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.

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.

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.

Distribution of blood flow during exercise after blood volume expansion in swine

1990 ◽  
Vol 69 (5) ◽  
pp. 1578-1586 ◽  
Author(s):  
K. I. Norton ◽  
M. D. Delp ◽  
M. T. Jones ◽  
C. Duan ◽  
D. R. Dengel ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Blood Volume ◽  
Volume Expansion ◽  
O2 Uptake ◽  
Miniature Swine ◽  
Blood Flows ◽  
Blood Volume Expansion

To study the distribution of blood flow after blood volume expansion, seven miniature swine ran at high speed (17.6-20 km/h, estimated to require 115% of maximal O2 uptake) on a motor-driven treadmill on two occasions: once during normovolemia and once after an acute 15% blood volume expansion (homologous whole blood). O2 uptake, cardiac output, heart rate, mean arterial pressure, and distribution of blood flow (with radiolabeled microspheres) were measured at the same time during each of the exercise bouts. Maximal heart rate was identical between conditions (mean 266); mean arterial pressure was elevated during the hypovolemic exercise (149 +/- 5 vs. 137 +/- 6 mmHg). Although cardiac output was higher and arterial O2 saturation was maintained during the hypervolemic condition (10.5 +/- 0.7 vs. 9.3 +/- 0.6 l/min), O2 uptake was not different (1.74 +/- 0.08 vs. 1.74 +/- 0.09 l/min). Mean blood flows to cardiac (+12.9%), locomotory (+9.8%), and respiratory (+7.5%) muscles were all elevated during hypervolemic exercise, while visceral and brain blood flows were unchanged. Calculated resistances to flow in skeletal and cardiac muscle were not different between conditions. Under the experimental conditions of this study, O2 uptake in the miniature swine was limited at the level of the muscles during hypervolemic exercise. The results also indicate that neither intrinsic contractile properties of the heart nor coronary blood flow limits myocardial performance during normovolemic exercise, because both the pumping capacity of the heart and the coronary blood flow were elevated in the hypervolemic condition.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

Circulation of sympathectomized dogs under pentobarbital anesthesia

1965 ◽  
Vol 208 (4) ◽  
pp. 790-794
Author(s):  
Shu Chien ◽  
Shunichi Usami
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Volume ◽  
Total Blood Volume ◽  
Central Blood Volume ◽  
Total Blood ◽  
Pentobarbital Anesthesia ◽  
Blood Flows ◽  
The Mean ◽  
Mean Circulation

In sympathectomized-splenectomized dogs under pentobarbital anesthesia, the total blood volume averaged 78 ml/kg, with 20% in the splanchnic circulation and 28% in the central blood volume. These values are almost the same as those found in the splenectomized (control) dogs with the sympathetic system intact. The over-all and the splanchnic Fcells factors are also not significantly different between these two groups. The sympathectomized animals had lower arterial pressure, cardiac output, and splanchnic blood flow, but the resistances calculated for the total and the splanchnic circulations were not significantly different from those of the control dogs. The mean circulation times for the total, the central, and the splanchnic circulations were all longer in the sympathectomized dogs. The data indicate that, under pentobarbital anesthesia, sympathectomized dogs are characterized by slower blood flows without any significant changes in either the blood volume or vascular resistance.

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.

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.

Splanchnic and systemic haemodynamic response to volume changes in patients with cirrhosis and portal hypertension

1999 ◽  
Vol 96 (5) ◽  
pp. 475-481 ◽  
Author(s):  
Panagiotis VLAVIANOS ◽  
Padraik MAC MATHUNA ◽  
Roger WILLIAMS ◽  
David WESTABY
Keyword(s):  
Cardiac Output ◽  
Portal Hypertension ◽  
Systemic Vascular Resistance ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Haemodynamic Response ◽  
Volume Depletion ◽  
Compensated Cirrhosis

We investigated the haemodynamic response to volume depletion and subsequent repletion in patients with cirrhosis and portal hypertension. Twelve patients with compensated cirrhosis and portal hypertension were included in the study. The haemodynamic changes occurring after removal of approx. 15% of the blood volume, and subsequently after isovolume repletion with colloid, were assessed. Baseline haemodynamic measurements showed increased cardiac output and a systemic vascular resistance at the lower limit of normal. The hepatic venous pressure gradient (HVPG) was increased, at 18 mmHg. After depletion, arterial pressure, cardiac output and all right-heart-sided pressures decreased, and systemic vascular resistance increased. HVPG decreased to 16.0 mmHg. All the above changes were statistically significant. After blood volume restitution, the haemodynamic values returned to baseline. In particular, an increase in HVPG was shown in four out of the twelve patients (two with ascites and two without), which was small in three of them. However, HVPG remained the same as or lower than the baseline in the other eight patients. Patients with cirrhosis and portal hypertension exhibit an abnormal haemodynamic response to blood volume depletion. After volume repletion, no increase in the portal pressure was noted in this group of patients as a whole, although four out of the twelve patients did show an increase, possibly due to extensive collateral circulation.

Studies of experimental cervical spinal cord transection

1980 ◽  
Vol 52 (2) ◽  
pp. 197-202 ◽  
Author(s):  
Phillip A. Tibbs ◽  
Byron Young ◽  
Edward P. Todd ◽  
R. G. McAllister ◽  
Steve Hubbard
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Cervical Cord ◽  
Regional Myocardial Blood Flow ◽  
Tissue Blood Flow ◽  
Coronary Vascular Resistance ◽  
Blood Flows

✓ Effects of cervical cord transection on total and regional myocardial blood flow and coronary vascular resistance were studied in anesthetized dogs using 15-µm microspheres. Left atrial catheters were inserted by thoracotomy in 10 dogs and iodine-125-labeled microspheres were injected to measure baseline tissue blood flows by means of the reference flow technique. Four dogs then underwent laminectomy of the C-6 vertebra (control group), and six underwent laminectomy and cord transection (experimental group). Microspheres labeled with cerium-141, strontium-85, and scandium-46 were injected at 15, 30, and 120 minutes, respectively, after surgical intervention. The dogs were sacrificed, and the radioisotope content of specimens of epicardial, mid-myocardial, and endocardial tissues was determined by differential spectrometry, and tissue blood flow was calculated in relation to arterial reference specimens. No significant differences in baseline endocardial, epicardial, or mid-myocardial blood flow were detected between the control and experimental groups. Tissue blood flows fell significantly in all regions (p < 0.05 or less) at 15, 30, and 120 minutes after transection. No major alteration of the endocardial/epicardial flow ratio occurred, and no electrocardiographic or pathological evidence of ischemia was seen. When corrected for variations in systemic arterial pressure, no differences in coronary vascular resistance between control and cord-transected dogs were observed. These findings suggest that the decreased coronary blood flow following cervical cord transection is secondary to decreased mean arterial pressure rather than to altered coronary vascular resistance. Pharmacological augmentation of perfusion pressure may therefore be necessary to maintain adequate coronary blood flow in patients with acute cord injury who have pre-existent cardiac disease.

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