Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers

1992 ◽  
Vol 43 (3) ◽  
pp. 245-249 ◽  
Author(s):  
H. Ensinger ◽  
T. Weichel ◽  
K. H. Lindner ◽  
A. Prengel ◽  
A. Grünert ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Plasma Catecholamine ◽  
Plasma Catecholamine Concentrations ◽  
Noradrenaline And Adrenaline

Decreased Platelet-Free Dopamine and Unchanged Noradrenaline and Adrenaline in Essential Hypertension

1988 ◽  
Vol 60 (02) ◽  
pp. 251-254 ◽  
Author(s):  
S E Kjeldsen ◽  
K Gjesdal ◽  
P Leren ◽  
I K Eide
Keyword(s):  
Body Weight ◽  
Essential Hypertension ◽  
Blood Platelets ◽  
Plasma Catecholamine ◽  
Catecholamine Synthesis ◽  
Hypertensive Group ◽  
Plasma Catecholamine Concentrations ◽  
Noradrenaline And Adrenaline ◽  
Over Time ◽  
Normotensive Control

SummaryThe content of free-catecholamines in blood platelets is much higher than in plasma and platelet catecholamines must be taken up from plasma, since platelets lack the enzymes for catecholamine synthesis. There is some evidence that platelet catecholamine content under certain circumstances may be an integrated measure of plasma catecholamine concentrations over time. Platelet-free catecholamines were therefore assayed in 18 untreated patients with essential hypertension and in 16 normotensive control subjects. Mean platelet-free dopamine in the hypertensive group was 3.7 ± 0.4 pg/mg platelet weight, i.e. significantly less than the 6.5 ± 0.9 pg/mg found in the normotensive (p <0.005). Platelet contents of noradrenaline and adrenaline did not differ. Decreased platelet-free dopamine and unchanged platelet noradrenaline and adrenaline persisted after adjustment for increased body weight in the hypertensive group. Although the reasons for decreased platelet-free dopamine in the hypertensive group remain unknown, this finding may add to previous result showing facilitated release of granular contents from blood platelets in patients with essential hypertension. Our data do not support platelet levels of free-catecholamines to be a marker of increased sympathetic tone in essential hypertension.

Effect of respiratory acidosis and alkalosis on plasma catecholamine concentrations in anaesthetized man

1993 ◽  
Vol 84 (1) ◽  
pp. 69-72 ◽  
Author(s):  
J. M. Low ◽  
T. Gin ◽  
T. W. Lee ◽  
K. Fung
Keyword(s):  
Carbon Dioxide ◽  
Plasma Concentration ◽  
Partial Pressure ◽  
Plasma Concentrations ◽  
Respiratory Acidosis ◽  
Gas Mixture ◽  
Plasma Catecholamine ◽  
Arterial Partial Pressure ◽  
Plasma Catecholamine Concentrations ◽  
Noradrenaline And Adrenaline

1. Plasma concentrations of noradrenaline and adrenaline were measured in 11 anaesthetized patients during normocapnia, hypocapnia and hypercapnia. Hypocapnia was produced by deliberate hyperventilation and hypercapnia by adding carbon dioxide to the inspired gas mixture. 2. With a median (range) arterial partial pressure of carbon dioxide of 4.7 (4.2–5.2) kPa, the median (range) plasma concentration of noradrenaline was 0.41 (0.12–0.94) nmol/l and of adrenaline was 0.15 (0.05–0.31) nmol/l. 3. With an arterial partial pressure of carbon dioxide of 2.6 (2.2–3.3) kPa, there was no change in the plasma concentration of noradrenaline [0.37 (0.12–0.86) nmol/l] or that of adrenaline [0.16 (0.05–0.32) nmol/l]. 4. However, with an arterial partial pressure of carbon dioxide of 10.4 (7.6–13.2) kPa, there were significant increases in the plasma concentrations of both noradrenaline [1.13 (0.79–2.05) nmol/l, P < 0.01] and adrenaline [0.67 (0.20–2.92) nmol/l, P < 0.05]. 5. This is the first demonstration in man that respiratory acidosis causes an increase in plasma concentrations of catecholamines.

Plasma Catecholamine Levels and Vascular Response in Deoxycorticosterone Acetate Hypertension of Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 315s-317s ◽  
Author(s):  
W. Rascher ◽  
R. Dietz ◽  
A. Schomig ◽  
J. Weber ◽  
F. Gross
Keyword(s):  
Hind Limb ◽  
Vascular Tone ◽  
Plasma Concentrations ◽  
Plasma Catecholamine ◽  
Vascular Response ◽  
Deoxycorticosterone Acetate ◽  
Pronounced Increase ◽  
Basal Plasma ◽  
Noradrenaline And Adrenaline ◽  
Catecholamine Levels

1. In rats with deoxycorticosterone acetate (DOCA) hypertension basal plasma concentrations of noradrenaline and adrenaline correspond to those of sham-treated controls. 2. In DOCA-treated rats frusemide caused a more pronounced increase in plasma noradrenaline than in control rats. This difference was not observed for adrenaline. 3. In the isolated perfused hind-limb preparation the sensitivity to noradrenaline was already enhanced before blood pressure was elevated. 4. These results suggest that the adrenergic vascular tone is increased in DOCA hypertension in rats.

Plasma Concentrations of Catecholamines in Two Strains of Spontaneously Hypertensive Rats at Different Ages

1981 ◽  
Vol 61 (s7) ◽  
pp. 199s-202s ◽  
Author(s):  
P. Ferrari ◽  
G. B. Picotti ◽  
E. Minotti ◽  
G. P. Bondiolotti ◽  
A. M. Caravaggi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Concentrations ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Adult Rats ◽  
Plasma Adrenaline ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Normotensive Strain ◽  
Noradrenaline And Adrenaline

1. Blood pressure was measured and plasma levels of noradrenaline and adrenaline were determined radioenzymatically under basal conditions and after 10% blood volume reduction in blood drawn through catheters previously implanted in young and adult rats of two different genetically hypertensive strains: the Kyoto strain (SHR) and the Milan strain (MHS), and in their respective controls: Wistar—Kyoto strain (WKY) and Milan normotensive strain (MNS). 2. Under basal conditions no differences were observed between plasma noradrenaline and adrenaline levels in SHR and MHS rats and in the controls, at any age. Haemorrhage produced a greater fall in the blood pressure (P &lt; 0.01) of young and adult hypertensive strains (SHR-MHS) than in WKY and MNS rats, and a greater rise in plasma adrenaline (P &lt; 0.01). 3. These results suggest that: (a) there may be differences in involvement of the sympathetic nervous system in the pathogenesis of hypertension in SHR and MHS rats but not such as to cause differences in plasma catecholamine levels in either young or adult rats; (b) haemorrhage activates the sympatho—adrenal systems more in SHR and MHS rats, than in controls, and the greater percentage fall in blood pressure is probably due to a difference in reflex venoconstriction.

Abstract 57: Therapeutic Effects of Small Molecule Gβγ Inhibition in Pressure Overload Heart Failure

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Fadia A Kamal ◽  
Alan V Smrcka ◽  
Burns C Blaxall
Keyword(s):  
Heart Failure ◽  
Small Molecule ◽  
Interstitial Fibrosis ◽  
Plasma Catecholamines ◽  
Pressure Overload ◽  
Plasma Catecholamine ◽  
Therapeutic Effects ◽  
Mrna Levels ◽  
Group V ◽  
Plasma Catecholamine Concentrations

Heart failure (HF) is a progressive disease with rapidly increasing rates of morbidity and mortality; it is the leading cause of death worldwide. Elevated sympathetic nervous system activity, a salient feature of HF progression, leads to pathologic attenuation and desensitization of β-adrenergic receptors (β-ARs) due in part to Gβγ-mediated signaling. We recently reported that novel small molecule Gβγ inhibitors selectively block specific Gβγ signals and halt HF progression in pharmacologic and transgenic mouse models of HF. We assessed the hypothesis that the Gβγ inhibitor Gallein could be salutary in treating pre-existing HF in a clinically relevant model. We utilized the pressure-overload HF model of mouse transverse aortic constriction (TAC). Four weeks post-TAC, mice received daily IP injections of vehicle (PBS; group V) or Gallein (10mg/Kg/day; group G) for eight weeks. Gallein treatment improved survival (7 of 9 mice survived vs. 5 of 9 mice in group V) and cardiac function (%EF 75.2 ± 7.5 vs 35.6 ± 17.2 in group V, +dP/dt (mmHg/sec) 7022 ± 485.3 vs. 3584 ± 598.6 in group V), -dP/dt (mmHg/sec) -5826 ± 910.7 vs. -3260 ± 62.3 in group V, LVEDP (mmHg) 11.5 ± 3.7 vs. 29.45 ± 3.6 in group V). In addition, gallein reduced cardiac hypertrophy (HW/BW (mg/g) 5.8 ± 0.3 vs. 8.8 ± 1.1 in group V) and plasma catecholamine concentrations (adrenaline (ng/ml) 1.3 ± 0.3 vs. 6.6 ± 2.8 in group V, noradrenaline (ng/ml) 3.6 ± 0.6 vs. 15.1 ± 3.6 in group V). Reduction of interstitial fibrosis as well as mRNA levels of α-SMA, TNF-α, and IL-6 was observed in the hearts of Gallein treated animals (59.7 ± 14.1%, 43.8 ± 9.3% and 28.5 ± 3.5% relative to group V, respectively). On the molecular level, Gallein treated mice showed less GRK2 and PI3Kγ membrane recruitment, and less Akt activation (42.9 ± 7.1%, 66.7 ± 13.3% and 46.2 ± 7.7% relative to group V, respectively) in myocardial lysates. In conclusion , these data suggest a possible therapeutic role for small molecule Gβγ inhibition in halting the progression of HF, potentially via inhibition of the Gβγ-GRK2-PI3Kγ-Akt pathway. The combined effect of halting HF progression and reducing plasma catecholamines suggests a possible systemic role for small molecule Gβγ inhibition in both the heart and the adrenal gland.

Plasma Catecholamine Concentrations and Haemodynamic Studies During Phaeochromocytoma Resection

1982 ◽  
pp. 249-250
Author(s):  
J. Marty ◽  
J. M. Desmonts ◽  
M. Fischler ◽  
G. Chalaux ◽  
F. Michon ◽  
...  
Keyword(s):  
Plasma Catecholamine ◽  
Plasma Catecholamine Concentrations

Reflex sympathetic activation in humans is accompanied by inhibition of gastric HCO3- secretion

1988 ◽  
Vol 255 (6) ◽  
pp. G752-G758 ◽  
Author(s):  
H. Sjovall ◽  
H. Forssell ◽  
J. Haggendal ◽  
L. Olbe
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
Sympathetic Activity ◽  
Plasma Catecholamine ◽  
Series Of Experiments ◽  
Plasma Catecholamine Concentrations ◽  
Peripheral Sympathetic Activity ◽  
Forearm Vascular Resistance

The study was performed to determine whether the sympathetic nervous system contributes to the reflex control of gastric HCO3- secretion in humans. Gastric HCO3- secretion was registered by a computerized technique based on measurements of pH and PCO2 in gastric effluent. To minimize formation of CO2 in the stomach, subjects were pretreated with the H2-receptor blocker ranitidine. Compensations were made for HCO3- of nongastric origin. As indicators of cardiovascular sympathetic activity, we measured heart rate, forearm vascular resistance, and plasma catecholamine concentrations. In one series of experiments, peripheral sympathetic activity was enhanced by the application of a negative pressure around the lower part of the body (lower body negative pressure, LBNP), at a rate sufficient to induce a slight decrease in systemic arterial pressure. In another series of experiments, peripheral sympathetic activity was inhibited by elevation of the legs, a procedure that simulates volume loading by redistributing blood volume toward the central circulation. LBNP at -20 mmHg decreased systolic pressure and pulse pressure and significantly increased heart rate, forearm vascular resistance, and plasma catecholamine levels. All these effects were observed in the first 15-min period of LBNP and were well maintained throughout the 45-min observation period. LBNP also inhibited basal gastric HCO3- secretion rate in seven of eight individuals, but this response was slower in onset with a latency of at least 15 min. Elevation of the legs increased pulse pressure and decreased forearm vascular resistance. Catecholamines were not measured in these experiments. Gastric HCO3- secretion tended to increase, but the magnitude of the response was highly variable.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of the α2-Agonist Dexmedetomidine on Cerebral Neurotransmitter Concentrations during Cerebral Ischemia in Rats

2002 ◽  
Vol 96 (2) ◽  
pp. 450-457 ◽  
Author(s):  
Kristin Engelhard ◽  
Christian Werner ◽  
Susanne Kaspar ◽  
Oliver Möllenberg ◽  
Manfred Blobner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Glutamate Release ◽  
Plasma Catecholamine ◽  
Doppler Flowmetry ◽  
Brain Norepinephrine ◽  
Arterial Blood ◽  
The Right ◽  
Plasma Catecholamine Concentrations

Background This study investigates whether neuroprotection seen with dexmedetomidine is associated with suppression of peripheral or central sympathetic tone. Methods Thirty fasted male Sprague-Dawley rats were intubated and ventilated with isoflurane and N2O/O2 (fraction of inspired oxygen = 0.33). Catheters were inserted into the right femoral artery and vein and into the right jugular vein. Cerebral blood flow was measured using laser Doppler flowmetry. Bilateral microdialysis probes were placed into the cortex and the dorsal hippocampus. At the end of preparation, the administration of isoflurane was replaced by fentanyl (bolus: 10 microg/kg; infusion: 25 microg x kg(-1) x h(-1)). Animals were randomly assigned to one of the following groups: group 1 (n = 10): control animals; group 2 (n = 10): 100 microg/kg dexmedetomidine administered intraperitoneally 30 min before ischemia; group 3 (n = 10): sham-operated rats. Ischemia (30 min) was produced by unilateral carotid artery occlusion plus hemorrhagic hypotension to a mean arterial blood pressure of 30-35 mmHg to reduce ipsilateral cerebral blood flow by 70%. Pericranial temperature, arterial blood gases, and pH were maintained constant. Cerebral catecholamine and glutamate concentrations and plasma catecholamine concentrations were analyzed using high-performance liquid chromatography. Results During ischemia, dexmedetomidine suppressed circulating norepinephrine concentrations by 95% compared with control animals. In contrast, brain norepinephrine and glutamate concentrations were increased irrespective of dexmedetomidine infusion before ischemia. Conclusions The current data show that the increase of circulating catecholamine concentrations during cerebral ischemia was suppressed with dexmedetomidine. In contrast, dexmedetomidine does not suppress elevation in brain norepinephrine and glutamate concentration associated with cerebral ischemia. This suggests that the neuroprotective effects of dexmedetomidine are not related to inhibition of presynaptic norepinephrine or glutamate release in the brain.

Sign in / Sign up

Export Citation Format

Share Document