Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats

1982 ◽  
Vol 243 (4) ◽  
pp. H560-H565
Author(s):  
F. Charocopos ◽  
P. Hatzinikolaou ◽  
W. G. North ◽  
H. Gavras
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Blood Flows ◽  
Fluid Load ◽  
Regional Blood Flows ◽  
Blood Pressures ◽  
Specific Antagonist

We investigated the systemic and regional hemodynamic alterations induced in normotensive anephric rats by stimulation of endogenous vasopressin with an acute sodium and fluid load and following vasopressin inhibition with a specific antagonist of its vasoconstricting action. Blood pressure and total peripheral resistance were significantly higher and cardiac output was lower in rats with stimulated vasopressin, and all were reversed to near control levels in rats receiving the vasopressin inhibitor. Regional blood flows were diminished in most organs and local vascular resistance was elevated compared with control animals, but the magnitude of change varied widely. In fact, heart blood flow did not decrease significantly and brain blood flow actually increased indicating small or no change in vascular resistance of these organs. Moreover, fractional distribution of the diminished cardiac output to these organs was significantly higher, so that blood flow to vital organs was maintained at the expense of blood flow to other tissues. In rats that received the vasopressin antagonist after the saline infusion, regional blood flows were similar to those of control animals. Blood pressures at the base line and after hypertonic NaCl infusion correlated closely with the corresponding plasma levels of control and stimulated vasopressin.

Regional blood flows in salt loading hypertension in the dog

1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Salt Loading ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
Regional Blood Flows

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

Peripheral vascular resistance and regional blood flows in hypertensive Dahl rats

1991 ◽  
Vol 261 (4) ◽  
pp. R934-R938 ◽  
Author(s):  
M. A. Boegehold ◽  
L. J. Huffman ◽  
G. A. Hedge
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
High Salt ◽  
Renal Vasculature ◽  
Blood Flows ◽  
High Salt Intake ◽  
Regional Blood Flows

The aim of this study was to determine whether different organs undergo similar increases in vascular resistance with hypertension in the Dahl salt-sensitive rat. Cardiac output and organ blood flows were measured with microspheres in anesthetized salt-sensitive and salt-resistant rats fed a high- (7%) or normal- (0.45%) salt diet for 4 wk. High salt intake produced hypertension only in salt-sensitive rats. Cardiac index for the hypertensive group was not different from that for any other group, whereas peripheral resistance index was elevated in proportion to arterial pressure. There were no differences among groups in the fraction of cardiac output supplying the myocardium, intestine, diaphragm, spinotrapezius muscle, or gracilis muscle. The fraction of cardiac output supplying the kidneys was lower in salt-sensitive rats (13%) than in salt-resistant rats (17%) and, among salt-sensitive rats, lowest in the high-salt group. Therefore all the organs studied contribute to increased total peripheral resistance in the hypertensive Dahl rat, with the renal vasculature undergoing the largest resistance increase. Different muscles undergo similar increases in vascular resistance, despite differences in the microvascular abnormalities accompanying salt-induced hypertension.

Effects of haemorrhage and volume expansion on portal–systemic collateral vascular resistance in conscious portal hypertensive rats

1990 ◽  
Vol 78 (2) ◽  
pp. 193-197 ◽  
Author(s):  
Abraham Koshy ◽  
Tatsuya Sekiyama ◽  
Jean-Michel Cereda ◽  
Antoine Hadengue ◽  
Catherine Girod ◽  
...  
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Portal Pressure ◽  
Blood Flows ◽  
Regional Blood Flows

1. In order to study the acute effects of blood volume changes on the vascular resistance of portal-systemic collaterals (collateral vascular resistance), a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the rat. In this model, we determined the haemodynamic effects of haemorrhage (1.8 ml/100 g body weight) or intravenous infusion of a volume expander (1.8 ml/100 g body weight). Cardiac output and regional blood flows were measured by the radioactive microsphere method. 2. Haemorrhage significantly reduced arterial pressure from 108 ± 4 to 92 ± 4 mmHg (mean ± sem), cardiac output from 56 ± 4 to 24 ± 2 ml min−1 100 g−1 body weight, portal pressure from 15.1 ± 1.5 to 10.0 ± 1.4 mmHg and portal tributary blood flow from 19.9 ± 2.3 to 8.3 ± 1.4 ml/min. Consequently, collateral vascular resistance significantly increased from 6.6 ± 0.9 × 103 to 11.1 ± 2.0 × 103 kPal−1 s. 3. Volume expansion reduced arterial pressure from 98 ± 3 to 90 ± 3 mmHg, and significantly increased cardiac output from 43 ± 3 to 55 ± 3 ml min−1 100 g−1 body weight, portal pressure from 13.9 ± 0.7 to 16.5 ± 0.8 mmHg and portal tributary blood flow from 16.4 ± 1.3 to 28.2 ± 3.2 ml/min. Consequently, collateral vascular resistance significantly decreased from 7.0 ± 0. 5 × 103 to 4.9 ± 0.4 × 103 kPa l−1 s. 4. This study shows that in rats with portal hypertension, portal-systemic collateral vascular resistance is modified by alterations in blood volume.

Derecruitment of filtration surface area in paraquat-injured isolated dog lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1581-1589 ◽  
Author(s):  
T. Shibamoto ◽  
J. C. Parker ◽  
A. E. Taylor ◽  
M. I. Townsley
Keyword(s):  
Blood Flow ◽  
Surface Area ◽  
Vascular Resistance ◽  
High Flow ◽  
Base Line ◽  
Flow Rates ◽  
Blood Flows ◽  
Capillary Filtration Coefficient ◽  
Specific Index ◽  
Filtration Surface

The capillary filtration coefficient (Kf,c) is a sensitive and specific index of vascular permeability if surface area remains constant, but derecruitment might affect Kf,c in severely damaged lungs with high vascular resistance. We studied the effect of high and low blood flow rates on Kf,c in papaverine-pretreated blood-perfused isolated dog lungs perfused under zone 3 conditions with and without paraquat (PQ, 10(-2) M). Three Kf,cs were measured successively at hourly intervals for 5 h. These progressed sequentially from isogravimetric blood flow with low vascular pressure (I/L) to high flow with low vascular pressure (H/L) to high flow with high vascular pressure (H/H). The blood flows of H/L and H/H were greater than or equal to 1.5 times that of I/L. There were no significant changes in Kf,c in lungs without paraquat over a 50-fold range of blood flow rates. At 3 h after PQ, I/L-Kf,c was significantly increased and both isogravimetric capillary pressure and total protein reflection coefficient were decreased from base line. At 4 and 5 h, H/L-Kf,c was significantly greater than the corresponding I/L-Kf,c (1.01 +/- 0.22 vs. 0.69 +/- 0.09 and 1.26 +/- 0.19 vs. 0.79 +/- 0.10 ml.min-1.cmH2O-1.100 g-1, respectively) and isogravimetric blood flow decreased to 32.0 and 12.0% of base line, respectively. Pulmonary vascular resistance increased to 12 times base line at 5 h after PQ. We conclude that Kf,c is independent of blood flow in uninjured lungs. However, Kf,c measured at isogravimetric blood flow underestimated the degree of increase in Kf,c in severely damaged and edematous lungs because of a high vascular resistance and derecruitment of filtering surface area.

Responses of reproductive and nonreproductive tissues to 17 beta-estradiol during ovine puerperium

1980 ◽  
Vol 239 (5) ◽  
pp. E333-E339 ◽  
Author(s):  
C. R. Rosenfeld
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Mammary Gland ◽  
Thyroid Gland ◽  
Vascular Reactivity ◽  
Progressive Increase ◽  
Fallopian Tubes ◽  
Blood Flows ◽  
Flow Response ◽  
Regional Blood Flows

The responses of regional blood flows and cardiac output to the systemic infusion of 17 beta-estradiol (E2) (1 microgram/kg) were studied with radionuclide-labeled microspheres in 11 chronically instrumented ewes 1-12 days after lambing. Blood flow to the uterine myometrium, endometrium, and caruncles increased 818 +/- 212, 1,149 +/- 376, and 544 +/- 160% (mean +/- SE, P < 0.025), respectively, within 90 min after the infusion of E2. There was, however, in each of these tissues a progressive increase in the magnitude of the response to E2 stimulation as the puerperium progressed, not attaining changes expected in the prepregnant ewe until the 12th postpartum day. Significant vasodilation also occurred in the fallopian tubes, cervix, vagina, ovaries, mammary gland, skin, and thyroid gland. The magnitude of the blood flow response in the tubes, cervix, and vagina increased as the puerperium progressed. Cardiac output rose 17 +/- 10% (P < 0.05) after the infusion of E2. Although the ovine reproductive tissues are sensitive to estrogen-induced vasodilation throughout the puerperium, the magnitude of the responses progressively increase, suggesting that vascular reactivity in these tissues is changing and is not similar to that of the prepregnant animal.

Effects of hematocrit variations on regional hemodynamics and oxygen transport in the dog

1980 ◽  
Vol 238 (4) ◽  
pp. H545-H522 ◽  
Author(s):  
F. C. Fan ◽  
R. Y. Chen ◽  
G. B. Schuessler ◽  
S. Chien
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Vessels ◽  
Oxygen Transport ◽  
Oxygen Supply ◽  
Blood Flows ◽  
Regional Hemodynamics ◽  
Regional Blood Flows ◽  
Splenic Vessels ◽  
The Brain

The responses of alterations in regional hemodynamics and oxygen transport rate to hematocrit (Hct) were studied in 20 pentobarbitalized dogs. Hemodilution was carried out by isovolemic exchange with plasma in 12 dogs and the hemoconcentration with packed cells in 8 dogs. The cardiac output and regional blood flows were determined with the microsphere technique. In hemodilution, the increases of blood flow to the myocardium and the brain were out of proportion to the increase of cardiac output; the oxygen supply to the myocardium remained unchanged while that to the brain decreased only slightly. In hemoconcentration, vasodilation occurred in the myocardium and the brain to maintain constant oxygen supply. Splenic vessels had marked vasoconstriction with Hct alteration in either direction. Blood vessels in the liver, intestine, and kidney responded with a milder vasoconstriction and maintained a constant oxygen supply between Hct of 30-55%. Therefore, during Hct alteration, redistribution of blood flow to myocardium and brain occurred. The optimal Hct range for constant oxygen supply was different among various organs.

Regional Blood Flows in High-Cardiac-Output Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 355s-356s ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Initial Increase ◽  
Water Load ◽  
Blood Flows ◽  
Vascular Bed ◽  
Regional Blood Flows ◽  
Electromagnetic Flow Meter ◽  
Secondary Rise

1. Mean arterial pressure, cardiac output (electromagnetic flow-meter) and regional blood flows (15 μm radioactive microspheres) were measured repeatedly in eight dogs receiving a salt and water load after renal mass reduction as well as in six control animals. 2. As previously observed, hypertension developed in the salt-loaded dogs with an initial increase in cardiac output followed by a secondary rise in total peripheral resistance. 3. Much of the early increase in cardiac output was distributed to the skeletal muscle vascular bed. 4. Total peripheral resistance changes did not reflect the resistance of individual vascular beds in the early stages of salt and water load hypertension; indeed, resistance in the muscle vascular bed was decreased and that in the splanchnic area and the bone increased on the first day of salt and water load when total peripheral resistance was unchanged.

Fever and regional blood flows in wethers and parturient ewes

1988 ◽  
Vol 65 (1) ◽  
pp. 165-172 ◽  
Author(s):  
C. M. Blatteis ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
T. A. Mashburn
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Full Term ◽  
Blood Flows ◽  
Pregnant Sheep ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Placental Blood Flow

To determine whether the reported absence of fever in full-term-pregnant ewes might be associated with shifts of regional blood flows from thermogenic tissues to placenta during this critical period, fevers were induced twice by injections of Escherichia coli lipopolysaccharide (LPS, 0.25 microgram/kg iv) into each of six Merino ewes from 8 to 1 days prepartum, and their regional blood flow distribution was measured with radioactive, 15-microns-diam microspheres before and during the rise in fever (when their rectal temperature had risen approximately 0.4 degree C). Unexpectedly, fever always developed, rising to heights not significantly different at any time before parturition [4-8 days prepartum = 0.81 +/- 0.23 degree C (SE); 1-3 days prepartum = 0.75 +/- 0.17 degree C) and similar to those in three wethers treated similarly (0.90 +/- 0.10 degree C). Generally, during rising fever, blood flow in the ewes shifted away from heat loss tissues (e.g., skin, nose) to heat production tissues (e.g., shivering muscle, fat) and cardiac output increased; blood flow through redistribution organs (e.g., splanchnic bed) decreased. The reverse occurred during defervescence. Utero-placental blood flow remained high in the febrile ewes. These regional blood flow distributions during febrigenesis and lysis are essentially the same as those during exposures to ambient cold and heat, respectively. Some differences in the responses of cardiac output and its redistribution, however, were apparent between wethers and pregnant ewes. We conclude that 1) the previously reported "absence of fever in the full-term-pregnant sheep" should not be regarded as a general phenomenon and 2) full-term-pregnant sheep support fever production without sacrificing placental blood flow.

Effects of exercise, hypoxia and feeding on the gastrointestinal blood flow in the Atlantic cod Gadus morhua

1991 ◽  
Vol 158 (1) ◽  
pp. 181-198 ◽  
Author(s):  
M. Axelsson ◽  
R. Fritsche
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Control Mechanisms ◽  
Artery Blood Flow ◽  
Blood Flows ◽  
Mesenteric Artery Blood Flow

Cardiac output, ventral and dorsal aortic blood pressure, heart rate, and coeliac and mesenteric artery blood flow were recorded simultaneously in the Atlantic cod, Gadus morhua L., at rest, during exercise, during hypoxia and after feeding. In the resting unfed animals, coeliac artery blood flow was 4.1 +/− 0.8 ml min-1 kg-1 and mesenteric artery blood flow was 3.5 +/− 1.1 ml min-1 kg-1 (mean +/− S.E.M., N = 10); together, these flows represent approximately 40% of the cardiac output. Exercise or exposure to hypoxia resulted in increased visceral vascular resistance, leading to reductions in the coeliac and mesenteric artery blood flows. Coeliac and mesenteric blood flows were increased 24 h after feeding and the coeliac and systemic vascular resistances decreased in comparison with the prefeeding values. Phentolamine did not affect the gastrointestinal artery blood flow, but produced a significant decrease in the mesenteric and systemic vascular resistance. Treatment with bretylium and phentolamine revealed differences between the coeliac and the mesenteric vasculature regarding the control mechanisms during hypoxia and during exercise and feeding. During hypoxia, an adrenergic control of the gastrointestinal vasculature with both nervous and humoral components was found, whereas during exercise and after feeding an additional non-adrenergic mechanism controlling gut blood flow was demonstrated.

Angiotensin II: nitric oxide interaction and the distribution of blood flow

1993 ◽  
Vol 265 (6) ◽  
pp. R1276-R1283 ◽  
Author(s):  
D. H. Sigmon ◽  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Conscious Rats

Nitric oxide (NO) contributes to the regulation of regional blood flow. Inhibition of NO synthesis increases blood pressure and vascular resistance. Using radioactive microspheres and the substrate antagonist N omega-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg) to block NO synthesis, we tested the hypothesis that there is a significant interaction between the vasodilator NO and the vasoconstrictor angiotensin II, which regulates regional hemodynamics. Further, we investigated the influence of anesthesia on this interaction. L-NAME increased blood pressure, decreased cardiac output, and increased total peripheral resistance in both anesthetized and conscious rats. In anesthetized rats, L-NAME decreased blood flow to visceral organs (i.e. kidney, intestine, and lung) but had little effect on blood flow to the brain, heart, or hindlimb. Treating anesthetized rats with the angiotensin II receptor antagonist losartan (10 mg/kg) attenuated the decrease in cardiac output and the increase in total peripheral resistance without affecting the pressor response to L-NAME. Losartan also attenuated the visceral hemodynamic responses to L-NAME. In conscious rats, L-NAME decreased blood flow to all organ beds. Treating these rats with losartan only marginally attenuated the increase in total peripheral resistance to L-NAME without significantly affecting the pressor response or the decrease in cardiac output. Losartan had no effect on the regional hemodynamic responses to L-NAME. These data suggest that NO-mediated vascular relaxation is an important regulator of total peripheral and organ vascular resistance. (ABSTRACT TRUNCATED AT 250 WORDS)

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