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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 2 (1968), S. 73-73 
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1433-8580
    Keywords: Arginine-hydrochloride ; Endogenous glucagon ; Insulin ; Arterial blood flow ; Arterial blood pressure ; Heart rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationship of arginine-mediated release of endogenous glucagon and insulin to renal and splanchnic arterial blood flow, blood pressure, and heart rate was studied in dogs. Intravenous injection of argininehydrochloride (arg-HCl) in logarithmically increasing doses increased the concentration of glucagon (pGl) in the femoral artery from 143 ± 39 pg/ml (pre-injection) to 282 ± 49 pg/ml (following maximum dosage of arg-HCl) and insulin concentration from 23 ± 5 to 41 ± 11 µU/ml. Sodium chloride (NaCl) and urea, isovolemic and isosmolar to arg-HCl, failed to change pGl and insulin. Arg-HCl depressed arterial blood pressure from 93 ± 13 (preinjection) to 60 ± 14 mm Hg (maximum dose), NaCl increased it from 89 ± 13 to 99 ± 13 mm Hg. The blood flow increase due to arg-HCl was comparable with that due to NaCl in renal as well as in celiac and left gastric artery. The former was more pronounced in superior and inferior pancreaticoduodenal artery by 61 and 102%, and in gastroduodenal and superior mesenteric artery by 11 and 35%. Infusion of arg-HCl increased pGl from 294 ± 90 to 731 ± 200 pg/ml, and insulin from 23 ± 5 to 63 ± 18 µU/ml; the resulting blood flow increase, however, only differed in both pancreatic arteries by 10–20% from the rise during NaCl infusion where no change of pGl was observed and a decline occurred in insulin from 64 ± 21 to 27 ± 8 µU/ml. It is concluded that physiological levels of pGl have no systemic effect on arterial blood flow. A local flow increasing effect of glucagon and/or insulin on the arteries next to the pancreas is discussed.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 2 (1968), S. i 
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 243 (1962), S. 351-351 
    ISSN: 1432-1912
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 312 (1980), S. 123-129 
    ISSN: 1432-1912
    Keywords: Histamine ; 2-Methylhistamine ; 4-Methylhistamine ; Mepyramine ; Gastrointestinal blood flow ; Clemastine ; Cimetidine ; H1-receptors ; H2-receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Evidence for the presence of specific histamine H1- and H2-receptors in the gastrointestinal circulation was obtained using histamine, 2-methylhistamine (a specific H1-agonist), 4-methylhistamine (a specific H2-agonist), and selective H1- and H2-receptor antagonists in the anesthetized dog. Histamine and 2-methylhistamine increased conductance in the vascular beds of the superior mesenteric artery, the left gastric artery and the common hepatic artery, whereas 4-methylhistamine mainly enhanced conductance in the vascular beds of the left gastric artery and the common hepatic artery. All three agents depressed systemic arterial blood pressure. The vasodilatory effect of histamine and 2-methylhistamine on the superior mesenteric artery bed occurred earlier and was of shorter duration than their effect on the two other vessels. The H1-receptor antagonists mepyramine and clemastine blocked the response of the superior mesenteric artery bed to histamine, but had a lesser inhibitory effect on the histamine response of the common hepatic artery and the left gastric artery. The addition of the H2-receptor antagonist cimetidine to mepyramine blockade augmented the inhibiting effect of mepyramine on the common hepatic artery. Cimetidine bolus injections prevented enhancement of vascular conductance by 4-methylhistamine, but did not influence conductance enhancement by histamine or 2-methylhistamine. These data demonstrate there are separable histamine H1- and H2-receptors in the gastrointestinal circulation which are distinguished by anatomic location, temporal relationships of receptor response, and response to specific histamine H1- and H2-agonists and antagonists.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-2013
    Keywords: Liver blood flow ; Splenic blood flow ; Pancreatic blood flow ; Regional gastrointestinal blood flow ; Sensitivity to catecholamines ; Norepinephrine ; Isoprenaline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Responses to norepinephrine (NE) and isoprenaline (ISO) (1–1024 ng/kg i.v.) were assessed by electromagnetic flowmetry on 18 arteries of the splanchnic region in anesthetized dogs. Measurements were judged according to the 2 criteria: 1. direction of effect; 2. sensitivity of vascular areas to catecholamines, expressed as D50 (i.e. the calculated dose inducing 50% of the maximum effect). NE decreased flow in all arteries (40–80%), but caused additionally an increase in the celiac, splenic and splenic artery proper. Thus changes in the spleen are responsible for the increase with NE. Flow reduction in the pancreatic branch of the cranial mesenteric artery was small. All flow reductions induced by NE had a similar D50 (about 30 ng/kg), except that in the hepatic artery (100 ng/kg). ISO increased all flows except that to the pancreas. Increase in the left gastric artery was higher (316%) than all other flow increases (62–168%). Activity of ISO is greatly different in the various vascular beds. D50 of flow to antrum and spleen were the lowest (4 ng/kg). Sensitivity decreases from cranial (D50 about 16 ng/kg) to caudal end (D50 about 70 ng/kg) of the gut. This gradual decrease is compared with functional and anatomical gradients reported in the literature. The varying response to ISO suggests presence of different vascular β-adrenergic receptors. The generally accepted distinction in cardiac β1-receptors and peripheral β2-receptors should be refined at least for β2-adrenergic vascular receptors.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-2013
    Keywords: Norepinephrine ; Isoprenaline ; Blood flow acceleration ; Cardiac inotropy ; Peripheral hemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In anesthetized dogs the norepinephrine (NE) and isoprenaline (ISO) (1–1024 ng/kg i.v.)-induced increase of maximum peripheral flow acceleration (celiac artery, cranial mesenteric artery, renal artery, and femoral artery) and the changes of the maximum first derivative of arterial pressure were compared with the increases of maximum ascending aortic flow acceleration and maximum first derivative of left ventricle pressure (LV dP/dt max). The maximum effect of each dose on maximum acceleration of flows (dF/dt max) and maximum first derivative of pressures (dP/dt max) occurred simultaneously for all variables. The effect was dose-dependent. Sensitivity was similar for NE (D50:2256–512 ng/kg) and for ISO (D50: 128–256 ng/kg). We demonstrated that other variables than inotropic action (heart rate, left ventricular end diastolic pressure and diastolic aortic pressure) played only a minor role in the increases of LV dP/dt max in our studies. In contrast with the uniform response of dF/dt max and dP/dt max, the reaction of peripheral vascular resistance varied. In particular in the gastrointestinal tract the resistance could either be increased (NE, D50: 115 ng/kg) or decreased (ISO, D50: 15 ng/kg). Gastrointestinal resistance was a more sensitive variable for catecholamine stimulation than dF/dt max and dP/dt max. The data show that under the present experimental conditions enhancement of peripheral flow acceleration induced by NE and ISO is due to increase of cardiac inotropy.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-2013
    Keywords: Pancreatic exocrine secretion ; Secretin ; O2 consumption ; Blood flow ; Model for the metabolic control of tissue oxygenation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Secretin stimulates pancreatic water and CO2 excretion as well as pancreatic blood flow. It has been questioned whether the production (i.e. water and CO2 excretion) is reflected in the input-output difference of nutrients. In pentobarbital anesthetised dogs, pancreatic exocrine secretion was stimulated by secretin, (Karolinska), 1 U/kg injected as an i.v. bolus. Secretion was maximally increased at 2 min after the secretin shot and returned to a basal value at between 16 and 32 min after secretin. Blood flow was also maximally increased at 2 min, but decreased to the basal value at between 8 and 16 min. O2 extraction first decreased (at 2 min) and then gradually increased until it was higher than the basal value (at 16 min) and then returned to the basal level (at 32 min). O2 consumption increased quickly, reached a plateau, lasting from 1 to 16 min, and then decreased to the basal level (32 min). CO2 transfer from blood to tissue reached a maximum at 4 min and then decreased to the basal value (at between 16 and 32 min). The curves for CO2 transfer from tissue to pancreatic secretion and for CO2 in the secretion had the same shape. It is concluded that the curve of production (of water and CO2 excretion) parallels the curve of O2 consumption fairly well. The O2 consumption curve did not correlate either with the blood flow curve or with the O2 extraction curve. About one quarter of the excreted CO2 originated from pancreatic metabolism and the remaining three quarters were transferred from blood, through the pancreatic tissue into the secretion. The increase in O2 consumption was achieved by an increase in blood flow, followed by an increase in O2 extraction. The release of a vasodilator metabolite by the pancreatic cells upon arrival of the secretin molecules, may explain both the increase in blood flow and the successive increase in O2 extraction. Therefore these data can be interpreted according to the model for metabolic control of tissue oxygenation.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-2013
    Keywords: Pancreatic exocrine secretion ; Secretin ; Vasopressin ; O2 consumption ; Blood flow ; Model for the metabolic control of tissue oxygenation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vasopressin decreases blood flow as well as secretory flow in the pancreas. The question raised was whether the blood flow decrease is the determinant of the decrease in secretion or quite the reverse. In pentobarbital anesthetized dogs, secretory flow was first increased to a steady level by infusion of secretin. At this steady state, O2 consumption and O2 extraction were increased, while blood flow remained at the control level, indicating an increase in the area available for exchange i.e. an increase in capillary density. At increasing doses of vasopressin, secretory flow decreased, arterial flow decreased, and O2 extraction increased, while O2 consumption decreased and venous-arterial CO2 concentration difference was not changed. At the same time CO2 transport decreased, CO2 concentration in the secretion was unchanged and CO2 output in the secretion was decreased. The decrease in blood flow was always seen about 25 s before the decrease in secretory flow, strongly suggesting that the decrease in blood flow induced the decrease in secretory flow. A higher dose of vasopressin was required to decrease the O2 consumption (i.e. this effect was less sensitive) than to increase O2 extraction. The decrease in secretory flow and the decrease in blood flow showed an intermediate sensitivity. So O2 consumption seems to be preserved at a high level by the increase in O2 extraction. It is concluded that the vasopressin-induced decrease in blood flow is the determinant of the decrease in secretory flow. This phenomenon is discussed in terms of the model for metabolic control of tissue oxygenation.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 2 (1961), S. 425-435 
    ISSN: 1432-2072
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tryptamine applied intracisternally can produce catatonia in cats. This effect can be antagonized by 5-H.T. which itself never causes catatonia. The central — autonomic effects elicited by injections of 5-H.T. and of Tryptamine in the cisterna magna are qualitatively the same; Tryptamine having the weaker effect. These facts lead us to the hypothesis that both substances act in the C.N. S. on the same receptors, Tryptamine having the lower intrinsic activity; thus, Tryptamine must be a competitive inhibitor of 5-H.T. The catatonia produced by Tryptamine might then be regarded as the consequence of a shortage of 5-H.T. on certain receptors in the C. N. S. The effect of Tryptamine lasts longer than that of 5-H.T.; Tryptamine also shows a cumulative pattern, 5-H.T. does not. After Iproniazld (Marsilid) administration this difference is not observed, being obviously dependent on the rate of de struction. Without Iproniazid, 5-H.T. can suppress or prevent the Tryptaminecatatonia only for a restricted period of time, with Iproniazid this suppression respectively prevention is unlimited.
    Type of Medium: Electronic Resource
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