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Acute impact of submaximal resistance exercise on immunological and hormonal parameters in young men.

https://arctichealth.org/en/permalink/ahliterature9539
Source
J Sports Sci. 2003 Dec;21(12):1001-8
Publication Type
Article
Date
Dec-2003
Author
Alfons Ramel
Karl-Heinz Wagner
Ibrahim Elmadfa
Author Affiliation
Unit for Nutrition Research, University of Iceland, PO Box Nyi Gardur, IS-101 Reykjavik, Iceland. ramel@hi.is
Source
J Sports Sci. 2003 Dec;21(12):1001-8
Date
Dec-2003
Language
English
Publication Type
Article
Keywords
Adult
CD4-CD8 Ratio
Comparative Study
Hematocrit
Humans
Hydrocortisone - blood
Killer Cells, Natural - physiology
Leukocyte Count
Lymphocyte Count
Male
Monocytes - physiology
Neutrophils - physiology
Norepinephrine - blood
Physical Education and Training - methods
Reference Values
T-Lymphocytes, Helper-Inducer - physiology
T-Lymphocytes, Regulatory - physiology
Time Factors
Abstract
In this study, we examined the acute effects of submaximal resistance exercise on immunological and hormonal parameters in 7 resistance-trained and 10 non-resistance-trained males. The participants, who were aged 29.5 +/- 7.1 years (mean +/- s), performed submaximal resistance exercise at 75% of their one-repetition maximum. Blood samples were taken before, during, immediately after, and 30, 60 and 120 min after exercise and analysed for leukocyte subpopulations and stress hormones. Total leukocytes, neutrophils and monocytes increased during exercise, reaching their maximum 2 h after exercise. Lymphocytes increased during exercise, T-helper cells returned to resting values after exercise, and natural killer cells and T-suppressor cells decreased below resting values. The CD4/CD8 ratio decreased during exercise but increased during recovery. The resistance-trained participants tended to have lower T-helper cell counts before, during and immediately after exercise and a lower CD4/CD8 ratio during recovery than the non-resistance-trained participants. Plasma cortisol correlated positively with leukocytes during exercise (r = 0.572, P
PubMed ID
14748457 View in PubMed
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Adrenal medullary overactivity in lean, borderline hypertensive young men.

https://arctichealth.org/en/permalink/ahliterature9447
Source
Am J Hypertens. 2004 Jul;17(7):611-8
Publication Type
Article
Date
Jul-2004
Author
Henrik M Reims
Eigil Fossum
Aud Høieggen
Andreas Moan
Ivar Eide
Sverre E Kjeldsen
Author Affiliation
Department of Cardiology, Ullevaal University Hospital, Oslo, Norway.
Source
Am J Hypertens. 2004 Jul;17(7):611-8
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Adolescent
Adrenal Gland Diseases - blood - physiopathology
Adrenal Medulla - metabolism - physiopathology
Adult
Biological Markers - blood
Blood Glucose - metabolism
Blood Pressure - physiology
Body mass index
Comparative Study
Heart Rate - physiology
Humans
Hypertension - blood - physiopathology
Insulin - metabolism
Male
Norepinephrine - blood
Norway - epidemiology
Obesity - blood - physiopathology
Regression Analysis
Research Support, Non-U.S. Gov't
Rest
Statistics
Stress, Psychological - blood
Thinness - blood - physiopathology
Abstract
BACKGROUND: There may be a link among stress, adrenal medullary activation, and the development of hypertension. Obesity is characterized by sympathetic activation and predisposes to hypertension, but may be associated with low or normal adrenal medullary activity. We hypothesized that plasma epinephrine (E) levels and adrenal medullary responsiveness to mental stress are lower in overweight than in lean borderline hypertensive subjects. METHODS: We compared groups of lean (n = 62) and overweight (n = 29) borderline hypertensive young men as well as lean (n = 36) and overweight (n = 7) normotensive young men from the same population. Plasma catecholamines and heart rate (HR) were measured at rest during a hyperinsulinemic glucose clamp and during mental arithmetic-induced stress. RESULTS: Plasma norepinephrine (NE) and E, HR, and responses to stress were increased in borderline hypertensive subjects. Our results showed that NE was increased only in lean borderline hypertensive subjects at rest, but in overweight subjects as well during stress, with DeltaNE being similar in lean and overweight subjects. We found that E was higher in lean than in overweight borderline hypertensive subjects at rest and during stress (both P
PubMed ID
15233980 View in PubMed
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Adrenomedullary catecholamine, pressor and chronotropic responses to human coagulation beta-FXIIa mediated by endogenous kinins.

https://arctichealth.org/en/permalink/ahliterature93828
Source
J Hypertens. 2008 Jan;26(1):61-9
Publication Type
Article
Date
Jan-2008
Author
Amfilochiadis Akis A
Backx Peter H
Floras John S
Author Affiliation
University Health Network and Mount Sinai Hospital Division of Cardiology, Department of Medicine, Canada.
Source
J Hypertens. 2008 Jan;26(1):61-9
Date
Jan-2008
Language
English
Publication Type
Article
Keywords
Adrenal Medulla - drug effects - physiology
Animals
Blood Pressure - drug effects
Bradykinin - blood - pharmacology
Catecholamines - blood
Dose-Response Relationship, Drug
Epinephrine - blood
Factor XIIa - pharmacology
Heart Rate - drug effects
Humans
Injections, Intravenous
Kininogens - blood - deficiency
Male
Norepinephrine - blood
Peptide Fragments - pharmacology
Rats
Rats, Inbred BN
Rats, Mutant Strains
Rats, Wistar
Time Factors
Abstract
OBJECTIVES: There is increasing evidence that blood coagulation factors can influence blood pressure. In the present study, we tested the hypothesis that the beta fragment of human coagulation factor XIIa (beta-FXIIa) induces adrenal catecholamine-mediated pressor and chronotropic responses via bradykinin generated from the plasma kallikrein-kinin system. METHODS AND RESULTS: In anaesthetized bioassay rats with blocked autonomic reflexes, in the Brown Norway strain a bolus injection of beta-FXIIa (1 microg/kg, administered intravenously) elicited a 170-fold rise in plasma epinephrine (from 0.12 +/- 0.02 to 20.58 +/- 2.42 nmol/l; P
PubMed ID
18090541 View in PubMed
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Alcohol and heat tolerance in warm-acclimated rats.

https://arctichealth.org/en/permalink/ahliterature11894
Source
Alcohol. 1992 Mar-Apr;9(2):129-32
Publication Type
Article
Author
P. Huttunen
Author Affiliation
Department of Forensic Medicine, University of Oulu, Finland.
Source
Alcohol. 1992 Mar-Apr;9(2):129-32
Language
English
Publication Type
Article
Keywords
Acclimatization
Animals
Body Temperature - drug effects
Body Temperature Regulation - drug effects
Epinephrine - blood - urine
Ethanol - administration & dosage - blood - pharmacology
Heat
Male
Norepinephrine - blood - urine
Rats
Rats, Inbred Strains
Abstract
The effect of chronic ethanol intake and warm acclimation on the heat tolerance of rats under the influence of alcohol was studied. The animals were divided into two groups: Group 1 received water as their fluid intake and, group 2 received a 10% ethanol solution, and both groups were exposed to a temperature of 30 degrees C for 4 weeks. Excretion of urinary catecholamines was measured prior to warm exposure at 22 degrees C and once a week during warm exposure at 30 degrees C. After warm acclimation a dose of alcohol 2 g/kg was injected in the rats intraperitoneally (i.p.), and then they were exposed to a heat stress of 40 degrees C for 45 min. During warm acclimation, the controls consumed more fluid and they excreted more norepinephrine into the urine than the alcohol-fed animals during the first week. After the period of acclimation there were no significant differences in urinary excretion of catecholamines between the groups. Colonic temperature of the controls was 0.7 degrees C higher than in the alcohol-fed animals. Acute alcohol administration (2 g/kg) increased the colonic temperature of the alcohol-fed animals during a heat stress of 40 degrees C more than in the controls. After heat stress, the concentration of catecholamines in the blood was significantly higher in the controls. The results show that the hyperthermic effect of ethanol was more considerable in the rats whose drinking water during warm acclimation was an ethanol solution.
PubMed ID
1599624 View in PubMed
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Altered cortical activation patterns associated with baroreflex unloading following 24 h of physical deconditioning.

https://arctichealth.org/en/permalink/ahliterature124175
Source
Exp Physiol. 2012 Dec;97(12):1249-62
Publication Type
Article
Date
Dec-2012
Author
J K Shoemaker
C W Usselman
A. Rothwell
S W Wong
Author Affiliation
Neurovascular Research Laboratory, Faculty of Health Sciences, The University of Western Ontario, London, Ontario, Canada. kshoemak@uwo.ca
Source
Exp Physiol. 2012 Dec;97(12):1249-62
Date
Dec-2012
Language
English
Publication Type
Article
Keywords
Adult
Analysis of Variance
Arterial Pressure
Autonomic Nervous System - metabolism - physiopathology
Baroreflex
Bed Rest
Biological Markers - blood
Brain - physiopathology
Brain Mapping - methods
Cardiovascular Deconditioning
Diuretics
Epinephrine - blood
Female
Head-Down Tilt
Heart rate
Humans
Hypovolemia - blood - chemically induced - physiopathology
Lower Body Negative Pressure
Magnetic Resonance Imaging
Male
Motor Activity
Norepinephrine - blood
Ontario
Plasma volume
Renin - blood
Spironolactone
Time Factors
Young Adult
Abstract
Cardiovascular arousal is associated with patterned cortical activity changes. Head-down-tilt bed rest (HDBR) dimishes the baroreflex-mediated cardiac control. The present study tested the hypothesis that HDBR deconditioning would modify the forebrain organization for heart rate (HR) control during baroreflex unloading. Heart rate variability (HRV), blood pressure and plasma hormones were analysed at rest, whereas HR and cortical autonomic activation patterns (functional magnetic resonance imaging) were measured during graded and randomly assigned lower body negative pressure treatments (LBNP, -15 and -35 mmHg) both before (Pre) and after (Post) a 24 h HDBR protocol (study 1; n = 8). An additional group was tested before and following diuretic-induced hypovolaemia (study 2; n = 9; spironolactone, 100 mg day(-1) for 3 days) that mimicked the plasma volume lost during HDBR (-15% in both studies; P
PubMed ID
22613740 View in PubMed
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Anaphylactic death: the effect of aminoguanidine and heparin on histamine and stress hormones in guinea pigs.

https://arctichealth.org/en/permalink/ahliterature12380
Source
Z Rechtsmed. 1989;102(5):297-304
Publication Type
Article
Date
1989
Author
J. Hirvonen
P. Rintahaka
T. Lapinlampi
P. Huttunen
Author Affiliation
Department of Forensic Medicine, University of Oulu, Finland.
Source
Z Rechtsmed. 1989;102(5):297-304
Date
1989
Language
English
Publication Type
Article
Keywords
Anaphylaxis - blood
Animals
Death, Sudden - blood
Epinephrine - blood
Female
Guanidines - pharmacology
Guinea Pigs
Heparin - pharmacology
Histamine - blood
Hydrocortisone - blood
Lung - pathology
Male
Norepinephrine - blood
Abstract
The modifying effect of aminoguanidine (a histaminase inhibitor) and heparin (a histaminase liberator) on anaphylactic shock in guinea pigs was studied using ovalbumin as an antigen and trigger. The animals died of the shock, the time to death remaining unaltered by the drugs. Serum histamine and cortisol values were high after shock, but were reduced by heparin. Both noradrenaline and adrenaline in plasma were also elevated after shock, the final concentration of the latter being lowered by heparin. The lungs were dilated, indicating bronchoconstriction. The results confirm the role of histamine in anaphylactic shock and its potential value for the diagnosis in this kind of rapid death, in which morphological signs are scarce or lacking. Its diagnostic value still requires confirmation, however, which only autopsy studies can supply. It also appears that pretreatment of the animals with heparin affected the blood cortisol and catecholamines, which are involved in the shock mechanism as countermeasures, although aminoguanidine did not have any effect.
PubMed ID
2728623 View in PubMed
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ARCTIC: assessment of haemodynamic response in patients with congestive heart failure to telmisartan: a multicentre dose-ranging study in Canada.

https://arctichealth.org/en/permalink/ahliterature5162
Source
Am Heart J. 1999 Nov;138(5 Pt 1):843-8
Publication Type
Article
Date
Nov-1999
Author
A B Parker
E R Azevedo
M G Baird
S J Smith
J M Arnold
D P Humen
G W Moe
J O Parker
R W Butt
J D Parker
Author Affiliation
University of Ottawa Heart Institute, Ottawa, Canada.
Source
Am Heart J. 1999 Nov;138(5 Pt 1):843-8
Date
Nov-1999
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Angiotensin II - blood
Angiotensin-Converting Enzyme Inhibitors - administration & dosage
Atrial Natriuretic Factor - blood
Benzimidazoles - administration & dosage
Benzoates - administration & dosage
Canada
Catheterization, Peripheral
Comparative Study
Coronary Care Units
Dose-Response Relationship, Drug
Double-Blind Method
Female
Heart Failure, Congestive - blood - drug therapy - physiopathology
Hemodynamic Processes - drug effects
Humans
Male
Middle Aged
Norepinephrine - blood
Renin - blood
Research Support, Non-U.S. Gov't
Safety
Treatment Outcome
Abstract
BACKGROUND: The aim of this study was to examine the acute hemodynamic and neurohormonal effects of the angiotensin II antagonist telmisartan relative to placebo in patients with chronic symptomatic (New York Heart Association class II to III) congestive heart failure and to explore the dose-response relation for these effects. METHODS AND RESULTS: After baseline hemodynamic and neurohormonal measurements made with the use of a pulmonary artery and radial arterial catheter, 82 patients were randomly assigned to placebo or 10, 20, 40, or 80 mg of telmisartan in a double-blind fashion. Hemodynamic and neurohormonal measurements were carried out over 24 hours. Telmisartan caused significant decreases in systemic arterial, pulmonary arterial, and pulmonary capillary wedge pressures with evidence of a dose-response relation for each of these parameters. The drug had no significant effects on heart rate, cardiac index, or systemic vascular resistance. Telmisartan did not have consistent effects on either plasma norepinephrine or plasma atrial natriuretic peptide levels, although it did cause significant increases in both plasma renin activity and angiotensin II levels at higher doses. CONCLUSIONS: The acute administration of the angiotensin II antagonist telmisartan was associated with significant dose-dependent reductions in systemic arterial blood pressure and pulmonary pressures. Long-term follow-up studies are required to translate changes in hemodynamic parameters into a clinical benefit.
PubMed ID
10539814 View in PubMed
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Are the blood pressure and endocrine responses of healthy subjects exposed to cold stress altered by an acutely increased sodium intake?

https://arctichealth.org/en/permalink/ahliterature10212
Source
Eur J Appl Physiol. 2001 Jan-Feb;84(1-2):48-53
Publication Type
Article
Author
O. Arjamaa
T. Mäkinen
L. Turunen
P. Huttunen
J. Leppäluoto
O. Vuolteenaho
H. Rintamäki
Author Affiliation
Institute of Arctic Medicine, PO BOX 5000, 90014 University of Oulu, Finland. olli.arjamaa@oulu.fi
Source
Eur J Appl Physiol. 2001 Jan-Feb;84(1-2):48-53
Language
English
Publication Type
Article
Keywords
Adult
Atrial Natriuretic Factor - blood
Blood Pressure - drug effects - physiology
Cold
Female
Hematocrit
Hemoglobins
Humans
Male
Natriuretic Peptide, Brain - blood
Norepinephrine - blood
Protein Precursors - blood
Sodium, Dietary - administration & dosage
Stress - physiopathology
Abstract
In the study reported here, we examined blood pressure and endocrine responses in cold conditions during salt load in young healthy subjects who had previously shown increased resting blood pressure during acutely increased sodium intake. Subjects (n = 53) added 121 mmol sodium into their normal diet for 1 week. If their mean arterial pressure had increased by a minimum of 5 mmHg compared to the previous measure they were selected for subsequent experiments. The subjects (n = 8) were given 121 mmol supplemental sodium.day-1 for 14 days. They were then put into a wind tunnel for 15 min (temperature--15 degrees C, wind speed 3.5.ms-1). Their blood pressure increased (P
PubMed ID
11394253 View in PubMed
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Blood pressure and endocrine responses of healthy subjects in cold pressor test after acutely increased dietary sodium intake.

https://arctichealth.org/en/permalink/ahliterature10173
Source
J Physiol Anthropol Appl Human Sci. 2001 May;20(3):207-12
Publication Type
Article
Date
May-2001
Author
O. Arjamaa
T. Mäkinen
L. Turunen
P. Huttunen
J. Leppäluoto
O. Vuolteenaho
H. Rintamäki
Author Affiliation
Center of Arctic Medicine, University of Oulu, Oulu, Finland. Olli.Arjamaa@oulu.fi
Source
J Physiol Anthropol Appl Human Sci. 2001 May;20(3):207-12
Date
May-2001
Language
English
Publication Type
Article
Keywords
Adult
Blood Pressure - physiology
Cold
Endocrine System - physiology
Female
Hand
Humans
Male
Natriuretic Agents - blood
Norepinephrine - blood
Pressoreceptors - physiology
Random Allocation
Sodium, Dietary
Abstract
The objective of the study was to compare blood pressure and endocrine responses in a cold pressure test in young healthy subjects who had shown increased blood pressure during an acutely increased sodium intake. Subjects (n = 53) added 121 mmol sodium into their normal diet for one week. If the mean arterial pressure had increased by a minimum of 5 mmHg compared to the control measure, they were selected for the experiments. The selected subjects (n = 8) were given 121 mmol supplemental sodium d-1 for 14 days after which they immersed the right hand into a cold (+10 degrees C) water bath for 5 min. The blood pressure increased (P
PubMed ID
11499168 View in PubMed
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65 records – page 1 of 7.