Plasma levels, heart rate, and blood pressure after intravenous, oral, and aerosol administration of reproterol in man

1988 ◽  
Vol 9 (3) ◽  
pp. 301-314 ◽  
Author(s):  
R. J. J. Hageman ◽  
R. A. De Zeeuw ◽  
J. E. Greving ◽  
J. J. Krann ◽  
G. H. Koëter
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Levels

The Involvement of Platelets and the Coronary Vasculature in Collagen-Induced Sudden Death in Rabbits

1985 ◽  
Vol 53 (01) ◽  
pp. 070-074 ◽  
Author(s):  
G Mallarkey ◽  
G M Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Platelet Count ◽  
Sudden Death ◽  
Myocardial Ischaemia ◽  
Plasma Levels ◽  
Sodium Citrate ◽  
Plasma Samples ◽  
Calcium Entry Blockers

SummaryThe mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TxB2) and 6-keto prostaglandin Fia (6-keto PGF1α). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBs), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TxB2 levels. 6-keto PGF1α could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TxB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KC1, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBs physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.

Downregulation of growth hormone in postural orthostatic tachycardia syndrome: insights from the SYSTEMA cohort

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Johansson ◽  
J Schulte ◽  
F Ricci ◽  
M Persson ◽  
R Sutton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Growth Hormone ◽  
Plasma Levels ◽  
Orthostatic Intolerance ◽  
Statistical Tests ◽  
Growth Hormone Level ◽  
Postural Orthostatic Tachycardia Syndrome ◽  
Funding Source ◽  
Significant Difference

Abstract Background Postural orthostatic tachycardia syndrome (POTS) is a variant of cardiovascular autonomic disorder occurring predominantly in young women. POTS is characterized by an excessive heart rate increase when assuming upright posture accompanied by symptoms of orthostatic intolerance. The pathophysiology of POTS has not been fully established and is believed to be multifactorial. Purpose We aimed to investigate the alterations in circulating growth hormone level in POTS. Methods We conducted an age-matched case-control study enrolling 42 patients with POTS (age 31±9 years; 36 women) verified by positive head-up tilt testing and cardiovascular autonomic tests, and 46 controls (32±9 years; 35 women) with negative active standing test and no history of syncope, orthostatic intolerance and endocrine disease. We measured plasma levels of growth hormone using a high-sensitivity chemiluminescence immunoassay in relation to presence of POTS diagnosis. All study participants completed the validated Orthostatic Hypotension Questionnaire (OHQ), consisting of two components: the symptoms assessment scale (OHSA) and daily activity scale (OHDAS) to evaluate the burden of symptoms. We applied standard statistical tests for group differences. Growth hormone values were log-transformed and standardized before the group comparison. Results POTS patients had significantly lower plasma levels of growth hormone (ng/mL) (median=0.53, IQR, 0.10–2.83 vs. median=2.33, IQR, 0.26–7.2, p=0.04) than controls. Levels of growth hormone were reversely related to OHDAS (p=0.049) among POTS patients. Supine heart rate was significantly higher in POTS patients (69.0±11.1 beats/min vs. 63.3±10.8 beats/min, p=0.02), as well as diastolic blood pressure (72.9±9.1 mmHg vs. 69.0±8.5 mmHg, p=0.04). We observed no significant difference in supine systolic blood pressure (116.6±13.3 mmHg vs. 115.2±10.0 mmHg, p=0.60). POTS patients had a significantly higher composite OHQ score than controls (60.0±18.6 vs. 4.2±7.5, p<0.001), as well as OHSA (36.2±10.0 vs. 3.6±6.4, p<0.001) and OHDAS (23.8±9.7 vs. 0.6±1.3, p<0.001). Conclusion(s) Our study shows that patients with POTS have significantly reduced plasma levels of circulating growth hormone. Lower growth hormone levels among POTS patients are associated with increased impairment of daily life activities. Further studies are necessary to confirm our findings in the independent populations and explain the mechanisms behind this alteration. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Crafoord Foundation, Swedish Heart and Lung Foundation

Prostaglandins, catecholamines, and cardiovascular responses to hemorrhage

1981 ◽  
Vol 240 (3) ◽  
pp. R166-R174 ◽  
Author(s):  
G. Feuerstein ◽  
D. C. Jimerson ◽  
I. J. Kopin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Levels ◽  
Recovery Rate ◽  
Heart Rate Recovery ◽  
Cardiovascular Responses ◽  
Pressure Recovery ◽  
Hemodynamic Effects ◽  
Transient Effect ◽  
Acute Hemorrhage

The effects of prostaglandins (PGE2 and 16,16-dimethyl-PGE1) on epinephrine (E) and norepinephrine (NE) release, in response to a hypotensive stimulus (bleeding 5 ml/300 g), were studied in relation to blood pressure and heart rate responses in the rat. PGE2 (10 micrograms/kg-1 . min-1) and 16,16-dimethyl-PGE1 (1 microgram . kg-1 . min-1) accelerated blood pressure and heart rate recovery rate following acute hemorrhage and increased plasma E and NE levels. Plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol (DHPG) were not affected by PG infusion. In bilaterally nephrectomized rats, PGE2 increased plasma levels of E, NE, and DHPG but failed to enhance the blood pressure and had only a mild effect on heart rate recovery following bleeding. In hexamethonium-treated rats, infusion of PGE2 had a small and transient effect on blood pressure recovery, but its effect on the heart rate was not affected; NE and E levels in the plasma of the hexamethonium-treated rats were still higher in the PGE2-infused rats. These studies indicate that in the intact rat, administered PGE potentiate the release of E and NE and facilitate blood pressure and heart rate recovery following acute hemorrhage. The hemodynamic effects of the PGE appear to be mediated by a renal factor whereas the effects of PGE on E and NE response to hemorrhage are independent of the presence of intact kidneys.

Effects of naloxone on catecholamine plasma levels in adult men. A dose-response study

1984 ◽  
Vol 106 (3) ◽  
pp. 357-361 ◽  
Author(s):  
Massimo Mannelli ◽  
Mario Maggi ◽  
Maria Laura De Feo ◽  
Silvana Cuomo ◽  
Giuseppe Delitala ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Levels ◽  
Plasma Insulin ◽  
Endogenous Opiates ◽  
Adult Men ◽  
Before And After ◽  
Normal Men ◽  
Dose Response Study

Abstract. To evaluate a possible role for endogenous opiates in modulating sympathetic-adrenal function in humans, we measured plasma epinephrine and norepinephrine (radioenzymatic method), blood pressure and heart rate in 8 normal men (aged 24–33 years) before and after placebo or different doses (0.4, 4.8, 10 mg) of naloxone. In 6 subjects plasma insulin and glucagon levels were also measured by radioimmunoassay after placebo and 10 mg naloxone. Naloxone had no significant effect upon blood pressure, heart rate, plasma insulin, glucagon or norepinephrine. Placebo, 0.4 and 4.8 mg naloxone caused no significant change in peripheral levels of epinephrine while 10 mg produced an increase in epinephrine concentrations 15 min after iv injection (186 ± 23 vs 99 ± 9 pmol/l, P < 0.01). Since naloxone did not modify plasma levels of insulin and glucagon, an indirect effect of naloxone on adrenal medullary secretion seems to be excluded. These results are in agreement with in vitro experimental data obtained in animals and suggest that endogenous opiates also have a role in modulating adrenal medullary secretion in man.

scholarly journals Alternations in the cardiovascular autonomic regulation and growth factors in autism

2021 ◽  
pp. 551-561
Author(s):  
Ingrid Tonhajzerova ◽  
Igor Ondrejka ◽  
Nikola Ferencova ◽  
Iveta Bujnakova ◽  
Marian Grendar ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Growth Factor ◽  
Frequency Band ◽  
Plasma Levels ◽  
Autism Spectrum ◽  
Autonomic Regulation ◽  
Autistic Children ◽  
Rr Intervals ◽  
Cardiovascular Autonomic Regulation

Autism spectrum disorder (ASD) represents a serious neurodevelopmental disorder associated with autonomic nervous system dysregulation. The aim was to study complex cardiovascular autonomic regulation using heart rate variability (HRV) and systolic blood pressure variability (SBPV) linear/non-linear analysis at rest and during orthostasis, and to assess plasma levels of epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) in autistic children. Twenty-five ASD boys and 25 age and gender-matched children at the age 7 15 years were examined. After venous blood taking, continuous ECG and blood pressure biosignals were recorded at rest and during orthostasis. Evaluated parameters: RR intervals, high- and low-frequency band of HRV spectral analysis (HF-HRV, LF-HRV), symbolic dynamics parameters 0V %, 1V %, 2LV %, 2UV %, low- and high-frequency band of SBPV (LF-SBPV, HF-SBPV), systolic, diastolic, mean blood pressure, EGF, VEGF plasma levels. RR intervals were significantly shortened and the HF-HRV, LF-SBPV, HF-SBPV parameters were significantly lower at rest, the HF-HRV and LF-SBPV remained lower during orthostasis in autistic children compared to controls (p0.05). EGF plasma levels were significantly lower in ASD compared to controls (p=0.046). No significant differences were found in remaining parameters. Our study revealed tachycardia, cardiovagal underactivity, and blunted sympathetic vasomotor regulation at rest and during orthostasis in autistic children. Additionally, complex heart rate dynamics are similar in autistic children than controls. Furthermore, EGF was reduced in autistic children without significant correlations with any autonomic parameters. We suggest that the abnormal complex cardiovascular reflex control could contribute to understanding the pathway linking autonomic features and autism.

scholarly journals Increase in epinephrine-induced responsiveness during microgravity simulated by head-down bed rest in humans

1999 ◽  
Vol 87 (5) ◽  
pp. 1614-1620 ◽  
Author(s):  
P. Barbe ◽  
J. Galitzky ◽  
C. Thalamas ◽  
D. Langin ◽  
M. Lafontan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Energy Expenditure ◽  
Systolic Blood Pressure ◽  
Plasma Levels ◽  
Simulated Microgravity ◽  
Bed Rest ◽  
Plasma Norepinephrine ◽  
Spectral Variability ◽  
Nonesterified Fatty Acids

The epinephrine (Epi)-induced effects on the sympathetic nervous system (SNS) and metabolic functions were studied in men before and during a decrease in SNS activity achieved through simulated microgravity. Epi was infused at 3 graded rates (0.01, 0.02, and 0.03 μg ⋅ kg−1 ⋅ min−1for 40 min each) before and on the fifth day of head-down bed rest (HDBR). The effects of Epi on the SNS (assessed by plasma norepinephrine levels and spectral analysis of systolic blood pressure and heart rate variability), on plasma levels of glycerol, nonesterified fatty acids (NEFA), glucose and insulin, and on energy expenditure were evaluated. HDBR decreased urinary norepinephrine excretion (28.1 ± 4.2 vs. 51.5 ± 9.1 μg/24 h) and spectral variability of systolic blood pressure in the midfrequency range (16.3 ± 1.9 vs. 24.5 ± 0.9 normalized units). Epi increased norepinephrine plasma levels ( P < 0.01) and spectral variability of systolic blood pressure ( P < 0.009) during, but not before, HDBR. No modification of Epi-induced changes in heart rate and systolic and diastolic blood pressures were observed during HDBR. Epi increased plasma glucose, insulin, and NEFA levels before and during HDBR. During HDBR, the Epi-induced increase in plasma glycerol and lactate levels was more pronounced than before HDBR ( P < 0.005 and P < 0.001, respectively). Epi-induced energy expenditure was higher during HDBR ( P < 0.02). Our data suggest that the increased effects of Epi during simulated microgravity could be related to both the increased SNS response to Epi infusion and/or to the β-adrenergic receptor sensitization of end organs, particularly in adipose tissue and skeletal muscle.

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