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At least 991 records · Page 55Linked to original sources
PubMed1992

[Catecholamine blood levels in sheep during superovulation in estrus].

The effects of a serum gonadotropin (SG) superovulation hormonal preparation were investigated on catecholamine levels (norepinephrine, dopamine and epinephrine) in the blood plasma of ewes with synchronized oestrus in the oestrus period. In this trial the blood plasma of eleven ewes of the Slovak Merino breed was analyzed to detect catecholamines in the oestrus period. Superovulation was induced by an i.m. administration of 1500 IU SG as soon as oestrus synchronization with Agelin vaginal tampons finished (20 mg chlorsuperlutin) which lasted for 10 days. Catecholamines were detected in the blood plasma before synchronization, on the day of Agelin vaginal tampons application, and in 48 and 72 hours after the hormone administration--on the days of the expected ovulation. Catecholamine concentrations in the blood plasma were determined by a radioenzymatic assay using a Catechola test (Praha). The results indicate that synchronization and hormonal stimulation influence plasma catecholamine levels. The norepinephrine (NE) concentration in the blood plasma of the control samples has the value of 8.31 +/- 0.732 pmol/ml. An insignificant increase in the NE levels (13.12 +/- 0.120 pmol/ml; Fig. 1) was recorded on day 1 of the trial, after the start of synchronization. On the day of the expected ovulation the NE concentrations rose to 17.12 +/- 1.289 pmol/ml (P less than 0.001) and they remained significantly increased (P less than 0.01) at the level of 12.89 +/- 1.020 pmol/ml on the following day of the experiment. The dopamine level (DA) in the plasma of a control sample is 6.42 +/- 0.350 pmol/ml (Fig. 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

[Influence of catecholamines on myocardium in experimental septic shock].

OBJECTIVE: To study the influence of catecholamine on myocardium in rats with septic shock and its mechanism by biochemical and pathophysiological methods to evaluate the underlying pathophysiologic mechanism of myocardial damage and the influence of catecholamine on the myocardial injury. METHODS: Septic shock was replicated in rats by cecal ligation and puncture (CLP). Dobutamine (DB), norepinephrine (NE) and combination of DB and NE were used in the lowest dose. The rats were randomly divided into sham operations, CLP control group, CLP+DB group, CLP+NE group and CLP+DB+NE group, 8 rats in each group. Troponin I (cTnI) and total creatine kinase (CK) were measured, and myocardial tissue was examined under light microscopy and electron microscopy. RESULTS: An significantly increased cTnI level was found in CLP septic shock rats, compared with sham rats (P<0.05). In the present study, the use of DB or NE alone, or the combination of the two drugs, was not found to influence the cTnI levels. But, the total CK levels in catecholamine-treated group were significantly increased (P<0.05). There was no statistically significant correlation between cTnI and CK levels. Morphological study confirmed the results of cTnI. Findings that were common in the myocardium of CLP septic shock rats included extracellular and intracellular edema as well as mitrochondrial injury. However, no conclusive evidence was found for the influence of catecholamine on myocardial damage. CONCLUSION: No evidence of the influence of catecholamine on myocardial damage is found. Pathological study suggests that myocardial injury is the result of ischemia.

Animals↗
PubMedDate not supplied

[Effect of catecholamines on migration and differentiation of gonadotropin releasing hormone-neurons in rats].

The GnRH producing neurons are the key link of neuroendocrine regulation of the adult reproductive system. Synthesis and secretion of GnRH are, in turn, under the afferent catecholaminergic control. Taking into account that catecholamines exert morphogenetic effects on target cells during ontogenesis, this study was aimed at investigation of the effects of catecholamines on development of GnRH neurons in rats during ontogenesis. We carried out comparative quantitative and semiquantitative analyses of differentiation and migration of GnRH neurons in fetuses of both sexes under the conditions of normal metabolism of catecholamines (administration of saline) or their pharmacologically induced deficiency (administration of alpha-methylparatyrosine). The inhibition of catecholamine synthesis from day 11 of embryogenesis led to an increasing number of GnRH neurons in rostral regions of the trajectory of their migration over the brain: in the area of olfactory tubercles on day 17 and in the area of olfactory bulb on days 18 and 21. In addition, the optical density of GnRH neurons located in the rostral regions of migration was higher in the fetuses after administration of alpha-methylparatyrosine during embryogenesis, as compared to the control. It has been concluded that catecholamines stimulate the migration of GnRH neurons and affect their differentiation.

Animals↗
PubMed1992

[Effects of insulin-induced hypoglycemia on catecholamine secretion and blood pressure in neurological disorders affecting autonomic nervous system].

The effects of insulin-induced hypoglycemia on catecholamine secretion were investigated in patients with various neurological disorders affecting the autonomic nervous system. In control subjects, insulin-induced hypoglycemia resulted in marked increases in plasma epinephrine and norepinephrine levels. Heart rates were increased within 15 minutes after the insulin injection which were associated with slight elevation and depression of systolic and diastolic blood pressure, respectively. In patients with upper level spinal cord lesions (C1-T6) of various etiology, Shy-Drager syndrome and familial amyloidosis, insulin-induced hypoglycemia failed to increase plasma epinephrine and norepinephrine levels and resulted in falls in systolic and/or diastolic blood pressure 15 minutes after the injection. Heart rates were increased at 30-45 minutes after the injection. In patients with lower spinal cord lesions (T10-L1), neurosyphilis or brain stem tumor with orthostatic hypotension, the catecholamine responses were normal and blood pressure did not fall during insulin-induced hypoglycemia. In patients with Parkinson's disease and spinocerebellar degeneration with autonomic symptoms catecholamine responses were not impaired. These findings suggest that any lesion involving the sympathetic efferent systems of baroreflex such as the spinal descending pathway, sympathetic preganglionic neuron and peripheral nervous system causes both impairment of catecholamine secretion and a fall in blood pressure during hypoglycemia, and that lesions in sympatho-afferent system may not affect the secretion of catecholamine and neural control of blood pressure.

Adult↗
PubMed1991

Cyanide-induced increases in plasma catecholamines: relationship to acute toxicity.

Cyanide is known to initiate release of catecholamines from chromaffin cells and isolated adrenals but the effect of cyanide on plasma catecholamine levels has not been reported. The present study demonstrates that cyanide produces marked elevation of plasma catecholamines in mice. A sublethal dose of KCN (5 mg/kg, sc) significantly increased plasma norepinephrine (NE) and epinephrine (EPI) at 5 min after administration, and the elevated levels returned to normal at 15 min. At a dose of 10 mg/kg, NE and EPI plasma levels remained elevated over a 15 min period. Multiple exposures to sublethal doses of KCN (5 mg/kg, sc, 4 doses at 15 min intervals) produced a steep, sustained rise in plasma NE and EPI. Administration of KCN (15.6 micrograms) directly into the lateral ventricles of the brain caused convulsions and respiratory depression, but did not affect plasma catecholamine levels. Pretreatment with pargyline did not alter the magnitude of the response to KCN. Adrenalectomy prevented the increase in plasma EPI and had no influence on plasma NE levels, indicating cyanide acts directly on the adrenals to stimulate EPI release. It is proposed that KCN directly stimulates the sympathoadrenal axis to increase plasma catecholamine levels.

Adrenal Glands↗
PubMed1977

Distortion of cyclic AMP responses to catecholamine due to destruction of the hormone.

The acute actions of low and moderate concentrations of catecholamines on cyclic AMP metabolism in SV40-transformed human lung fibroblasts (VA13) were seriously distorted by non-enzymatic destruction of the agonist. Catecholamine destruction, as measured directly with an isotopic method, was slowed by a variety of anti-oxidants and chelating agents. A combination of two anti-oxidants, ascorbate and thiourea, was very effective in protecting isoproterenol in the cell culture system. That is, there was a 10-fold increase in the sensitivity of VA13 to isoproterenol and the duration of action of the catecholamine was greatly prolonged. However, the anti-oxidants did not alter the responses of the cells to prostaglandins. We conclude that any quantitative studies of cyclic AMP responses to catecholamines must address the question of agonist destruction if meaningful results are to be expected. The use of anti-oxidants, especially the combination of ascorbate and thiourea, would appear to be advisable, particularly in situations where the catecholamine concentrations are less than supramaximal.

Antioxidants↗
PubMed1990

[Catecholamines in the treatment of the low cardiac output syndrome following heart surgery with extracorporeal circulation].

The aim of this study was to estimate the effectiveness of different mono- and combination therapies with catecholamines (dopamine, dobutamine, adrenaline and noradrenaline) in the treatment of low cardiac output syndrome after open-heart surgery. All together 425 patients treated at the Intensive Care Unit of the Clinic for Anaesthesiology and Intensive Care Therapy of the Martin Luther University Halle-Wittenberg after open-heart surgery from 1985-1986 were examined. The low cardiac output syndromes were characterised by the following parameters: mean arterial pressure (MAP), heart frequency (HF), central venous pressure (CVP), diuresis and mixed venous oxygen saturation (SvO2). Recommendations were given for evaluating the grade of low cardiac output syndrome and for selecting whether a mono- or a combination therapy is necessary and which dose should be given. Thus, the pretherapeutical signs MAP 50 mm Hg and presence of 3 disturbed signs characterise severe low cardiac output syndrome and make necessary the primary combined application of catecholamines. Two investigated signs connected in a mathematical formula can help to determine when during a low-cardiac output state a dopamine-monotherapy should be replaced by a combination therapy of catecholamines. It was found, that the doses of dopamine increased proportionally to the reached level of catecholamine combination. Therefore, doses of catecholamines should be kept in their recommended range with their specific receptor-mediated effect.

Cardiac Output, Low↗
PubMed1990

Involvement of protein kinase C in prostaglandin E2-induced catecholamine release from cultured bovine adrenal chromaffin cells.

We recently reported that prostaglandin (PG) E2 stimulated phosphoinositide metabolism in cultured bovine adrenal chromaffin cells and that PGE2 and ouabain induced a gradual secretion of catecholamines from the cells (Yokohama, H., Tanaka, T., Ito, S., Negishi, M., Hayashi, H., and Hayaishi, O. (1988) J. Biol. Chem. 263, 1119-1122). Here we examined the involvement of two signal pathways, Ca2+ mobilization and protein kinase C activation resulting from phosphoinositide metabolism, in the PGE2-induced catecholamine release. Either the Ca2+ ionophore ionomycin or 12-O-tetradecanoylphorbol 13-acetate (TPA) could enhance the release in the presence of ouabain, and ionomycin-induced release was additive to PGE2-induced release, but TPA-induced release was not additive. PGE2 dose-dependently stimulated the formation of diacylglycerol and caused the translocation of 4% of the total protein kinase C activity to become membrane-bound within 5 min. These effects were specific for PGE2 and PGE1 among PGs tested (PGE2 = PGE1 greater than PGF2 alpha greater than PGD2). Furthermore, the phosphoinositide-specific phospholipase C inhibitor neomycin inhibited PGE2-induced accumulation of inositol phosphates, diacylglycerol formation, translocation of protein kinase C, and also stimulation of catecholamine release. Both PGE2- and TPA-induced release were inhibited by the depletion of protein kinase C caused by prolonged exposure to TPA, but ionomycin-induced release was not inhibited. We recently found that the amiloride-sensitive Na+, H+-antiport participates in PGE2-evoked catecholamine release (Tanaka, T., Yokohama, H., Negishi, M., Hayashi, H., Ito, S., and Hayaishi, O. (1990) J. Neurochem. 54, 86-95). In agreement with our recent report, PGE2 and TPA induced a sustained increase in intracellular pH that was abolished by the protein kinase C inhibitor staurosporine but not by the calmodulin inhibitor W-7. Ionomycin also induced a marked increase in intracellular pH, but this increase was abolished by W-7 but not by staurosporine. These results demonstrate that PGE2-induced activation of the Na+, H(+)-antiport and catecholamine release in the presence of ouabain are mediated by activation of protein kinase C, rather than by Ca2+ mobilization, resulting from phosphoinositide metabolism.

Adrenal Medulla↗
PubMed1990

[The content of catecholamines in the adrenergic plexuses of the spleen and intestines during cold and emotional stresses].

The content of catecholamines in adrenergic plexuses of the spleen and small intestine of rats has been studied histochemically using a computer analysis. It is shown that the content increases both during the short-term cold and emotional stress. Intraperitoneally administered guanethidine (10 mg/kg) does not prevent cold-induced accumulation of catecholamines in these adrenergic plexuses, but the emotional-induced one remains. Putative mechanisms of the catecholamine accumulation in the splenic and small intestinal adrenergic plexuses during different stresses are discussed. It is suggested that the cold stress induces an increase of the catecholamine synthesis in adrenergic terminals of prevertebral ganglion neurons, whereas emotional stress leads to the catecholamine uptake by adrenergic terminals from the blood.

Adrenergic Fibers↗
PubMed1989

Adrenal growth and ontogeny of adrenal substance P, enkephalins and catecholamines in the ovine fetus.

Biologically active peptides have been identified in the adrenal glands of several adult mammalian species. Some of these peptides appear to modulate the nicotine-induced catecholamine release from the adrenal medulla. The present study was carried out to investigate the presence and ontogeny of the peptides substance P, met-enkephalin and leu-enkephalin in the ovine fetal adrenal gland from 70 to 140 days gestation (term = 145-150 days). Concurrently, the growth of the fetal adrenal as well as the gestational changes in catecholamine content were determined. The maternal adrenal glands were also studied for comparison. The ovine fetal adrenal gland increased in weight with advancing gestation at a single exponential rate. Total adrenal substance P content correlated with gestational age, while met-enkephalin, leu-enkephalin and total catecholamine contents correlated with adrenal weight. The adrenal content (normalized as per unit protein) of substance P was highest in the young fetuses at 70 days gestation, decreased progressively towards term and, in the adult levels were significantly lower than those measured in the fetuses. The contents of met-enkephalin and leu-enkephalin were low in the young fetuses at 70 days gestation, but reached high levels at 130 to 140 days gestation. Maternal adrenal contents of the two enkephalins were significantly lower than those measured in the near-term fetal adrenal. Total catecholamine content in the fetal adrenal medulla increased as the fetus matured. Norpinephrine was the primary catecholamine present in the medulla of fetuses at 70 and 80 days gestation, while epinephrine was the major one in the adult.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1978

The stimulation by catecholamines of guanylate cyclase activity in a cell-free system.

Cytosolic guanylate cylase activity in cell-free preparations of the rabbit renal cortex was increased 3- to 5-fold by catecholamines. The plasma membrane-bound enzyme was not activated, although hormone receptors were present. Stimulation was augmented by NaN3, which by itself had little effect on the soluble enzyme activity. With a partially purified enzyme, activity was enhanced by 0.1 muM 1-epinephrine and activated half-maximally by about 1 muM. In decreasing potency, epinephrine greater than isoproterenol greater than norepinephrine greater than dopamine greater than catechol. Phenylephrine and metanephrine did not stimulate. 1-Epinephrine-stimulation of the enzyme was reversed by dialysis and the deactivated enzyme was reactivatable by a second exposure to the catecholamine. Activation by catecholamines was not stereospecific. Epinephrine-stimulated guanylate cyclase activity in the crude cytosolic fraction was partially inhibited by alpha-adrenergic antagonists, but neither alpha- nor beta-blockers inhibited when the partially purified enzyme was used; thus, leaving open the question of a role for typical alpha- or beta-adrenergic mechanisms in this regulation of the soluble enzyme. Adrenochrome was the most potent activator of the partially purified guanylate cyclase, being approximately 10-times more effective than epinephrine. Epinephrine and adrenochrome activated in the presence of reducing agents, i.e., ascorbate, DTT and N2, although the enzyme in a more SH-reduced form and in an oxygen-deficient medium had a decreased sensitivity to both effectors. Epinephrine activated soluble guanylate cyclase in several tissues, including cerebrum, cerebellum, brain stem, lung, heart, liver, ductus deferens and colon. Although the precise mechanism by which low concentrations of catecholamines stimulated guanylate cyclase activity is unknown and the physiological significance of the activation remains to be established, these findings direct attention to an interesting interaction of catecholamines with the cytosolic enzyme system and stress the need for further studies.

Adrenochrome↗
PubMed1987

Characterization of vasopressor response to sympathetic stimulation in the pithed rat: differential regulation of neuronally stimulated and blood-borne catecholamine-stimulated pressor responses in rats harboring pheochromocytoma.

The vasopressor response to sympathetic stimulation in the pithed rat was characterized both by analyzing the effects of chemical sympathectomy, adrenalectomy and selective antagonists on the vasopressor response and by measurement of changes in plasma concentrations of catecholamines. Stimulation of the spinal sympathetic outflow evoked a biphasic pressor response: an initial transient component was caused mainly by postganglionic sympathetic nerve stimulation (the direct response); a slowly developing secondary component was mediated predominantly by circulating catecholamines released from the adrenal medulla (the adrenal response). Parallel analysis of plasma catecholamines showed that the rise in epinephrine appeared to be closely related to this adrenal component. The pressor response in adrenalectomized rats was selectively blocked by prazosin but not by yohimbine; however, in sympathectomized rats, the pressor response was abolished by prazosin and yohimbine together but not by either drug given alone. These results suggest that the direct, neurogenic component is mediated mainly by alpha-1 adrenoceptors whereas the secondary, adrenally mediated response occurs by activation of both alpha-1 and alpha-2 adrenoceptors. Furthermore, the in vivo regulation of each component of the pressor response was studied in rats harboring pheochromocytoma (PHEO), a tumor causing marked elevations in endogenous catecholamine concentrations. In PHEO rats, the direct pressor response was found to be relatively intact but the adrenal response was blunted. Inasmuch as there was normal rise in plasma epinephrine to electrical stimulation in PHEO rats, the results suggest a differential regulation of neuronally stimulated and blood-borne catecholamine-mediated pressor responses in PHEO rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗
PubMed1988

Phosphorylation of bovine adrenal chromaffin cell tyrosine hydroxylase. Temporal correlation of acetylcholine's effect on site phosphorylation, enzyme activation, and catecholamine synthesis.

Tryptic peptide fragments of tyrosine hydroxylase isolated from 32PO4-prelabeled bovine adrenal chromaffin cells are resolved into seven phosphopeptides by reverse phase-high performance liquid chromatography. All seven of the peptides are phosphorylated on serine residues. Three of these putative phosphorylation sites, peptides 3, 5, and 6, are rapidly phosphorylated (5-fold in 15 s) by both acetylcholine stimulation and potassium depolarization of the cells, and this phosphorylation is accompanied by a similarly rapid activation of the enzyme. Both phosphorylation and activation are transient and do not account for the prolonged increase in catecholamine biosynthesis produced by these stimuli. Peptides 4 and 7 show a much slower and sustained increase in phosphorylation (3-fold in 4 min) in response to acetylcholine and potassium. Phosphorylation of these peptides correlates with the sustained increase in catecholamine biosynthesis rather than enzyme activation. Peptides 1 and 2 are not stimulated by any agonist yet employed and thus show no relation to enzyme activation or catecholamine biosynthesis. Phosphorylation of all five peptides by acetylcholine or potassium is calcium-dependent. In contrast to the stimulation of phosphorylation of tyrosine hydroxylase on multiple sites, forskolin stimulates the phosphorylation of only peptide 6, and this is accompanied by a coordinated activation of tyrosine hydroxylase and increased catecholamine biosynthesis. These findings show that the phosphorylation of tyrosine hydroxylase in intact cells is more complex than predicted from in vitro results, that at least two protein kinases are involved in the secretagogue-induced phosphorylation of tyrosine hydroxylase, and that the regulation of catecholamine biosynthesis, in response to phosphorylation, appears to involve both tyrosine hydroxylase activation and other mechanisms.

Acetylcholine↗
PubMedDate not supplied

[Catecholamines of the blood vessels of Rana temporaria frogs].

In histochemical (with the glyoxylic acid) and biochemical (spectrofluorimetric trioxyindolic method) investigations sources and content of catecholamines (dopa, noradrenalin, adrenalin) in the blood vessels, sympathetic chains, adrenals and cardiac ventricles have been studied in autumn-winter and spring-summer frogs at various temperatures. It was found that the catecholamines in the studied tissues are located in the sympathetic neurons, adrenergic terminals and chromaffin cells. The ratio of these structures in different tissues was various. It was found that the catecholamine level in frog blood vessels and various organs undergoes seasonal and temperature variations. The increase of temperature from + 5 to 20 degrees caused a decrease in the catecholamine level in the autumn-winter frogs, but increased the catecholamine concentrations over 60--100% in the spring-summer ones.

Adrenal Glands↗
PubMed1986

Simultaneous liquid-chromatographic determination of 3,4-dihydroxyphenylglycol, catecholamines, and 3,4-dihydroxyphenylalanine in plasma, and their responses to inhibition of monoamine oxidase.

This is a reversed-phase liquid-chromatographic method, with electrochemical detection, for simultaneously measuring, in plasma, the concentrations of the catecholamine precursor dihydroxyphenylalanine (DOPA); the endogenous catecholamines norepinephrine, epinephrine, and dopamine; and the deaminated catecholamine metabolites dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG). We used this method to assess effects of monoamine oxidase (EC 1.4.3.4) inhibition in humans. Plasma DHPG concentrations as determined by the present method (mean 826, SEM 61 ng/L) were similar to those found by other methods. Inhibition of monoamine oxidase (by administering deprenyl or tranylcypromine) decreased plasma DHPG by greater than 65%, plasma DOPAC by greater than 50%, and plasma DOPA by about 20%, without consistently affecting norepinephrine or epinephrine. Simultaneous measurement of DOPA, catecholamines, and DHPG may be useful for examining the synthesis, release, and intraneuronal metabolism of norepinephrine. The assay method is rapid, reliable, and simple, and it provides a more comprehensive assessment of noradrenergic nervous function than does measurement only of catecholamines.

Alzheimer Disease↗
PubMed1987

[Measurement of platelet catecholamine content for the diagnosis of pheochromocytoma with intermittent hypertension].

We have compared platelet and plasma catecholamines (radioenzymatic assay with catechol-O-methyl transferase) and urinary metanephrines (high performance liquid chromatography) in 16 patients with phaeochromocytoma, 12 essential hypertensives, and 15 normotensive volunteers. Hypertensive patients with or without phaeochromocytoma had labile or paroxysmal hypertension with normal or borderline blood pressures between paroxysms. Catecholamine concentrations in platelets and plasma did not differ in essential hypertensives and controls, but were higher in patients with phaeochromocytoma than in subjects without tumour, with values overlapping between groups. Metanephrine excretion was markedly higher in phaeochromocytoma than in essential hypertension, with no intergroup overlap. Platelet adrenaline plus noradrenaline content was highly correlated to urinary metanephrines (r' = 0.830, n = 28 p less than 0.01). Using as a cut-off point the highest values measured in essential hypertensives, the sensitivity of each measurement was 1.00 for metanephrines, 0.87 for platelet catecholamines and 0.50 or less for plasma catecholamines. Measurement of platelet catecholamine content is a sensitive test and an appropriate alternative to metanephrine measurement in the difficult cases of suspected phaeochromocytoma with intermittent hypertension.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

[Effect of an external electrostatic field on catecholamine secretion by rat adrenals].

Experimental rats were exposed to an electrostatic field of 200 kW/m for 1, 24 or 6 hours a day for 6 days. The effect of this exposure on the structure and function of adrenal chromaffin bodies and the concentration of catecholamines and their precursors in blood and adrenals was investigated. Using histochemical, fluorescent-microscopic and spectrofluorimetric methods, it was found that the exposure may modify the structure and function of adrenal chromaffins and the concentration of catecholamines in blood and adrenals. These changes depended on the exposure time. An hour exposure activated the secretory apparatus of adrenal chromaffins and enhanced catecholamine secretion to blood. A 24-hour exposure led to an increase in the concentration of catecholamines in adrenals and blood and a change in the organ cytoangioarchitectonics. A 6-day fractionated exposure resulted in a decrease of catecholamines both in blood and adrenals.

Adrenal Glands↗
PubMed1988

Quantitative analysis of the contribution of hepatic, renal and portal circulation to the clearance of exogenous catecholamines.

The contribution of hepatic, renal and portal circulation to the clearance of exogenous catecholamines was analyzed quantitatively. During infusion of clinical doses of norepinephrine, epinephrine and dopamine in dogs, the plasma level of catecholamine and the plasma flow were measured simultaneously. Percentage of contribution was calculated from the following equation; transorgan difference of plasma catecholamine (ng/ml) x plasma flow (ml/min) x 100/dose (ng/min). This value means the percentage of the amount of catecholamine cleared by an organ to the amount of catecholamine administered into the body. Significant transorgan gradients of plasma levels of norepinephrine, epinephrine and dopamine were observed in each of hepatic, renal and portal circulation. The calculated contribution values indicate that hepatic circulation clears 15.9% of norepinephrine, 24.2% of epinephrine and 9.0% of dopamine administered exogenously. The corresponding figures for renal circulation are 8.7, 22.0 and 9%, and those for portal circulation are 11.5, 21.5 and 10.4%.

Animals↗