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1.
The contribution of pulmonary and hind limb 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 (nanograms per milliliter) X plasma flow (milliliters per minute) X 100/dose (nanograms per minute). This value means the percentage of the amount of catecholamine cleared by an organ to the amount of catecholamine administered into the body. Small but significant transpulmonary gradients of plasma levels of norepinephrine, epinephrine and dopamine and large translimb gradients of plasma levels of these catecholamines were observed. The plasma flow of pulmonary circulation was increased by infusion of epinephrine and dopamine, whereas it remained unchanged by infusion of norepinephrine. The plasma flow of hind limb circulation showed no significant change by infusion of catecholamines. The calculated contribution values indicate that pulmonary circulation clears 35.7% of norepinephrine (at 0.2 ng X kg-1 X min-1), 27.1% of epinephrine (0.2 ng X kg-1 X min-1) and 21.5% of dopamine (10 micrograms X kg-1 X min-1) administered exogenously, and that the corresponding figures for hind limb circulation are 8.2, 7.8 and 4.5%.  相似文献   

2.
A series of studies were performed to determine the relationship between physiologic levels of circulating plasma norepinephrine and epinephrine and human platelet alpha-2 binding site number and the affinity (KD) of these sites for antagonist radioligands. In one study, alpha-2-adrenergic binding site number and affinity were compared using both [3H]yohimbine and [3H]dihydroergocryptine as radioligands. There was good absolute and relative comparison for binding site number, but only a relative relationship for KD. In 46 normal subjects, there was no significant relationship between site number or KD and age, plasma epinephrine, or plasma norepinephrine concentration. Even after plasma epinephrine was raised nearly 20-fold by means of an intravenous infusion for 4 h in seven normal subjects, neither sites (608 +/- 68 vs. 567 +/- 120 sites/platelet) nor KD (2.01 +/- 0.94 vs. 2.14 +/- 1.15 nM) were significantly changed. Similarly, neither sites (445 +/- 55 vs. 421 +/- 53 sites/platelet) nor KD (1.44 +/- 0.29 vs. 2.10 +/- 0.75 nM) were significantly changed in six normal subjects when plasma norepinephrine levels increased during oral administration of prazosin for 1 wk. Thus, in a cross-sectional analysis and after a change in plasma catecholamine concentrations, there was no relationship in normal subjects between platelet alpha-2 binding site number or affinity of these sites for antagonist radioligands and the circulating catecholamine levels to which the platelets were exposed. In a group (n = 7) of patients who lack epinephrine-induced platelet aggregation due to abnormal thrombopoiesis, binding site number was decreased (304 +/- 36 vs. 572 +/- 29 sites/platelet, P less than 0.001) and KD tended to be greater (8.69 +/- 2.44 vs. 5.40 +/- 0.31 nM, P = NS) than in normal subjects (n = 46), despite having similar plasma catecholamine levels. There was no difference in binding site number (491 +/- 116 sites/platelet) and KD (5.61 +/- 0.84 nM) in patients (n = 5) with autonomic insufficiency and low levels of upright plasma norepinephrine when compared with the normal subjects. Two patients were examined before and after the removal of a pheochromocytoma. Their binding site number and KD were normal before the operation and essentially unchanged after the tumor removal and fall of plasma catecholamines. Thus, this study demonstrates that within the physiologic and pathophysiologic range of plasma catecholamines (in men), there is no relationship between the circulating catecholamine concentration and either platelet alpha-2 adrenergic binding site number or the affinity of these sites for antagonist radioligands.  相似文献   

3.
The effect of the potent specific cholecystokinin (CCK) receptor antagonist loxiglumide on meal-stimulated plasma concentrations of CCK, gastrin, pancreatic polypeptide (PP), neurotensin, glucose-dependent insulinotropic polypeptide (GIP), insulin and C peptide was investigated in a placebo-controlled study in 10 healthy male volunteers. Intravenous infusion of loxiglumide (10 mg kg-1 h-1) significantly augmented integrated incremental IR-CCK levels 7.3-fold after stimulation by a standard breakfast (504 +/- 54 vs 3.665 +/- 365 pmol-1 135 min-1, P less than 0.001), as measured by a specific CCK radioimmunoassay. Basal IR-CCK concentrations were not affected by administration of loxiglumide. Oral treatment with bile acids (2 g ursodeoxycholic acid plus 2 g chenodeoxycholic acid) together with the meal abolished this augmentation, whereas high-dose substitution with pancreatic enzymes (4.2 g pancreatin) reduced elevated IR-CCK levels by only 38%. CCK-like bioactivity, determined by a bioassay using rat pancreatic acini, was not detectable in all samples that contained loxiglumide at plasma concentrations of 100-250 micrograms ml-1. Plasma gastrin concentrations in response to the breakfast were elevated 3.2-fold during loxiglumide infusion and not influenced by substitution with bile acids or pancreatic enzymes. Meal-stimulated integrated incremental plasma PP concentrations were significantly suppressed (55-65% inhibition, P less than 0.01) by loxiglumide. Infusion of the CCK receptor antagonist only slightly increased postprandial peak plasma glucose, insulin and C-peptide levels, whereas GIP and neurotensin levels were not significantly influenced. These findings suggest: (i) CCK secretion is under feedback control by intraduodenal bile acids and to a lesser extent by pancreatic enzymes; (ii) simultaneous extraction of CCK and loxiglumide results in circulating plasma CCK-like bioactivity of zero; (iii) gastrin secretion is feedback controlled via an indirect mechanism probably involving CCK-induced somatostatin secretion; (iv) release of PP is under inhibitory control of CCK; (v) CCK does not play a major role as insulinotropic hormone in the entero-insular axis in humans.  相似文献   

4.
A defect of conjugation may play a role in the elevated plasma free norepinephrine observed in patients with cirrhosis. Plasma free, sulfoconjugated, and glucuronoconjugated catecholamine concentrations were assessed in 15 patients with cirrhosis and in 15 age-matched control subjects. Plasma free norepinephrine and epinephrine levels were significantly higher in patients with cirrhosis (481 +/- 75 and 96 +/- 16 pg/ml, respectively) than in those of the control group (307 +/- 33 and 42 +/- 10 pg/ml, p less than 0.05 and p less than 0.01, respectively). Plasma free dopamine levels were similar in both groups. Sulfoconjugated catecholamines were the predominant form in plasma from both cirrhotic patients and control subjects. The ratio of conjugated to total catecholamines was similar in the two groups. Therefore, it is unlikely that a defect in conjugation of catecholamines is contributing to the excessive plasma free norepinephrine and epinephrine concentrations found in patients with cirrhosis. Moreover, in patients with cirrhosis, no significant relation was found between plasma conjugated catecholamines and the severity of liver disease. This study shows that cirrhosis does not induce alteration in conjugation of catecholamines and that hepatocellular function is not essential for conjugation of circulating catecholamines.  相似文献   

5.
BACKGROUND: Analysis of urinary free catecholamines was automated recently, but analysis of plasma samples posed special difficulties. The present study was undertaken to evaluate a new method for the automated analysis of plasma catecholamines. METHODS: The procedure is based on an improved sample handling system that includes dialysis and sample clean-up on a strong cation trace-enrichment cartridge. The catecholamines norepinephrine, epinephrine, and dopamine are then separated by reversed-phase ion-pair chromatography and quantified by electrochemical detection. RESULTS: Use of a 740- microL sample is required to give the catecholamine detection limit of 0.05 nmol/L and analytical imprecision (CV) between 1.1% and 9.3%. The assay can be run unattended, although >12 h of analysis time is not recommended without cooling of the autosampler rack. Comparison (n = 68) of the automated cation-exchange clean-up with the well-established manual alumina procedure gave excellent agreement (mean, 3.78 +/- 2.76 and 3.8 +/- 2.89 nmol/L for norepinephrine and 0.99 +/- 1.72 and 1.08 +/- 1.78 nmol/L for epinephrine). Hemodialysis had no clear effect on plasma norepinephrine. Epinephrine concentrations were similar (0.05 < P < 0.1) in chronic renal failure patients (0.24 +/- 0.3 nmol/L; n = 15) and healthy controls (0.5 +/- 0.24 nmol/L; n = 31). Dopamine was not quantified, being usually <0.2 nmol/L. CONCLUSION: The availability of such a fully automated procedure should encourage the more widespread use of plasma catecholamine estimation, e.g., after dialysis, exercise, or trauma/surgery and in the investigation of catecholamine-secreting tumors, particularly in the anuric patient.  相似文献   

6.
To evaluate the effect of endurance exercise on plasma catecholamines, we exercise trained eight dogs (group T) by treadmill running for 8 weeks. Six sedentary dogs constituted a nontrained control group (group NT). Heart rate response to a graded submaximal stress test was reduced in group T dogs (p less than 0.05), but mean resting aortic blood pressure (NT, 84 +/- 5 mm Hg; T, 82 +/- 4 mm Hg) and heart rate (NT, 87 +/- 1 bpm; T, 84 +/- 2 bpm) were unchanged by exercise, and no cardiac hypertrophy occurred after exercise. Plasma norepinephrine and epinephrine levels were reduced in group T at rest and during a fixed exercise workload. Plasma conjugated dopamine showed a marked increase in group T dogs (NT, 1398 +/- 130 pg/ml; T, 11346 +/- 1291 pg/ml; p less than 0.01) at rest, and no change in conjugated dopamine occurred in either group after short-term exercise stress. No intergroup differences were noted in resting coronary flow or coronary arteriovenous oxygen, or in myocardial oxygen consumption. The data verify previous findings of lower plasma levels of norepinephrine and epinephrine after training, and indicate that a marked rise in conjugated dopamine occurs after training. These findings suggest that norepinephrine and epinephrine metabolism is shifted toward conjugated dopamine by exercise training, thereby reducing active catecholamines in plasma, but retaining a large pool of usable metabolite.  相似文献   

7.
Changes in plasma catecholamine (CA) levels and hemodynamic responses after a dopamine (DA) infusion of 20 micrograms/kg body weight per min were studied in dogs with a normal acid-base state (pH 7.4, PaCO2 40 torr) and in the same animals after induction of severe metabolic acidosis (pH 7.0, PaCO2 40 torr). DA increased plasma norepinephrine (NE) levels from .487 +/- .109 ng/ml to 3.077 +/- 0.357 ng/ml in the normal acid-base state, and from 1.762 +/- .521 ng/ml to 9.533 +/- 1.403 ng/ml in acidosis. Plasma epinephrine (E) levels in normal and acidotic states were also increased by DA infusion. In the normal acid-base state DA increased myocardial contractility and cardiac index (CI). DA also increased myocardial contractility during acidosis, but the response of CI to DA was abolished. DA significantly decreased systemic vascular resistance index (SVRI) in the normal acid-base state and significantly increased SVRI in acidosis. Acidosis appears to enhance the rate of conversion of DA to NE and E. The failure of DA to increase CI in acidosis may be a result of the increased afterload on the left ventricle.  相似文献   

8.
Ventricular myocardial catecholamines in primates   总被引:1,自引:0,他引:1  
We report myocardial catecholamine levels in primate ventricles assayed by high-pressure liquid chromatography with electrochemical detection. The norepinephrine content of the left ventricles of 11 monkeys (four rhesus and seven cynomolgus) was 1391 +/- 362 ng/gm (+/-SD) with a definite gradient from base (highest) to apex (lowest concentration). Dopamine and epinephrine were present in much lower concentrations (51.8 +/- 24.5 ng/gm and 59.2 +/- 20.0 ng/gm, respectively), but were similarly distributed throughout the left ventricle. There was considerable variation in norepinephrine concentration between animals, but the dopamine/norepinephrine ratio was very consistent within a given animal, averaging 3.7% +/- 1.4%. These values are probably indicative of what normal concentrations of catecholamines are likely to be in humans, and provide a basis for interpretation of results obtained in disease studies.  相似文献   

9.
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.  相似文献   

10.
Clonidine hydrochloride via the central nervous system lowers blood pressure, inhibits ACTH and catecholamine release, and stimulates growth hormone secretion. To evaluate the effect of this drug on the release of glucoregulatory hormones during hypoglycemia, we studied the responses to insulin-induced hypoglycemia (0.1 units/kg) in 10 patients with mild essential hypertension before and after treatment for 16 weeks with transdermal clonidine. Clonidine significantly lowered blood pressure, basal plasma norepinephrine levels, and epinephrine and renin activity but did not affect basal growth hormone concentrations. Clonidine significantly reduced the norepinephrine and epinephrine responses to hypoglycemia (norepinephrine AUC from 207 +/- 16 SE to 156 +/- 25 nmol/L/min, epinephrine from 157 +/- 28 to 99 +/- 29 nmol/L/min; both p less than 0.05) and increased the growth hormone response (AUC from 763 +/- 148 ng/min/ml to 1164 +/- 292 ng/min/ml; p less than 0.05) but did not affect the cortisol response or the magnitude or rate of glucose recovery from hypoglycemia. Thus transdermal clonidine has several effects on glucose counterregulatory hormones that do not significantly alter insulin sensitivity or impair recovery from hypoglycemia.  相似文献   

11.
Pancreatic polypeptide was infused intravenously in healthy fasting subjects at 1 pmol kg-1 (n = 7) and 4 pmol kg-1 min-1 (n = 10) producing plasma PP concentrations of 223 +/- 37 pmol/l (mean +/- SEM) and 891 +/- 64 pmol/l respectively. These levels are similar to and four-fold higher than those seen after a normal mixed breakfast in healthy young adults. In a separate study five healthy subjects ingested a small breakfast during infusion of PP on different days at 1 pmol kg-1 min-1 and 2 pmol kg-1 min-1 respectively. PP at 1 pmol kg-1 min-1 caused a marked reduction in fasting plasma motilin concentrations to 20% of the basal level (p less than 0.001). There were, however, no significant changes in plasma concentrations of insulin, glucagon, gastrin, secretin, enteroglucagon, gastric inhibitory peptide or neurotensin. Despite previous reports possibly implicating PP in metabolism, there were no significant effects on blood levels of glucose, alanine lactate, 3-hydroxybutyrate, glycerol or non-esterified fatty acids, either in the fasting state or after the ingestion of food. Although it seems unlikely that PP is a major hormonal regulator of intermediary metabolism in man, its ability to suppress motilin at physiological concentrations suggests the possibility of an indirect influence on digestive motor function.  相似文献   

12.
Synthetic oxyntomodulin, a predicted product of the glucagon gene, which is produced in the human lower intestinal mucosa, was infused in doses of 100 and 400 ng kg-1 h-1 into six volunteers to study its pharmacokinetics and effects on pentagastrin-stimulated gastric acid secretion (100 ng kg-1 h-1). The concentration of oxyntomodulin in plasma measured with a cross-reacting glucagon assay increased from 37 +/- 5 to 106 +/- 17 and 301 +/- 40 pmol l-1, respectively. The metabolic clearance rate was 5.2 +/- 0.7 ml kg-1 min-1 and the half-life in plasma was 12 +/- 1 min. Oxyntomodulin reduced the pentagastrin-stimulated acid secretion by 20 +/- 9% during the low-rate infusion (P less than 0.05) and by 76 +/- 10% during the high-rate infusion (P less than 0.05). In accordance with the homology with glucagon, there was a small, significant rise in plasma concentrations of insulin and insulin C-peptide during oxyntomodulin infusion. Oxyntomodulin may therefore be included among the potential incretins and enterogastrones in man.  相似文献   

13.
OBJECTIVE--To clarify whether the circulating insulin level influences hormonal responses, glucagon secretion in particular, during hypoglycemia in patients with insulin-dependent (type I) diabetes. RESEARCH DESIGN AND METHODS--Nine type I diabetic patients were studied. During two separate experiments, hypoglycemia was induced by low-dose (244 pmol.kg-1.h-1) and high-dose (1034 pmol.kg-1.h-1) intravenous insulin infusions for 180 min in each case. The arterial blood glucose level was directly monitored every 1.5 min, and glucose was infused in the high-dose test to clamp the arterial blood glucose level to be identical as in the low-dose test. RESULTS--Despite the fact that the plasma insulin level was four times higher in the high-dose than in the low-dose test (740 +/- 50 vs. 180 +/- 14 pM), a close to identical arterial hypoglycemia of approximately 3.3 mM was obtained in the two experiments. During hypoglycemia, a significant rise of the plasma glucagon level was found only in the low-dose test (188 +/- 29 vs. 237 +/- 37 ng/L, P less than 0.05), and the incremental area under the glucagon curve was significantly greater in the low-dose than in the high-dose test (140 +/- 19 vs. -22.7 +/- 34 ng/L.h-1, P less than 0.005). The responses of plasma epinephrine, norepinephrine, growth hormone, pancreatic polypeptide, and somatostatin were similar in both tests and, consequently, were not significantly modified by the circulating insulin level. CONCLUSIONS--This study demonstrates that, in type I diabetic patients, the glucagon response to hypoglycemia is suppressed by a high level of circulating insulin within the physiological range. Our findings may help to explain the impairment of glucagon secretion during hypoglycemia frequently seen in these patients.  相似文献   

14.
Growth hormone (GH) hypersecretion in insulin-dependent diabetes mellitus (IDDM) subjects has been shown to be causally related to early-morning hyperglycemia. We studied the effect of nocturnal GH suppression on acute glycemic control in six IDDM patients during a constant overnight insulin infusion (0.075 mU.kg-1.min-1). In control experiments (infusion of insulin alone), plasma glucose increased from 5.6 +/- 0.6 mM at 2400 to 11.1 +/- 1.3 mM at 0900 (P = .0024). When in addition the cholinergic muscarinic antagonist pirenzepine was given (100 mg at 2200 and again at 2400), plasma glucose increased from 5.6 +/- 0.3 mM at 2400 to 8.4 +/- 1.4 mM at 0900 (P greater than .05). The nocturnal surges of GH that were demonstrated in all patients during the control nights were suppressed during the treatment nights. There were no significant changes in insulin, cortisol, or epinephrine concentrations. Mean glucagon and norepinephrine concentrations. Mean glucagon and norepinephrine concentrations were reduced from 127 +/- 2.7 ng/L and 8.7 +/- 0.5 nM to 101 +/- 1.9 ng/L (P less than .001) and 3.5 +/- 0.2 nM (P less than .001) on control and treatment nights, respectively. Neither glucagon nor norepinephrine concentrations changed significantly between 2400 and 0900 on either control or treatment nights. We conclude that nocturnal GH suppression by pirenzepine during a constant low-rate insulin infusion is associated with an attenuation of the early-morning plasma glucose rise.  相似文献   

15.
High levels of beta receptor agonist have previously been shown to down-regulate beta receptor density on circulating leukocytes in man; however, the factors controlling receptor density under physiological conditions have not previously been defined. To determine whether beta receptor density is normally down-regulated by circulating, physiological levels of catecholamines we have examined the relationship between receptor density and catecholamine levels. Urinary epinephrine and norepinephrine were significantly reciprocally correlated to lymphocyte receptor density. A similar relationship existed between beta receptor density and supine plasma epinephrine, norepinephrine, upright epinephrine, and norepinephrine levels. Change in sodium intake from 10 to 400 meq/d caused a 52% increase in lymphocyte and a 48% increase in polymorphonuclear beta receptor density. The changes in receptor density were accompanied by an increase in the sensitivity to isoproterenol measured as a fall in the dose of isoproterenol required to raise the heart rate by 25 beats per minute. Beta receptor density on both lymphocyte and polymorphonuclear cells was significantly correlated to the cardiac sensitivity to isoproterenol. Propranolol administration resulted in an increase in the density of beta receptors on lymphocyte and polymorphonuclear cells that correlated with the subject's pretreatment catecholamine levels.These findings, therefore, suggest that physiological levels of catecholamines normally down-regulate beta receptors in man and that blockade of this down-regulation by propranolol allows receptor density to increase.  相似文献   

16.
Plasma, platelet and erythrocyte contents of free and conjugated norepinephrine, epinephrine and dopamine were determined by radioenzymatic assay in 12 resting healthy volunteers. Mean platelet/plasma concentration ratios were 533 for free norepinephrine, 502 for free epinephrine and 149 for free dopamine. Corresponding erythrocyte/plasma ratios were 1.04, 1.13 and 4.5, respectively. The presence of conjugated catecholamines in platelets and erythrocytes could be confirmed; however, their relative proportion within these cells, particularly in platelets, was lower than that in plasma. Upon intravenous infusion of dopamine for 3 hr at 5 micrograms kg-1 min-1, concentrations of free dopamine in plasma increased rapidly (280-970-fold), whereas conjugated dopamine only reached maximal values (14-19-fold increase) at 30 to 60 min after cessation of the infusion. The relative distribution of unconjugated dopamine in whole blood between plasma, platelets and erythrocytes changed from mean values of 1:0.33:3.7 at rest to 1:1.1:0.5 at the end of the infusion. As a result of the subsequent rapid decrease of dopamine in plasma and erythrocytes, this distribution was 1:17:1 shortly thereafter and remained constant up to the end of the investigation period. The relative distribution for conjugated dopamine of 1:0.001:0.5 at rest changed to about 1:0.2:0.1 at the termination of the infusion. Oral administration of norepinephrine and dopamine led to increases in the plasma concentrations of these amines in their conjugated forms only, whereas epinephrine concentrations remained constant. These elevations were not accompanied by corresponding increases in platelet and erythrocyte norepinephrine, epinephrine and dopamine contents.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

17.
Plasma catecholamines and resuscitation from prolonged cardiac arrest   总被引:1,自引:0,他引:1  
Plasma catecholamine levels rise markedly with cardiac arrest and attempted resuscitation. We examined whether epinephrine (EPI) or norepinephrine (NE) plasma concentrations could predict resuscitation outcome. In nine mongrel dogs, EPI and NE levels were drawn before cardiac arrest and after 8 and 14 min of cardiac arrest and CPR. Intravenous EPI (1 mg) was given 1 min before the last plasma level was drawn. Catecholamines were quantitated by high-performance liquid chromatography with triple-electrode coulometric electrochemical detection. Plasma catecholamines increased significantly with cardiac arrest, EPI levels increased from a control level of 15.9 +/- 3.0 to 396.0 +/- 63.3 pmol/ml after 8 min of cardiac arrest (p less than .05), and NE levels similarly increased from 4.4 +/- 1.7 to 66.5 +/- 12.0 pmol/ml (p less than .01). Neither the absolute catecholamine plasma concentration nor the response to cardiac arrest of the endogenous catecholamine concentrations could predict outcome, but catecholamine responses to exogenous EPI did correlate with outcome. Animals which were subsequently resuscitated had a greater increase in the plasma EPI concentrations after exogenous EPI than animals that were not resuscitated, a 53-fold vs. a 23-fold increase (p less than .05). Successfully resuscitated animals also had increased NE levels after exogenous EPI, while unsuccessfully resuscitated animals had either no change or a decrease (p less than .02). Successfully resuscitated animals had an increase in coronary perfusion pressure (p less than .01) in response to exogenous EPI, in contrast to those that were not resuscitated. This suggests that the exogenous administration of EPI during prolonged CPR is beneficial despite markedly elevated endogenous catecholamine levels.  相似文献   

18.
Ethanol, administered i.p., produced a dose-dependent increase in plasma norepinephrine and epinephrine concentrations in LS/Ibg (LS) but not in SS/Ibg (SS) lines of mice. Ethanol-induced elevations of plasma epinephrine in LS mice were approximately 10-fold greater than those observed in SS mice. Plasma epinephrine and norepinephrine attained peak concentrations at 20-min post-ethanol administration at doses ranging from 2.8 to 4.1 g/kg. Plasma catecholamines remained elevated for approximately 1 hr and returned to basal values 2 hr after ethanol administration. Significant correlations were obtained between blood ethanol (r = 0.99), plasma epinephrine (r = 0.92) and plasma glucose (r = 0.98) as a function of ethanol dose in LS mice. Chlorisondamine (3 mg/kg), a ganglionic blocker, abolished completely the ethanol-induced increase in plasma catecholamines. These results confirm previous suggestions that the response is centrally mediated through an increased sympathetic outflow rather than by a direct effect on the adrenal medulla. The increase in plasma epinephrine and associated hyperglycemia produced by ethanol was not observed with pentobarbital or halothane anesthesia. Ethanol-induced hypothermia was diminished markedly (47%) by an elevated ambient temperature (28 degrees C) without reducing the hyperglycemic response to ethanol. These results suggest that ethanol-induced hypothermia does not mediate ethanol-induced adrenomedullary catecholamine secretion and concomitant hyperglycemia. It is proposed that the differential ethanol-induced secretion of adrenomedullary catecholamines in LS and SS mice is due to differential central nervous system sensitivities to ethanol.  相似文献   

19.
Dopa in plasma increases during acute exercise and after exercise training   总被引:2,自引:0,他引:2  
Plasma dihydroxyphenylalanine (dopa) has been shown to originate in sympathetic neurons, and it has been suggested that plasma level reflects activity of tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of catecholamines. In this study, we measured the effects of acute exercise and exercise training on the levels of dopa and catecholamines in the plasma of healthy, older individuals. Venous blood was drawn from 19 men, from 52 to 75 years of age, at rest, at a standard submaximal work load, at peak exercise, and 3 minutes after exercise on a cycle ergometer. Ten of 12 men then completed 12 to 16 weeks of supervised training, and seven continued normal activity. All 17 men were then retested. The seven control subjects subsequently underwent exercise training as above and were retested again. Levels of dopa and catecholamines in plasma samples were measured by high-performance liquid chromatography with electrochemical detection. Dopa levels at rest were considerably higher than free dopamine, epinephrine, and norepinephrine. During short-term exercise, levels of dopa and catecholamines increased. The absolute increase in dopa was greater than the increase in epinephrine or dopamine but was not greater than that in norepinephrine. After the training period, basal dopa levels increased significantly and correlated with the increase in peak oxygen uptake. There was no change in basal conjugated norepinephrine or dopamine levels with exercise or training, but the level of conjugated epinephrine decreased slightly. No changes occurred in levels of dopa or catecholamines in the untrained group. Free dopamine, norepinephrine, and epinephrine levels at peak exercise were increased after exercise training.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

20.
BACKGROUND: A gastrin receptor antagonist, CR2194 (spiroglumide), was used to explore the physiological role of gastrin in regulating gastric acid secretion in humans. MATERIALS AND METHODS: The effect of CR2194 on inhibition of gastrin-stimulated acid output was evaluated in a four-period crossover study. Each subject received intravenous doses of 1, 2.5 or 7.5 mg kg-1 h-1 CR2194 or saline (control) followed by graded increasing doses of gastrin (6.4-800 pmol kg-1 h-1). Secondly, the effect of CR2194 on meal-stimulated intragastric acidity was evaluated by infusing either saline (control) or CR2194 (7.5 mg kg-1 h-1) before and after food ingestion. RESULTS: Acid secretion was dose-dependently inhibited by CR2194. With CR2194, acidity was significantly reduced in the pre-meal and post-prandial period (P < 0.01 and 0.002 respectively), and the integrated gastrin response was augmented to 8.0 +/- 1.4 ng mL-1 240 min compared with 1.5 +/- 0.8 ng mL-1 240 min in the control experiment (P < 0.01). Finally, acid secretion in response to sham feeding was significantly reduced: 15.9 +/- 0.9 mmol 90 min-1 in the control experiment compared with 2.8 +/- 0.9 mmol 90 min-1 during CR2194 infusion (P < 0.05). CONCLUSION: Gastrin receptor blockade with CR2194 alters gastric acid secretion in response to food ingestion or to sham feeding. The results support a physiological role for gastrin in regulating acid secretion in humans.  相似文献   

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