Time-Course Effects of Adrenergic and Cholinergic Antagonists on Systemic Arterial Blood Pressure, Heart Rate and Temperature in Conscious Squirrel Monkeys

1981 ◽  
Vol 10 (2-3) ◽  
pp. 81-92 ◽  
Author(s):  
L.D. Byrd ◽  
F.A. Gonzalez
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Time Course ◽  
Squirrel Monkeys ◽  
Cholinergic Antagonists ◽  
Systemic Arterial Blood Pressure ◽  
Arterial Blood

Regulation of Cardiac Output during 2,4-Dinitrophenol-Induced Tissue Hypermetabolism in the Dog

1977 ◽  
Vol 53 (1) ◽  
pp. 17-25
Author(s):  
C. Liang ◽  
W. B. Hood
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
The Other ◽  
Pulmonary Artery Wedge Pressure ◽  
Systemic Arterial Blood Pressure ◽  
Arterial Blood ◽  
Wedge Pressure

1. Cardiac output increased in proportion to oxygen consumption in intact chloralose-anaesthetized dogs after four successive intravenous infusions of 2,4-dinitrophenol (11 μmol/kg; 2 mg/kg). 2. Splenectomy abolished the increase in cardiac output after the first three doses of 2,4-dinitrophenol. β-Adrenoreceptor blockade by practolol, on the other hand, did not prevent the cardiac output rise after the first 2,4-dinitrophenol infusion, but further increases by 2,4-dinitrophenol infusion were abolished. When splenectomy and β-adrenoreceptor blockade were combined, cardiac output did not increase significantly after all four doses of 2,4-dinitrophenol. 3. Cardiac output and mean systemic arterial blood pressure increased when the splenic venous blood collected after 2,4-dinitrophenol infusion was infused intraportally. 4. In a vascularly isolated, but normally innervated, lower half-body cross-perfusion preparation, cardiac output and mean systemic arterial blood pressure increased in the upper half-body when tissue hypermetabolism was produced in the cross-perfused area by 2,4-dinitrophenol. Neither pulmonary artery wedge pressure nor heart rate changed significantly. 5. This circulatory stimulation, after regional 2,4-dinitrophenol infusion, was abolished or was prevented from occurring by splenectomy. 6. It appears that the normal cardiac output response to tissue hypermetabolism requires both an intact spleen and normally functioning β-adrenoreceptors.

Compression Stocking Length Effects on Arterial Blood Pressure and Heart Rate Following Head-Up Tilt in Healthy Volunteers

2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Arterial Blood Pressure ◽  
Compression Stocking ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Length Effects

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

scholarly journals Rhythmic Breath Holding and Its Effect on Arterial Blood Pressure and Its Correlation With Blood Gases

2020 ◽  
Author(s):  
Bharti Bhandari ◽  
Manisha Mavai ◽  
Yogendra Raj Singh ◽  
Bharati Mehta ◽  
Omlata Bhagat
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular System ◽  
Arterial Blood Pressure ◽  
Blood Gases ◽  
Total Power ◽  
Breath Holding ◽  
Single Episode ◽  
Arterial Blood ◽  
Maximum Inspiration

A single episode of breath-holding (BH) is known to elevate the blood pressure, and regular breathing exercise lowers the blood pressure. This prompted us to investigate how a series of BH epochs would affect the cardiovascular system. To observe arterial blood pressure (ABP) and heart rate (HR) changes associated with a series of “BH epochs” following maximum inspiration and maximum expiration and find the underlying mechanisms for the change by autonomic activity. Thirty-five healthy young adults were instructed to hold their breath repetitively, for 5 minutes, in two patterns, one following maximum inspiration and other following maximum expiration. ABP and ECG (for Heart Rate Variability) were continuously recorded at rest and during both the maneuvers. Capillary blood gases (BG) were zanalyzed at baseline and at the breakpoint of the last epoch of BH. ABP rose significantly at the breakpoint during both the maneuvers. No change in HR was observed. There was significant fall in PO2 from 94.7 (4.1) mmHg at baseline to 79.1 (9.0) mmHg during inspiratory and 76.90 (12.1) mmHg during expiratory BH. Similarly, SPO2 decreased from 96.3 (1.9) % at baseline to 95.4 (1.5) % and 94.5 (2.7) % during inspiratory and expiratory BH, respectively. Rise in PCO2 from 39.5(3.1) mmHg at baseline to 42.9 (2.7) mmHg and 42.1 (2.8) mmHg during inspiratory and expiratory BH respectively was observed. There was no significant correlation between blood gases and arterial blood pressure. Among HRV parameters, a significant decrease in SDNN, RMSSD, HFnu, total power and SD1/SD2 and the significant increase in LFnu, LF/HF and SD2 were observed during both BH patterns. Rhythmic BH patterns affect the cardiovascular system in similar way as a single episode of BH. Sympathetic overactivity could be the postulated mechanism for the same. © 2019 Tehran University of Medical Sciences. All rights reserved. Acta Med Iran 2019;57(8):492-498.

scholarly journals Methane, a gut bacteria-produced gas, does not affect arterial blood pressure in normotensive anaesthetized rats.

2021 ◽  
Author(s):  
Ewelina Zaorska ◽  
Marta Gawrys-Kopczynska ◽  
Ryszard Ostaszewski ◽  
Dominik Koszelewski ◽  
Marcin Ufnal
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Acute Administration ◽  
Hemodynamic Effects ◽  
Arterial Blood ◽  
Anaesthetized Rats ◽  
Carbohydrate Fermentation ◽  
Oxidative Effects ◽  
Lines Of Evidence

Methane is produced by carbohydrate fermentation in the gastrointestinal tract through the metabolism of methanogenic microbiota. Several lines of evidence suggest that methane exerts anti-inflammatory, anti-apoptotic and anti-oxidative effects. The effect of methane on cardiovascular system is obscure. The objective of the present study was to evaluate the hemodynamic response to methane. A vehicle or methane-rich saline were administered intravenously or intraperitoneally in normotensive anaesthetized rats. We have found no significant effect of the acute administration of methane-rich saline on arterial blood pressure and heart rate in anaesthetized rats. Our study suggests that methane does not influence the control of arterial blood pressure. However, further chronic studies may be needed to fully understand hemodynamic effects of the gas.

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