AN EFFECT OF REDUCED BAROMETRIC PRESSURE ON THE PERIPHERAL CIRCULATION

1957 ◽  
Vol 35 (10) ◽  
pp. 777-783
Author(s):  
F. Girling ◽  
F. A. Sunahara
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Barometric Pressure ◽  
Peripheral Circulation ◽  
Arterial Oxygen ◽  
Blood Flows ◽  
The Past

Several groups of investigators have noted in the past that exposure to a reduced barometric pressure results in a decrease in peripheral blood flow.In the present study human subjects were exposed to a pressure of 225 mm. Hg with maintenace of arterial oxygen saturation, and forearm and hand blood flows were measured plethysmographically. Forearm blood flow was not affected by the exposure whereas hand blood flow was reduced in all subjects. Blood pressure and heart rate were also measured and showed no change during the experiment.

AN EFFECT OF REDUCED BAROMETRIC PRESSURE ON THE PERIPHERAL CIRCULATION

1957 ◽  
Vol 35 (1) ◽  
pp. 777-783
Author(s):  
F. Girling ◽  
F. A. Sunahara
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Barometric Pressure ◽  
Peripheral Circulation ◽  
Arterial Oxygen ◽  
Blood Flows ◽  
The Past

Several groups of investigators have noted in the past that exposure to a reduced barometric pressure results in a decrease in peripheral blood flow.In the present study human subjects were exposed to a pressure of 225 mm. Hg with maintenace of arterial oxygen saturation, and forearm and hand blood flows were measured plethysmographically. Forearm blood flow was not affected by the exposure whereas hand blood flow was reduced in all subjects. Blood pressure and heart rate were also measured and showed no change during the experiment.

scholarly journals Testing individual baroreflex responses to hypoxia-induced peripheral chemoreflex stimulation

2020 ◽  
Vol 30 (6) ◽  
pp. 531-540
Author(s):  
Hendrik Kronsbein ◽  
Darius A. Gerlach ◽  
Karsten Heusser ◽  
Alex Hoff ◽  
Fabian Hoffmann ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Recovery Period ◽  
Arterial Oxygen ◽  
Heart Rate Regulation ◽  
Peripheral Chemoreflex ◽  
Collective Influence

Abstract Introduction Baroreflexes and peripheral chemoreflexes control efferent autonomic activity making these reflexes treatment targets for arterial hypertension. The literature on their interaction is controversial, with suggestions that their individual and collective influence on blood pressure and heart rate regulation is variable. Therefore, we applied a study design that allows the elucidation of individual baroreflex–chemoreflex interactions. Methods We studied nine healthy young men who breathed either normal air (normoxia) or an air–nitrogen–carbon dioxide mixture with decreased oxygen content (hypoxia) for 90 min, with randomization to condition, followed by a 30-min recovery period and then exposure to the other condition for 90 min. Multiple intravenous phenylephrine bolus doses were applied per condition to determine phenylephrine pressor sensitivity as an estimate of baroreflex blood pressure buffering and cardiovagal baroreflex sensitivity (BRS). Results Hypoxia reduced arterial oxygen saturation from 98.1 ± 0.4 to 81.0 ± 0.4% (p < 0.001), raised heart rate from 62.9 ± 2.1 to 76.0 ± 3.6 bpm (p < 0.001), but did not change systolic blood pressure (p = 0.182). Of the nine subjects, six had significantly lower BRS in hypoxia (p < 0.05), two showed a significantly decreased pressor response, and three showed a significantly increased pressor response to phenylephrine in hypoxia, likely through reduced baroreflex buffering (p < 0.05). On average, hypoxia decreased BRS by 6.4 ± 0.9 ms/mmHg (19.9 ± 2.0 vs. 14.12 ± 1.6 ms/mmHg; p < 0.001) but did not change the phenylephrine pressor response (p = 0.878). Conclusion We applied an approach to assess individual baroreflex–chemoreflex interactions in human subjects. A subgroup exhibited significant impairments in baroreflex blood pressure buffering and BRS with peripheral chemoreflex activation. The methodology may have utility in elucidating individual pathophysiology and in targeting treatments modulating baroreflex or chemoreflex function.

General and regional circulatory effects of synthetic eledoisin in man

1964 ◽  
Vol 19 (1) ◽  
pp. 113-116 ◽  
Author(s):  
Hermes A. Kontos ◽  
William Shapiro ◽  
H. Page Mauck ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Normal Subjects ◽  
Average Increase ◽  
Pronounced Increase ◽  
Blood Flows ◽  
Circulatory Effects ◽  
Arterial Blood ◽  
Flow Effects

The circulatory effects of intravenous infusions of synthetic eledoisin were studied in nine normal subjects. Infusions of 0.6 μg/min of eledoisin in eight experiments on eight subjects produced a transient fall in mean arterial blood pressure, tachycardia (average 14.3 beats/min), marked increase in cardiac index (average 3.4 liters/min m2), increase in stroke volume (average 58.3 ml/beat) and fall in systemic vascular resistance (average 6 mm Hg/liter min). Blood flow to hand and forearm increased (average increase in four experiments on four subjects 7.9 and 2.9 ml/min 100 ml tissue, respectively). More marked hypotension and tachycardia and a more pronounced increase in hand and forearm blood flows were observed during infusions of 2–5 μg/min of eledoisin in four experiments on four subjects. These results indicate that eledoisin is a powerful dilator of vessels in skin and skeletal muscle, and quite probably of vessels in other vascular areas. vasodilatation; effects on cardiac output; effects on hand blood flow; effects on forearm blood flow; hypotensive agent Submitted on July 1, 1963

scholarly journals Cardiovascular adjustments to acute hypoxemia superimposed on chronic hypoxemia in lambs

1995 ◽  
Vol 268 (3) ◽  
pp. H974-H979
Author(s):  
M. Dalinghaus ◽  
J. W. Gratama ◽  
W. G. Zijlstra ◽  
J. R. Kuipers
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Supply ◽  
Pulmonary Stenosis ◽  
Arterial Oxygen Saturation ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Blood Flows ◽  
Regional Blood Flows ◽  
Chronic Hypoxemia

Cardiovascular responses to acute hypoxemia are in part mediated through adrenergic and chemoreceptor stimulation. In chronic hypoxemia the response to these stimuli may be blunted. Therefore, we determined whether the cardiovascular responses to acute hypoxemia superimposed on 3–4 wk of chronic hypoxemia were blunted in lambs with an experimental cardiac right-to-left shunt (combination of atrial septal defect and variable pulmonary stenosis). Cardiovascular variables and regional blood flows were determined during chronic hypoxemia and after acutely reducing the arterial oxygen saturation by increasing the cardiac right-to-left shunt. Arterial oxygen saturation decreased (65 +/- 7 to 40 +/- 7%, P < 0.001) and systemic blood flow increased (164 +/- 63 to 233 +/- 100 ml.min-1.kg-1, P < 0.01), maintaining systemic oxygen supply and oxygen uptake. Blood flow to the myocardium (P < 0.01), the adrenals (P < 0.05), and the brain (0.05 < P < 0.10) increased, and oxygen supply to these organs was maintained. Conversely, blood flow to the kidneys and the gastrointestinal tract was unaltered, so that oxygen supply to these organs was decreased. The responses to acute hypoxemia in chronically hypoxemic lambs were similar to those previously reported in normoxemic lambs. We conclude that the cardiovascular responses to acute hypoxemia in chronically hypoxemic lambs are not blunted.

COMPARISON OF ANTIHYPERTENSIVE EFFECT OF MOXONIDINE VERSUS CLONIDINE IN RENAL FAILURE PATIENTS.

2018 ◽  
Vol 6 (9) ◽  
Author(s):  
DR.MATHEW GEORGE ◽  
DR.LINCY JOSEPH ◽  
MRS.DEEPTHI MATHEW ◽  
ALISHA MARIA SHAJI ◽  
BIJI JOSEPH ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Blood Flow ◽  
Blood Vessel ◽  
Blood Vessels ◽  
High Blood Pressure ◽  
Antihypertensive Effect ◽  
The Body ◽  
Ability To Work ◽  
Blood Flows

Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. Factors that can increase this force include higher blood volume due to extra fluid in the blood and blood vessels that are narrow, stiff, or clogged(1). High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.

scholarly journals BIOCHEMICAL STUDIES ON SHOCK

1944 ◽  
Vol 79 (1) ◽  
pp. 9-22 ◽  
Author(s):  
Frank L. Engel ◽  
Helen C. Harrison ◽  
C. N. H. Long
Keyword(s):  
Blood Pressure ◽  
Amino Acids ◽  
Oxygen Saturation ◽  
Hepatic Artery ◽  
Arterial Oxygen Saturation ◽  
Amino Nitrogen ◽  
Arterial Oxygen ◽  
High Positive Correlation ◽  
Peripheral Tissues ◽  
Arterial Blood

1. In a series of rats subjected to hemorrhage and shock a high negative correlation was found between the portal and peripheral venous oxygen saturations and the arterial blood pressure on the one hand, and the blood amino nitrogen levels on the other, and a high positive correlation between the portal and the peripheral oxygen saturations and between each of these and the blood pressure. 2. In five cats subjected to hemorrhage and shock the rise in plasma amino nitrogen and the fall in peripheral and portal venous oxygen saturations were confirmed. Further it was shown that the hepatic vein oxygen saturation falls early in shock while the arterial oxygen saturation showed no alteration except terminally, when it may fall also. 3. Ligation of the hepatic artery in rats did not affect the liver's ability to deaminate amino acids. Hemorrhage in a series of hepatic artery ligated rats did not produce any greater rise in the blood amino nitrogen than a similar hemorrhage in normal rats. The hepatic artery probably cannot compensate to any degree for the decrease in portal blood flow in shock. 4. An operation was devised whereby the viscera and portal circulation of the rat were eliminated and the liver maintained only on its arterial circulation. The ability of such a liver to metabolize amino acids was found to be less than either the normal or the hepatic artery ligated liver and to have very little reserve. 5. On complete occlusion of the circulation to the rat liver this organ was found to resist anoxia up to 45 minutes. With further anoxia irreversible damage to this organ's ability to handle amino acids occurred. 6. It is concluded that the blood amino nitrogen rise during shock results from an increased breakdown of protein in the peripheral tissues, the products of which accumulate either because they do not circulate through the liver at a sufficiently rapid rate or because with continued anoxia intrinsic damage may occur to the hepatic parenchyma so that it cannot dispose of amino acids.

The physiology of extracorporeal membrane oxygenation: The Fick principle

Perfusion ◽  
2021 ◽  
pp. 026765912110559
Author(s):  
Hoong Lim
Keyword(s):  
Blood Flow ◽  
Extracorporeal Membrane Oxygenation ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Fick Principle ◽  
Membrane Oxygenation ◽  
Lung Failure ◽  
Va Ecmo ◽  
The Relationship ◽  
Vv Ecmo

Extracorporeal membrane oxygenation (ECMO) can be delivered in veno-arterial (VA) and veno-venous (VV) configurations based on the cannulation strategy. VA and VV ECMO are delivered primarily for haemodynamic and respiratory support in patients with severe heart and lung failure, respectively. The Fick principle describes the relationship between blood flow and oxygen consumption – key parameters in the physiological management of extracorporeal support. This review will discuss the application of the Fick principle in: (i) recirculation in VV ECMO; (ii) the quantification of oxygen delivery (DO2) in VV ECMO and (iii) the quantification of transpulmonary blood flow and systemic arterial oxygen saturation in VA ECMO.

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

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