized and CRF binding to liver, spleen and testicular membranes was determined at 5, 7 or 14 days following adrenalectomy. An additional group of adrenalectomized rats received subcutaneous injections of dexamethasone (75 micrograms/day) for 14 days. Adrenalectomy of rats for 14 days increased CRF binding to liver, kidney, testis, spleen and ventral prostate by approximately 65%-125% above sham-control values. CRF binding to membrane preparations obtained from the pancreas of sham-operated rats was undetectable; however, adrenalectomy produced detectable CRF binding in this tissue. Adrenalectomy produced a time-related increase in CRF binding to ventral prostate, spleen and liver tissue. Administration of dexamethasone to adrenalectomized animals prevented increased CRF binding to peripheral tissues observed following adrenalectomy alone. In vitro dexamethasone treatment of prostatic or hepatic homogenates from adrenalectomized rats resulted in a dose-related decrease in CRF binding activity. However, similar in vitro treatment of prostatic or hepatic homogenate with progesterone exhibited no significant effects on CRF binding. Our results suggest that glucocorticoids may be a regulator of peripheral CRF receptors.

Adrenalectomy↗
PubMed1998

Effect of chronic administration of L-arginine, NG-nitro-L-arginine or their combination on morphine concentration in peripheral tissues and urine of the mouse.

1. Chronic administration of L-arginine (200 mg/kg, i.p) twice a day for 4 days decreased the antinociceptive response to subcutaneously, but not to intracerebroventricularly, administered morphine in male Swiss-Webster mice, as measured by the tail-flick test. 2. The decreased antinociceptive response to morphine was reversed by concurrent administration of NG-nitro-L-arginine (L-NNA) (5 mg/kg, IP), an inhibitor of nitric oxide synthase. 3. The concentrations of morphine in mice treated chronically with L-arginine and then given morphine (10 mg/kg, SC) were determined in the peripheral tissues. L-Arginine treatment significantly increased the concentration of morphine in spleen and lungs, did not modify it in liver, kidneys and urine. L-NNA by itself had no effect on the distribution of morphine in peripheral tissues but reversed the changes induced by chronic treatment with L-arginine. 4. Acute administration of L-arginine (200 mg/kg, IP) did not modify either the morphine antinociception or the morphine distribution in peripheral tissues. 5. Previous studies from this laboratory indicated that chronic treatment with L-arginine decreases the concentration of morphine in several brain regions and spinal cord of mice. 6. The facts that chronic treatment with L-arginine does not alter antinociception induced by ICV administered morphine and it increases the concentration of morphine in peripheral tissues while decreasing it in brain regions after peripheral administration of morphine suggest that the decreased antinociception induced by subcutaneously administered morphine may be related to its decreased entry into the brain.

Analgesics, Opioid↗
PubMed1977

[Effects of somatostatin on pancreatic isolated islets and peripheral tissues of rats].

This study was performed in order to evaluate the effects of somatostatin on insulin releasing mechanisms and on glucose uptake in peripheral tissues using isolated pancreatic islets, isolated rat diaphragms and epididymal fat pads. Insulin release by various concentrations of glucose were examined, and it was found that 100 ng/ml of somatostatin significantly inhibited insulin release at the glucose concentration of 200 mg/dl. Somatostatin also significantly inhibted insulin release by the administration of 5microgram/ml of glucagon with 200 mg/dl of glucose concentration and 20 mM of orginine with 200mg/dl of glucose concentrations. But at the glucose concentration of 50mg/dl, no significant inhibition of somatostatin on insulin release was observed even when various concentrations of glucagon or arginine were added. The influence of somatostatin on peripheral tissues was examined in vitro, and no significant change on glucose uptake compared with the control group was shown in either tissues. The results indicated that somatostatin directly inhibited insulin release from rat pancreatic islets but had no effect on glucose uptake in peripheral tissues. The inhibitory effect of somatostatin on insulin release may act through the common mechanism of both glucose and other substances in leading to insulin release.

Animals↗
PubMed1999

Differential effects of chemical sympathectomy on expression and activity of tyrosine hydroxylase and levels of catecholamines and DOPA in peripheral tissues of rats.

Tyrosine hydroxylase (TH) mRNA and activity and concentrations of 3,4-dihydroxyphenylalanine (DOPA) and catecholamines were examined as markers of sympathetic innervation and catecholamine synthesis in peripheral tissues of sympathectomized and intact rats. Chemical sympathectomy with 6-hydroxydopamine (6-OHDA) markedly decreased norepinephrine and to a generally lesser extent TH activities and dopamine in most peripheral tissues (stomach, lung, testis, duodenum, pancreas, salivary gland, spleen, heart, kidney, thymus). Superior cervical ganglia, adrenals and descending aorta were unaffected and vas deferens showed a large 92% decrease in norepinephrine, but only a small 38% decrease in TH activity after 6-OHDA. Presence of chromaffin cells or neuronal cell bodies in these latter tissues, indicated by consistent expression of TH mRNA, explained the relative resistance of these tissues to 6-OHDA. Stomach also showed consistent expression of TH mRNA before, but not after 6-OHDA, suggesting that catecholamine synthesizing cells in gastric tissue are sensitive to the toxic effects of 6-OHDA. Tissue concentrations of DOPA were mainly unaffected by 6-OHDA, indicating that much of the DOPA in peripheral tissues is synthesized independently of local TH or sympathetic innervation. The differential effects of chemical sympathectomy on tissue catecholamines, DOPA, TH mRNA and TH activity demonstrate that these variables are not simple markers of sympathetic innervation or catecholamine synthesis. Other factors, including presence of neuronal cell bodies, parenchymal chromaffin cells, non-neuronal sites of catecholamine synthesis and alternative sources of tissue DOPA, must also be considered when tissue catecholamines, DOPA and TH are examined as markers of sympathetic innervation and local catecholamine synthesis.

Animals↗
PubMed1979

Insulin in portal, hepatic and peripheral venous blood after glucose, tolbutamide and glipizide stimulation. Indication of insulin release from peripheral tissues.

Insulin in portal, hepatic and/or peripheral venous blood was determined in 16 patients admitted to a surgical ward for various diseases. Portal venous blood was obtained via a catheter introduced into the portal vein either through the umbilical vein remnant or transhepatically. Four subjects were given a peroral load of glucose, followed after 60 min by i.v. tolbutamide. In simultaneous blood samples, two of these subjects showed higher insulin concentrations in peripheral venous blood than in portal venous blood. Twelve subjects were given i.v. glipizide. In one subject blood samples were drawn from the portal vein, a hepatic vein and a peripheral vein and in six subjects from the portal vein and a hepatic vein. Two subjects showed higher insulin concentrations in peripheral venous blood than in portal venous blood. The mean peripheral insulin response (six subjects) was of the same magnitude as the mean hepatic insulin response (six subjects). It is suggested that these findings reflect a release of previously bound insulin from peripheral tissues.

Adult↗
PubMed1989

Effect of indomethacin on peripheral tissue perfusion after coronary artery bypass surgery.

The effect of indomethacin on peripheral tissue perfusion in the early phase after coronary artery bypass grafting (CABG) was investigated in ten patients randomly allocated to receive indomethacin 25 mg i.v. or placebo 'double-blind'. The patients were coupled to a respirator with FiO2 30 v/v %. Central haemodynamics, intrapulmonary shunt and blood gases showed no significant change in either group during the 2-hour study period. The thromboxane A2 metabolite P-TXB2 decreased significantly (p less than 0.05) in the indomethacin group, but the prostacyclin metabolite P-6-K PGF1 alpha showed no significant change in either group. The PtcO2 index (transcutaneous oxygen tension/arterial PO2), measured in the upper extremity, rose (p less than 0.05) after indomethacin infusion, but was almost unchanged in the controls. The mean subcutaneous tissue oxygen tension and the laser-Doppler skin red-cell flux underwent no significant change. The data thus suggested that indomethacin administered intravenously post-CABG may exert beneficial effects on peripheral tissue perfusion and oxygenation, possibly mediated by improvements in prostacyclin-thromboxane balance and microcirculation.

Coronary Artery Bypass↗
PubMed1998

Hepatosplanchnic and peripheral tissue oxygenation during treatment of hemorrhagic shock: the effects of pentoxifylline administration.

OBJECTIVE: To evaluate the effects of pentoxifylline (PF) administration on liver, gut, and peripheral oxygenation during crystalloid resuscitation of hemorrhagic shock. SUMMARY BACKGROUND DATA: Hypoperfusion of the hepatosplanchnic vascular bed and hypoxia of vital organs may be prolonged despite adequate therapy of hemorrhagic shock. Vasoconstriction, leukostasis, platelet aggregation, and red blood cell plugging could be the underlying causes. PF has been shown to counteract these effects, but its effects in a large animal shock model have been less studied. METHODS: Thirteen anesthetized piglets (mean weight 19.6 kg) were bled steadily to a mean arterial pressure (MAP) of 40 to 50 mmHg and a 70% reduction in cardiac output during 1 hour. These levels were maintained for an additional hour. The animals were resuscitated with acetated Ringer's solution according to MAP and cardiac output values and followed for 80 minutes (total 3 hours and 20 minutes). Seven piglets were given PF boluses (12.5 mg/kg) and infusion (0.2 mg/kg x min), and the rest (n = 6) served as controls. Hemodynamic and systemic oxygen transport variables were recorded. Liver parenchymal and peripheral tissue (subcutaneous, transcutaneous, conjunctival) oxygen tensions (PO2) were measured continuously with polarographic electrodes. Jejunal intramucosal pH (pHi) was calculated every hour by the luminal PCO2, obtained with a balloon tonometer, and arterial bicarbonate concentration. RESULTS: Cardiac output decreased by a mean of 76% during shock and was restored during resuscitation in both groups. MAP decreased from 110 to 40 mmHg but remained at 70 to 80 mmHg during resuscitation in both groups despite remarkable volume load (2.6 ml/min per kg). Liver parenchymal PO2 decreased from 29+/-1 to 15+/-1 mmHg during shock and increased to 36+/-2 mmHg in the PF group, whereas in control group it remained at 26 mmHg. The difference between groups was significant, but at the end of follow-up the liver PO2 decreased to 21 mmHg in both groups. Gut pHi, peripheral tissue oxygen tensions, and the plasma adrenaline and noradrenaline concentrations did not differ between the groups. CONCLUSIONS: Pentoxifylline improved specifically, although only transiently, liver tissue oxygenation. Perhaps the microvascular abnormalities after resuscitation of hemorrhagic shock are more prominent in the hepatic vascular bed, rendering PF specifically effective in that area. The lack of any effect of PF on gut and peripheral tissue oxygenation may have resulted from the persistent vasoconstriction and inadequate restoration of blood volume with crystalloid solution.

Animals↗
PubMed1987

Mean residence time in peripheral tissue.

The published methods for determining the mean residence time for drugs in peripheral tissue are reviewed in terms of assumptions involved, advantages and disadvantages. A method for determining mean transit time in peripheral tissue is proposed; this may be a more useful indicator of the tissue retention properties for drug compounds.

Half-Life↗
PubMed1992

Distribution of protein phosphatase inhibitor-1 in brain and peripheral tissues of various species: comparison with DARPP-32.

The distribution of inhibitor-1, a cyclic AMP-regulated inhibitor of protein phosphatase-1, was analyzed in various brain regions and peripheral tissues of various species by immunolabeling of sodium dodecyl sulfate-poly-acrylamide gel transfers using specific antibodies. The distribution of inhibitor-1 was directly compared to that of DARPP-32, a structurally related cyclic AMP-regulated inhibitor of protein phosphatase-1. In rat CNS, a single immunoreactive protein of M(r) 30,000, identified as inhibitor-1, was widely distributed. In contrast, DARPP-32 was highly concentrated in the basal ganglia. Inhibitor-1 was detected in brain tissue from frog (M(r) 27,000), turtle (M(r) 29,000/33,000), canary (M(r) 26,000), pigeon (M(r) 28,000), mouse (M(r) 30,500), rabbit (M(r) 26,500), cow (M(r) 27,000), and monkey (M(r) 27,500), but not from goldfish. Inhibitor-1 was detected at various levels in most peripheral tissues of the species studied; however, it was not detectable in certain tissues of particular species (e.g., rat and cow liver). DARPP-32 was detected in brain tissue of all the species tested except frog and goldfish, but was not detectable in most peripheral tissues. Both inhibitor-1 and DARPP-32 were concentrated in the cytosol and synaptosomal cytosol of rat striatum. The developmental expressions of inhibitor-1 and DARPP-32 in rat striatum differed: the level of inhibitor-1 peaked in the first postnatal week and then declined by the third postnatal week, whereas the level of DARPP-32 increased to a peak level by the third postnatal week and remained elevated thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Fluorometric determination of peripheral tissue histamine levels using Bio-Rex 70.

Bio-Rex 70, a weak cation exchange resin, has been incorporated into a column chromatographic extraction procedure for the determination of peripheral tissue levels of histamine. The extracted histamine is quantified fluorometrically after condensation with o-phthaldialdehyde (OPT). The sensitivity of the procedure allows for the chromatographic extraction, using Bio-Rex 70, of 10 ng histamine to give fluorescence twice that of the blank. Because this extraction procedure does not separate histamine from spermidine it cannot be applied in determining levels of brain histamine. However, because spermidine in concentrations of up to 400 times that of histamine does not interfere with OPT-histamine fluorescence, the histamine levels of all peripheral tissues (including nerves) and fluids may be confidently examined. The relative simplicity of the procedure allows for the determination of 30 tissue samples within a working day. The method has been applied to determine peripheral tissue levels of histamine in naïve Wistar rats and the effects of compound 48/80 on these levels in several selected tissues have been investigated. Compound 48/80 decreased the levels of histamine in the heart, kidney and ileum, whereas these levels were initially elevated in the liver and lung without subsequent depletion. Since the reliability of existing histamine extraction procedures is questionable under certain conditions, it is suggested that the use of Bio-Rex 70 is a valuable addition in evaluating the possible physiological role(s) of tissue histamine.

Animals↗
PubMed1987

Opioids and opioid receptors in peripheral tissues.

Opioid peptides belonging to the enkephalin, beta-endorphin or dynorphin family, acting on specific opiate receptors may be found in peripheral tissues. Enkephalins have a widespread peripheral distribution, while beta-endorphin and dynorphin may be found locally in the enteric nervous system. The peptides of the various families are formed from specific precursor molecules. Apart from the enteric nervous system, opioids are also found in the adrenal medulla as well as in several autonomic ganglia. There is some evidence of three different classes of opioid receptors in peripheral tissues, i.e. mu-, delta- and kappa-receptors. These receptors are not only found on enteric nervous and mucosa cells but also on various cells in the immune system where opioid peptides seem to have important actions and appear to link the neuroendocrine and immune systems to control immunological functions. The physiological as well as the pathophysiological role of opioid peptides in the periphery is gradually being elucidated and, based on such knowledge, new therapeutic implications in gastrointestinal or immune diseases may be developed.

Animals↗
PubMed1993

Distribution of C-type natriuretic peptide and its messenger RNA in rat central nervous system and peripheral tissue.

In rat, the highest concentration of immunoreactive (ir-) C-type natriuretic peptide (CNP) was found in the central nervous system, as is the case in pig and human. Although its concentration in peripheral tissue was much lower than that in brain, CNP was present mainly as CNP-53 in ileum-jejunum, colon-cecum, stomach, kidney, lung, testis and submaxillary gland, but not in heart. By Northern blot analysis, CNP mRNA was detected in ileum-jejunum, testis, thymus, adrenal gland and submaxillary gland as well as in brain and spinal cord. CNP mRNA was further verified by reverse transcription-polymerase chain reaction to be present in most peripheral tissue, including aorta and bone marrow. These results indicate that CNP is synthesized in peripheral tissue and possibly functions as a local regulator in addition to acting as a neuropeptide in the central nervous system.

Animals↗
PubMed1991

Characterization of macaque 3 beta-hydroxy-5-ene steroid dehydrogenase/delta 5-delta 4 isomerase: structure and expression in steroidogenic and peripheral tissues in primate.

The conversion of 3 beta-hydroxy-5-ene steroids by the enzyme complex 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4 isomerase (3 beta-HSD) is an obligatory step in the biosynthesis of all classes of hormonal steroids in classical steroidogenic as well as in peripheral tissues. To develop a model more closely related to the human, we have isolated and characterized cDNA clones encoding macaque 3 beta-HSD by screening a rhesus monkey ovary lambda gt11 cDNA library using a human 3 beta-HSD cDNA probe. Nucleotide sequence of 1629 bp from overlapping cDNA clones predicts a protein of 372 amino acids with a calculated molecular mass of 41,874 (excluding the first Met). The deduced amino acid sequence of macaque 3 beta-HSD displays 79.4% and 93.9% similarity with that of bovine and human 3 beta-HSD, respectively. RNA blot analysis performed under high stringency conditions of macaque poly(A)+ RNA samples using full-length 32P-labeled macaque 3 beta-HSD cDNA revealed the presence of an approximately 1.7 kb mRNA species in classical steroidogenic tissues, namely the ovary, testis and adrenal glands as well as in several peripheral tissues including the liver, kidney and epididymis. Computer analysis of the deduced macaque 3 beta-HSD protein sequence predicts the presence of an NH2-terminal membrane-associated segment as well as four additional membrane-spanning segments, thus suggesting that 3 beta-HSD is an integral protein. The availability of macaque cDNA should permit detailed studies concerning the tissue-specific expression as well as the hormonal regulation of 3 beta-HSD mRNA in classical steroidogenic glands as well as in peripheral tissues which are an important site of steroidogenesis in primates.

Adrenal Glands↗
PubMed1999

Immunohistochemical localization of delta opioid receptors in peripheral tissues.

The distribution of delta opioid receptor (DOR) immunoreactivity (ir) was examined in various peripheral tissues of Sprague-Dawley rats and macaque monkeys, including glabrous and hairy skin, corneas, eyelids, and the lip. DOR-ir was observed in all tissues examined. In addition to the presence of DOR-immunoreactive fibers in subcutaneous nerve bundles and the papillary dermis, we report the existence of positively labeled fibers and terminals in close association with peripheral structures not traditionally assigned a primarily nociceptive function, such as hair follicles, glandular apparatus, and blood vessels. In every case, staining was restricted to small-diameter axons that appeared to terminate as free nerve endings. To further classify DOR-immunoreactive fibers, we examined the extent of colocalization between DOR and three commonly used neuronal subtype markers; tyrosine hydroxylase (TH), calcitonin gene-related peptide (CGRP), and RT-97, a monoclonal antibody which preferentially labels neurons with myelinated axons. Additional double-labeling experiments using the nonspecific neuronal marker Protein Gene Product 9.5 were performed in glabrous skin to determine the percentage of total fiber count that displayed DOR-ir. No colocalization was observed between DOR and RT-97, indicating that DOR-ir is localized to unmyelinated axons. In addition, DOR colocalized with CGRP, but did not colocalize with TH. Taken together, these data support the hypothesis that delta opioid receptors in peripheral tissues are associated with sensory fibers, but not with the terminals of postganglionic sympathetic neurons.

Animals↗
PubMed2005

'Mature' nerve growth factor is a minor species in most peripheral tissues.

The classic neurotrophin hypothesis is based on the idea that innervating neurons derive 'mature' neurotrophin provided by the target for their survival. Yet large precursor forms of the neurotrophin nerve growth factor (NGF) have been reported in both central and peripheral tissues. In the present study, immunoblotting was used to survey peripheral tissues containing NGF-responsive neurons and to characterize various NGF species. These results demonstrate that 'mature' forms of NGF, i.e., the 13 and 16kDa species, are rare in sympathetic and sensory ganglia and in their peripheral targets, and that large molecular weight NGF precursors are abundant. In addition, certain NGF forms predominate in a given tissue, with each tissue exhibiting a characteristic NGF expression pattern. These findings suggest that NGF processing in peripheral tissues and in NGF-responsive ganglia may involve a variety of NGF species.

Animals↗
PubMed1998

Humoral signals mediate the circadian expression of rat period homologue (rPer2) mRNA in peripheral tissues.

Northern blot analysis revealed the circadian expression of rat period homologue (rPer2) mRNA in peripheral mononuclear leukocytes that have no neuronal connections. The mRNA expression in the suprachiasmatic nucleus (SCN), peripheral mononuclear leukocytes, and other peripheral tissues exhibited prominent, synchronous circadian oscillation with peaks at early night. As we have previously shown the peripheral circadian expression of rPer2 mRNA is abolished in SCN-lesioned rats [Sakamoto, K., Nagase, T. Fukui, H., Horikawa, K., Okada, T., Tanaka, H., Sato, K., Miyake, Y., Ohara, O., Kako, K. and Ishida, N., J. Biol. Chem., 273 (1998) 27039-27042], our findings suggest that some humoral signals, driven by the SCN, mediate the circadian expression of mammalian per homologues in peripheral tissues.

Animals↗
PubMed1984

Adrenal function and the action of propranolol in surgical stress-mediated insulin resistance of glucose utilization by peripheral tissues in vivo. Inhibition of glucose accumulation in skeletal muscle.

The effect of acute adrenalectomy and the action of propranolol on insulin-stimulated glucose utilization was investigated in an in vivo model of peripheral tissues of the rabbit after evisceration and nephrectomy. The lactate/pyruvate ratios in muscle and blood and the content of energy-rich phosphate compounds in muscle were not altered during the experiments. The results obtained in animals with and without intact adrenals were compared. The insulin-mediated glucose utilization was inhibited by 34% in animals with intact adrenals. In the semimembranosus muscle of adrenalectomized rabbits the parameters of glucose metabolism corresponded to those in the 'resting state'. In the muscle of animals with intact adrenals the content of glycogen was decreased and that of glycolytic intermediates was elevated; free glucose was accumulated in the muscle cell. Alterations of the glucose content in skeletal muscle were inversely correlated with the glucose utilization of peripheral tissues. DL-Propranolol (0.05 mg/kg) administered before surgery i.v. to rabbits with intact adrenals not only prevented glycogenolysis and accumulation of glycolytic intermediates but also the stress-mediated glucose accumulation in skeletal muscle. Propranolol abolished the insulin resistance of glucose utilization of peripheral tissues mediated by the adrenals after surgical preparation of the rabbits.

Adrenal Glands↗
PubMed1988

Reduced activities of thiamine-dependent enzymes in the brains and peripheral tissues of patients with Alzheimer's disease.

A report of cell loss in the nucleus basalis of Meynert in patients with Wernicke-Korsakoff disease prompted the examination of thiamine pyrophosphate (TPP)-dependent enzymes in the brain and peripheral tissues of patients with Alzheimer's disease. In these brains, the activities of the 2-ketoglutarate dehydrogenase complex were reduced more than 75% and those of transketolase more than 45%. Decreases occurred in histologically damaged and in relatively undamaged areas. Small but statistically significant abnormalities of transketolase, but not of 2-ketoglutarate dehydrogenase complex, were identified in red blood cells and cultured fibroblasts. Previous studies have shown deficiencies in the brain and variable effects in peripheral tissues on another TPP-dependent enzyme--the pyruvate dehydrogenase complex. Activities of TPP-dependent enzymes appear to be deficient in the brain and perhaps in some peripheral tissues in patients with Alzheimer's disease.

Aged↗