Vascular responses to catecholamines during respiratory changes in pH

1961 ◽  
Vol 200 (4) ◽  
pp. 755-758 ◽  
Author(s):  
C. W. Nash ◽  
C. Heath
Keyword(s):  
Blood Pressure ◽  
Peripheral Resistance ◽  
Artery Blood Flow ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Vasomotor Tone ◽  
Vascular Responses ◽  
Blood Ph ◽  
Geometric Factors ◽  
Anesthetized Dogs

The influences of hypercapnia and hyperventilation on peripheral vascular responses to adrenaline and noradrenaline were observed in lightly anesthetized dogs. Changes in the carotid artery blood flow and pressure induced by intra-arterial doses of these amines were measured before, during and after the respiratory changes. During hypercapnia and low blood pH there was a reduced peripheral vascular response, while during hyperventilation and a high pH the vascular response to these drugs increased. However, a fall in blood pressure and flow, and a reflex elevation of the peripheral resistance occurred during both the hyperventilation and the posthypercapnic periods. It appeared that the elevated responses to the amines during those periods of high vasomotor tone may have been produced, in part at least, by the geometric factors involved in resistance, and not entirely by an increased response of the vascular smooth muscle.

Hemodynamics of hemorrhage in the conscious rat and chicken

1986 ◽  
Vol 251 (5) ◽  
pp. R846-R850 ◽  
Author(s):  
J. M. Ploucha ◽  
G. D. Fink
Keyword(s):  
Vascular Tone ◽  
Peripheral Resistance ◽  
Fluid Loss ◽  
Pulsed Doppler ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Conscious Rat ◽  
Vascular Responses ◽  
Anesthetic Agents ◽  
On Line

Hemodynamic responses to hemorrhage in conscious chicks (n = 10, 233 g) and rats (n = 10, 309 g) were compared. The animals were fitted with miniature pulsed Doppler aortic flow probes 2 days (chickens) or 5 days (rats) before catheterization, and the experiment began 1 (chickens) or 2 (rats) days later. Mean arterial pressure (MAP) and cardiac output (CO) were recorded continuously and simultaneously digitized to compute total peripheral resistance (TPR). MAP, CO, and TPR values were graphed on-line by a microcomputer and stored for later analysis. A 4-ml hemorrhage reduced MAP and CO by 25 and 43% in the rat, and 15 and 4% in the chickens, respectively. The fall in CO in the rat was due to reduction of stroke volume (SV) unlike the birds where SV was well maintained. TPR was elevated 65% in the rats and fell 13% in the chickens. The minimal fall in CO and SV in these conscious birds suggests that anesthetic agents used previously (i.e., urethane, paraldehyde, phenobarbital, and pentobarbital sodium) suppressed cardiac function. However, they do not account for the lack of a peripheral vascular response during hemorrhage. The chicken apparently maintains MAP by a volume regulating mechanism operating independently of peripheral vascular tone inasmuch as circulating fluid volume restitution is rapid and occurs without vasoconstriction. The rat maintains MAP through reflex cardiac and peripheral vascular responses which eventually may contribute to transvascular fluid loss and the ultimate collapse after prolonged hemorrhagic hypotension.

Peripheral vascular responses during acute anemia

1981 ◽  
Vol 59 (2) ◽  
pp. 102-107 ◽  
Author(s):  
C. K. Chapler ◽  
W. N. Stainsby ◽  
M. A. Lillie
Keyword(s):  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Vascular ◽  
Vasomotor Tone ◽  
Vascular Responses ◽  
Acute Anemia ◽  
Blood Exchange ◽  
Anesthetized Dogs ◽  
Pressure Changes ◽  
Arteries And Veins

Peripheral vascular responses during acute anemia were studied in 19 anesthetized dogs. In one study (n = 9) hindlimb weight and venous pressures were measured prior to and during acute anemia produced by isovolemic dextran-for-blood exchange. In another series of five control and five anemic dogs (hematocrit = 14 ± 1% (mean ± SE)), flow to the limb was occluded and arterial and venous pressure changes in the occluded limb were measured as an index of neurally mediated alterations in limb vasomotor tone. Following reduction of the hematocrit to 14 ± 0.3%, hindlimb weight decreased by an average of 10.0 g (P < 0.01) at 15 min and 12.8 g (P < 0.01) at 30 min of anemia. The decrease in limb weight was associated with a rise (P < 0.01) in limb venous pressure. There was also a relatively greater degree of vasomotor tone in the occluded hindlimb of anemic dogs as compared with control animals. Although both arterial and venous pressures decreased in an occluded hindlimb following the production of anemia, the decreases in vascular pressures were significantly less than those observed in control experiments. It was not possible to distinguish between tone changes in arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone.

Peripheral vascular responses to hyperthermia in the rat

1988 ◽  
Vol 64 (6) ◽  
pp. 2582-2588 ◽  
Author(s):  
K. C. Kregel ◽  
P. T. Wall ◽  
C. V. Gisolfi
Keyword(s):  
Elevated Level ◽  
Heat Stroke ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Sharp Decline ◽  
Vascular Responses ◽  
Doppler Flow ◽  
Arterial Blood ◽  
Unanesthetized Animals ◽  
Skin Temperatures

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70–150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10–15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.

scholarly journals Diets Containing Pistachios Reduce Systolic Blood Pressure and Peripheral Vascular Responses to Stress in Adults With Dyslipidemia

Hypertension ◽  
2012 ◽  
Vol 60 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Sheila G. West ◽  
Sarah K. Gebauer ◽  
Colin D. Kay ◽  
Deborah M. Bagshaw ◽  
David M. Savastano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Peripheral Vascular ◽  
Vascular Responses

scholarly journals Renal Vascular Response to Angiotensin II Administration in Two Kidneys-One Clip Hypertensive Rats Treated with High Dose of Estradiol: The Role of Mas Receptor

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Samira Choopani ◽  
Mehdi Nematbakhsh
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Ovariectomized Rats ◽  
Ang Ii ◽  
Vascular Response ◽  
Hypertensive Rats ◽  
Vascular Responses ◽  
Mas Receptor ◽  
Renal Vascular

Backgrounds. High blood pressure is one of the most important causes of death around the world. The renin-angiotensin system (RAS) and estradiol are two important items that regulate arterial blood pressure in women. However, hypertension, RAS, and sex hormone estradiol may influence renal vascular responses. This study was designed to determine the role of Mas receptor (MasR) on renal vascular response to angiotensin II (Ang II) administration in two kidneys-one clip (2K1C) hypertensive rats treated with estradiol. Method. The ovariectomized rats were subjected to 2K1C or non-2K1C and simultaneously treated with estradiol (500 μg/kg/weekly) or placebo for a period of 4 weeks. Subsequently, under anesthesia, renal vascular responses to graded doses of Ang II administration with MasR blockade (A779) or its vehicle were determined. Results. A779 or its vehicle did not alter mean arterial pressure (MAP), renal perfusion pressure (RPP), and renal blood flow (RBF). However, in non-2K1C rats, Ang II infusion decreased RBF and increased renal vascular resistance (RVR) responses in a dose-related manner ( P treat < 0.0001 ). The greatest responses were found in ovariectomized estradiol-treated rats that received A779 ( P group < 0.05 ) in non-2K1C rats. Such findings were not detected in 2K1C hypertensive rats. For example, in estradiol-treated rats that received A779, at 1000 ng/kg/min of Ang II infusion, RBF reduced from 1.6 ± 0.2 to 0.89 ± 0.19  ml/min in non-2K1C rats, and it reduced from 1.6 ± 0.2 to 1.2 ± 0.2  ml/min in 2K1C rats. Conclusion. Hypertension induced by 2K1C may attenuate the role of A779 and estradiol in renal vascular responses to Ang II infusion. Perhaps, this response can be explained by the reduction of Ang II type 1 receptor (AT1R) expression in the 2K1C hypertensive rats.

α-Adrenoceptor blockade and class III antiarrhythmic activity combined: hemodynamic and electrophysiological effects of melperone in the dog

1986 ◽  
Vol 64 (10) ◽  
pp. 1286-1290
Author(s):  
Eivind S. Platou ◽  
Eivind S. P. Myhre ◽  
Helge Refsum
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Peripheral Resistance ◽  
Antiarrhythmic Activity ◽  
Left Ventricular ◽  
Antiarrhythmic Action ◽  
Conduction Time ◽  
Class Iii ◽  
Anesthetized Dogs ◽  
Electrophysiological Effects

Melperone has been found to possess vasodilating and slight positive inotropic properties in addition to its class III antiarrhythmic action. To determine whether some of these effects might be related to an α-adrenoceptor blocking action of melperone, phenoxybenzamine (10 mg/kg) was given as a 2-h infusion to 12 pentobarbital-anesthetized dogs. In addition, six of the dogs were given atenolol 0.5 mg/kg i.v. After a 1-h stabilizing period, melperone (0.5,2.5, and 12.5 mg/kg) was given i. v. in cumulative doses to both series of dogs. In the presence of α-blockade as well as combined α- and β-blockade, atrial, atrioventricular (AV) nodal, and ventricular refractoriness increased and heart rate and AV nodal conduction time decreased, as previously reported after addition of melperone alone. A slight increase in left ventricular (dP/dt)max occurred after the addition of melperone (2.5 mg/kg) in the presence of α- and β-blockade, but only after the highest dose of melperone were small decreases in blood pressure and total peripheral resistance induced. The present study indicates that melperone combines the properties of class III antiarrhythmic action, slight positive inotropy, and α-adrenoceptor mediated vasodilation.

Effect of a left atrium-pulmonary vein baroreflex on peripheral vascular beds

1977 ◽  
Vol 233 (5) ◽  
pp. H587-H591 ◽  
Author(s):  
T. C. Lloyd ◽  
J. J. Fried
Keyword(s):  
Left Atrial ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Radioactive Microspheres ◽  
Peripheral Vascular ◽  
Blood Flows ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Response Peak ◽  
Vascular Beds

A step increase of left atrial and pulmonary venous pressure from 0 to 25 mmHg was used in anesthetized dogs with controlled arterial blood pressure to generate reflex systemic vasodilation. The resultant response of total peripheral resistance was an initial transient fall of about 40% which spontaneously regressed while the stimulus was maintained. Injections of differently tagged radioactive microspheres were used to measure selected organ blood flows prior to raising atrial pressure, at the response peak, during the steady state, and after recovery. Resistances of skin, skeletal muscle, kidney, and large intestine significantly fell upon atriovenous distention. The response in muscle, which greatly exceeded that of the other organs, was not sustained, whereas resistances of other responding beds remained depressed until the stimulus was removed. No significant responses occurred in small intestine, liver (hepatic artery), or adrenal gland.

Plasma norepinephrine variations correlate with peripheral vascular resistance in resting humans

1994 ◽  
Vol 266 (2) ◽  
pp. H435-H439 ◽  
Author(s):  
B. Kennedy ◽  
D. Shannahoff-Khalsa ◽  
M. G. Ziegler
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Inverse Relationship ◽  
Nervous Activity ◽  
Peripheral Resistance ◽  
Sympathetic Nervous Activity ◽  
Plasma Norepinephrine ◽  
Peripheral Vascular ◽  
Sympathetic Nervous

Plasma levels of norepinephrine (NE) vary rhythmically in humans and animals with an ultradian (shorter than 1 day) periodicity. We repeatedly measured plasma NE levels, blood pressure, cardiac output, and total peripheral resistance in nine normal resting subjects over 5 h. Plasma NE correlated with total peripheral resistance (Z = 0.322, P < 0.0002) and inversely with cardiac output (Z = -0.276, P < 0.0002) for the nine subjects overall. The correlations were strongest in subjects with the most spontaneous variability in total peripheral resistance. These findings suggest that spontaneous oscillations in plasma NE levels reflect alterations in sympathetic nervous activity to resistance blood vessels. The negative correlation between cardiac output and plasma NE levels may result from the very minor cardiac NE spillover into plasma and the inverse relationship between cardiac output and total peripheral resistance.

Role of Haemodynamics, Catecholamines and Renin in Acute Hypercalcaemic Hypertension in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 369s-371s ◽  
Author(s):  
C. Marone ◽  
C. Beretta-Piccoli ◽  
P. Weidmann
Keyword(s):  
Blood Pressure ◽  
Plasma Volume ◽  
Plasma Catecholamines ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Peripheral Vascular ◽  
Plasma Adrenaline ◽  
Adrenaline Release ◽  
Calcium Infusion

1. The effect of acute hypercalcaemia on blood pressure, blood volume, haemodynamic indices, plasma catecholamines, renin and aldosterone levels was investigated in 10 patients. 2. Calcium infusion (15 mg/kg over 3 h) increased (P&lt;0.05) plasma calcium and adrenaline levels, blood pressure, total peripheral resistance and packed cell volume. Plasma volume was decreased, and heart rate, cardiac output and plasma renin, aldosterone or dopamine levels were not significantly changed. Plasma noradrenaline was increased only minimally after 3 h of calcium infusion. 3. Mean blood pressure before and during calcium infusion correlated with concomitant serum calcium (r = 0.39; P&lt;0.02) or adrenaline levels (r = 0.57; P&lt;0.01); changes in blood pressure correlated with variations in plasma adrenaline (r = 0.68; P&lt;0.001). 4. Acute hypercalcaemic hypertension is mediated by an increase in peripheral vascular resistance and may be induced by a direct effect of calcium on blood vessels. The calcium-mediated increase in adrenaline release may play a contributory, and plasma volume contraction an inhibitory, role.

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