scholarly journals Long-Term Urban Particulate Air Pollution, Traffic Noise, and Arterial Blood Pressure

2011 ◽  
Vol 119 (12) ◽  
pp. 1706-1711 ◽  
Author(s):  
Kateryna Fuks ◽  
Susanne Moebus ◽  
Sabine Hertel ◽  
Anja Viehmann ◽  
Michael Nonnemacher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Arterial Blood Pressure ◽  
Traffic Noise ◽  
Particulate Air Pollution ◽  
Arterial Blood

Long-term Urban Background Particulate Air Pollution Increases Arterial Blood Pressure

2010 ◽  
Author(s):  
Kateryna Fuks ◽  
Sabine Hertel ◽  
Anja Viehmann ◽  
Michael Nonnemacher ◽  
Susanne Moebus ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Arterial Blood Pressure ◽  
Urban Background ◽  
Particulate Air Pollution ◽  
Arterial Blood

scholarly journals Mechanisms of Inhaled Fine Particulate Air Pollution–Induced Arterial Blood Pressure Changes

2009 ◽  
Vol 117 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Carlo R. Bartoli ◽  
Gregory A. Wellenius ◽  
Edgar A. Diaz ◽  
Joy Lawrence ◽  
Brent A. Coull ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Arterial Blood Pressure ◽  
Particulate Air Pollution ◽  
Arterial Blood ◽  
Fine Particulate ◽  
Pressure Changes

Effects of isoproterenol on the cardiovascular system of fetal sheep exposed to long-term high-altitude hypoxemia

1995 ◽  
Vol 78 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. Kamitomo ◽  
T. Ohtsuka ◽  
R. D. Gilbert
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Right Ventricular ◽  
High Altitude ◽  
Arterial Blood Pressure ◽  
Left Ventricular ◽  
Arterial Blood ◽  
Isoproterenol Infusion

We exposed fetuses to high-altitude (3,820 m) hypoxemia from 30 to 130 days gestation, when we measured fetal heart rate, right and left ventricular outputs with electromagnetic flow probes, and arterial blood pressure during an isoproterenol dose-response infusion. We also measured the distribution of cardiac output with radiolabeled microspheres during the maximal isoproterenol dose. Baseline fetal arterial blood pressure was higher in long-term hypoxemic fetuses (50.1 +/- 1.3 vs. 43.4 +/- 1.0 mmHg) but fell during the isoproterenol infusion to 41.3 +/- 1.4 and 37.5 +/- 1.4 mmHg, respectively, at the highest dose. Heart rate was the same in both groups and did not differ during isoproterenol infusion. Baseline fetal cardiac output was lower in the hypoxemic group (339 +/- 18 vs. 436 +/- 19 ml.min-1.kg-1) due mainly to a reduction in right ventricular output. During the isoproterenol infusion, right ventricular output increased to the same extent in both hypoxemic and normoxic fetuses (approximately 35%); however, left ventricular output increased only approximately 15% in the hypoxemic group compared with approximately 40% in the normoxic group. The percent change in individual organ blood flows during isoproterenol infusion in the hypoxemic groups was not significantly different from the normoxic group. All of the mechanisms that might be responsible for the differential response of the fetal left and right ventricles to long-term hypoxia are not understood and need further exploration.

Long-Term Telemetry of Direct Arterial Blood Pressure in Unrestricted Hypertensives

2015 ◽  
pp. 211-215
Author(s):  
B. Kr�nig ◽  
K. Dufey ◽  
P. Reinhardt ◽  
J. Jahnecke ◽  
H. P. Wolff
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Direct Arterial Blood Pressure

scholarly journals Significance of the Cerebrovascular Effects of Immobilization Stress in the Rabbit

1984 ◽  
Vol 4 (3) ◽  
pp. 397-406 ◽  
Author(s):  
Pierre Lacombe ◽  
Jacques Seylaz
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Immobilization Stress ◽  
Sampling Technique ◽  
Stress Reaction ◽  
Acute Hypertension ◽  
Cerebrovascular Autoregulation ◽  
Arterial Blood ◽  
Systemic Factors

The question of the significance of the cerebrovascular effects of stressful situations in animals is still controversial. In the present article, an experimental model of immobilization stress in the rabbit is described, and its specificity in relation to arterial blood pressure and PaCO2 is investigated. CBF was measured with the multiregional tissue sampling technique using [14C]-ethanol as tracer. After dissipation of althesin anesthesia, the stress reaction was elicited by tactile abdominal stimuli. The response was evidenced by an instantaneous acute hypertension (+ 33.8% during the CBF measurement period). Within the first minute of the reaction, the CBF was significantly increased in all nine structures studied by 39% (caudate nucleus) to 82% (parietotemporal cortex). The study of the influence of arterial blood pressure and the PaCO2 on CBF showed that cerebrovascular autoregulation and CO2 sensitivity were differently affected in the various structures during the stress reaction. However, the stress response of the brain circulation could not be entirely ascribed to one or both of these two systemic factors, thus suggesting the contribution of a local intrinsic activation. The model presented here could be useful for long-term studies of cerebrovascular repercussions of repeated acute hypertensions of a stressful nature.

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