Effect of increased intraabdominal pressure on cardiac output and tissue blood flow assessed by color-labeled microspheres in the pig

2001 ◽  
Vol 15 (2) ◽  
pp. 149-155 ◽  
Author(s):  
Y. Yavuz ◽  
K. Rønning ◽  
O. Lyng ◽  
R. Mårvik ◽  
J. E. Grønbech
1985 ◽  
Vol 248 (1) ◽  
pp. H98-H108
Author(s):  
D. G. van Wylen ◽  
L. G. D'Alecy

Regional blood flow distribution (microspheres) and cardiac output (CO, thermal dilution) were measured during the Cushing response in unblocked (UB), beta-receptor-blocked (BB, 2 mg/kg propranolol iv), or alpha-receptor blocked (AB, 0.5 mg/kg + 0.5 mg X kg-1 X min-1 phentolamine iv) chloralose-anesthetized dogs. Intracranial pressure was increased to 150 mmHg by infusion of temperature-controlled artificial cerebrospinal fluid into the cisterna magna. Similar increases in mean arterial pressure were seen in UB and BB, but in AB a Cushing response could not be sustained. In UB, cerebral blood flow (CBF) decreased 50%, coronary blood flow (CoBF) increased 120%, and peripheral tissue blood flow was reduced only in the kidneys (18%) and the intestines (small 22%, large 35%). Blood flow to the other viscera, skin, and skeletal muscle was unchanged. CO (16%) and heart rate (HR, 38%) decreased, and total peripheral resistance (TPR, 68%) and stroke volume (SV, 38%) increased. In BB, CBF decreased 50%, CoBF decreased 20%, and blood flow was reduced 40-80% in all peripheral tissues. CO (69%) and HR (62%) decreased, TPR increased 366%, and SV was unchanged. We conclude that the Cushing response in UB animals combines an alpha-receptor-mediated vasoconstriction with a beta-receptor cardiac stimulation. The beta-mechanism is neither necessary nor sufficient for the hypertension. However, the combination of alpha- and beta-adrenergic mechanisms maintains cardiac output and peripheral tissue blood flow relatively constant while producing a systemic hypertension.


1986 ◽  
Vol 64 (9) ◽  
pp. 1252-1258 ◽  
Author(s):  
Stephanie W. Y. Ma ◽  
David O. Foster

Starvation results in an energy-conserving reduction in metabolic rate that has features of an adaptive response. Tissue and organ sites of this response were investigated by examining the effects of starvation for 5 d on tissue blood flow (microsphere method) and regional arteriovenous O2 differences [Formula: see text] in conscious rats resting quietly at 28 °C. Comparison was with fed and overnight-fasted animals. Whole body resting metabolic rates (MR), colonic temperatures (Tc), and tissue weights were also determined. Quantitative changes in energy expenditure (as O2 consumption) were obtained for two regions: the portal-drained viscera (PDV) and the hindquarters (HQ). Fasting overnight resulted in increased blood flow to white adipose tissue (WAT) and decreased flow to the brain, PDV, testes, and skin; however, MR, Tc, the two regional [Formula: see text], and the weights of most tissues were not significantly altered. In comparison with overnight fasting, starvation for 5 d resulted in a 13% reduction in body weight, weight loss in many tissues and organs, a 26% reduction in MR, a decline of 0.5 °C in Tc, decreased [Formula: see text] across both the PDV and HQ, reduced cardiac output, and decreased blood flow to the heart, PDV, skin, WAT, leg muscle, HQ, and the musculoskeletal body as a whole. Utilization of O2 by the PDV and HQ [Formula: see text] declined by amounts that accounted for 22 and 18%, respectively, of the reduction in MR. The reductions in cardiac output (18%) and heart blood flow (36%) indicate that the heart also made a contribution to energy conservation (roughly estimated as 5%). Overall, the data suggest that gut and muscle together accounted for two-thirds to three-quarters of the starvation-induced energy conservation.


1985 ◽  
Vol 58 (4) ◽  
pp. 1225-1230 ◽  
Author(s):  
S. Gelman ◽  
K. C. Fowler ◽  
S. P. Bishop ◽  
L. R. Smith

Cardiac output distribution and regional blood flow were studied during hypocarbia independent of changes in ventilatory parameters. Fifteen cynomolgus monkeys were anesthetized with methohexital sodium (8 mg/kg im) and hyperventilated through an endotracheal tube. Hypocarbia at two levels, 28 +/- 1.8 and 17 +/- 0.6 Torr, was achieved by a stepwise decreasing CO2 flow into the semiclosed system. Regional blood flow was determined with labeled microspheres. At each stage of experiments two sets of microspheres (9 and 15 microns diam) were used simultaneously. The use of two microsphere sizes allowed evaluation of the relationship between total (nutritive and nonnutritive) tissue blood flow, determined with 15-microns spheres, and nutritive blood flow, determined with 9-microns spheres. There was no change in cardiac output or arterial pressure during both degrees of studied hypocarbia. Hypocarbia was accompanied by a decrease in myocardial blood flow determined with 15-microns spheres and preservation of the flow determined with 9-microns spheres. Splenic blood flow was decreased, whereas hepatic arterial blood flow was increased during both levels of hypocarbia. Blood flow through the brain, renal cortex, and gut showed a biphasic response to hypocarbia: during hypocarbia at 28 +/- 1.8 Torr, blood flow determined with 15-microns spheres was unchanged (in the gut) or decreased (in the brain and kidneys), whereas blood flow determined with 9-microns spheres was decreased. During hypocarbia at 17 +/- 0.6 Torr, blood flow determined with 9-microns spheres had a tendency to restore to base-line values.


1979 ◽  
Vol 57 (5) ◽  
pp. 995-1002 ◽  
Author(s):  
David R. Jones ◽  
Robert M. Bryan Jr. ◽  
Nigel H. West ◽  
Raymond H. Lord ◽  
Brenda Clark

The regional distribution of blood flow, both before and during forced diving, was studied in the duck using radioactively labelled microspheres. Cardiac output fell from 227 ± 30 to 95 ± 16 mL kg−1 min−1 after 20–72 s of submergence and to 59 ± 18 mL kg−1 min−1 after 144–250 s of submergence. Mean arterial blood pressure did not change significantly as total peripheral resistance increased by four times during prolonged diving. Before diving the highest proportion of cardiac output went to the heart (2.6 ± 0.5%, n = 9) and kidneys (2.7 ± 0.5%, n = 9), with the brain receiving less than 1%. The share of cardiac output going to the brain and heart increased spectacularly during prolonged dives to 10.5 ± 3% (n = 5) and 15.9 ± 3.8% (n = 5), respectively, while that to the kidney fell to 0.4 ± 0.26% (n = 3). Since cardiac output declined during diving, tissue blood flow (millilitres per gram per minute) to the heart was unchanged although in the case of the brain it increased 2.35 times after 20–75 s of submergence and 8.5 times after 140–250 s of submergence. Spleen blood flow, the highest of any tissue predive (5.6 ± 1.3 mL g−1 min−1, n = 4), was insignificant during diving while adrenal flow increased markedly, in one animal reaching 7.09 mL g−1 min−1. The present results amplify general conclusions from previous research on regional distribution of blood flow in diving homeotherms, showing that, although both heart and brain receive a significant increase in the proportionate share of cardiac output during diving only the brain receives a significant increase in tissue blood flow, which increases as submergence is prolonged.


1978 ◽  
Vol 55 (3) ◽  
pp. 317-320 ◽  
Author(s):  
C. R. Hiley ◽  
M. S. Yates

1. Radioactive 15 μm and 50 μm diameter microspheres were used to determine cardiac output, its regional distribution and tissue blood flow in adult normotensive Wistar and Okamoto spontaneously hypertensive rats. 2. Cardiac output in the spontaneously hypertensive rats was the same as in Wistar normotensive rats, but its distribution in the hypertensive rats appeared to differ: there was a significant increase in the proportion of microspheres trapped in the liver whereas fewer were found in the gastrointestinal tract. This indicates that a greater fraction of the cardiac output passes along the hepatic artery and less through the splanchnic bed. 3. Blood flow in skin and skeletal muscle in spontaneously hypertensive rats was approximately 50% of that in Wistar normotensive rats.


1984 ◽  
Vol 246 (3) ◽  
pp. R331-R337 ◽  
Author(s):  
C. H. Lang ◽  
G. J. Bagby ◽  
J. L. Ferguson ◽  
J. J. Spitzer

Cardiac output (CO) and the distribution of blood flow were studied in chronically catheterized conscious rats during sustained (4 days) sepsis. Septicemia was induced by intraperitoneal administration of a pooled fecal inoculum, and tissue blood flow and CO were determined daily with 15-micron radioactive microspheres. Mean arterial blood pressure (MABP, 113 +/- 2 mmHg), CO (244.5 +/- 11.4 ml X min-1 X kg-1), and total peripheral resistance (TPR, 1.36 +/- 0.07 mmHg X ml-1 X min) were stable in control rats over the 4 days postinoculation. Septic animals showed a consistent tachycardia with MABP significantly reduced only on days 3 and 4 (86 +/- 4 mmHg). A hyperdynamic response to sepsis was indicated by an elevated CO (27%) and similarly reduced TPR on day 2. The calculated stroke volume averaged 0.22 +/- 0.01 ml/beat and did not vary over time or between the two groups. There was a 40-70% increase in blood flow to the heart, spleen, adrenal glands, and small intestine, and a greater than sixfold increase in hepatic arterial blood flow. The sustained elevation of coronary blood flow, observed in septic animals, was independent of myocardial work and is consistent with impaired myocardial function. Pancreas, stomach, and skeletal muscle blood flow was consistently compromised (24, 39, and 52%, respectively) during sepsis. Blood flow in other organs remained unchanged over time. Sepsis-induced changes in the fractional distribution of blood flow to various organs were similar to those described for absolute flow. (ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 79 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Anders Edlund ◽  
Alf Sollevi ◽  
Birgitta Linde

1. Haemodynamic and metabolic effects of intravenous infusion of adenosine, an endogenous vasodilator, were studied in healthy humans. 2. Catheters were inserted into pulmonary and brachial arteries and into the hepatic and subclavian veins. Cardiac output was determined according to the Fick principle, and splanchnic blood flow was measured by using extraction of Indocyanine Green. Skin blood flow was estimated by a laser Doppler technique, calf blood flow by venous occlusion plethysmography and skeletal muscle and adipose tissue blood flow by a local isotope clearance technique. 3. Adenosine (infused in steps from 40 to 80 μg min−-1 kg−-1 into a central vein) elicited a gradual reduction in the peripheral vascular resistance to less than 50% of the basal level. There was a slight increase in the systemic blood pressure, but the pulmonary arterial and the ventricular filling pressures were unchanged. Cardiac output was doubled, accomplished by a combination of a positive chronotropic effect and an increase in stroke volume, which may be secondary to diminished peripheral resistance. 4. Skin blood flow increased by 100% at 50 μg of adenosine min−-1 kg−-1, whereas splanchnic blood flow rose significantly at 60 μg of adenosine min−-1 kg−-1. Blood flow in the calf, gastrocnemius muscle and adipose tissue did not change significantly. 5. Arterial concentrations of noradrenaline and adrenaline increased by 62 and 43%, respectively, during infusion of adenosine. Arterial levels of glycerol were depressed by more than 50%, but those of glucose and pyruvate were unchanged. 6. In conclusion, exogenous adenosine caused a marked systemic vasodilatation, with different responsiveness in the investigated vascular beds. The vasodilatation occurred in the presence of an increase in generalized sympathetic activity. Adipose tissue blood flow was unaltered despite a considerable reduction in fat mobilization.


1995 ◽  
Vol 83 (6) ◽  
pp. 1067-1071 ◽  
Author(s):  
Ole J. Kirkeby ◽  
Ingunn R. Rise ◽  
Lars Nordsletten ◽  
Sigmund Skjeldal ◽  
Cecilie Risøe

✓ The authors hypothesized that the combination of hemorrhage and increased intracranial pressure (ICP) has deleterious effects on cardiovascular function. The effect of blood loss during normal and increased ICP was studied in eight pigs. The mean arterial pressure (MAP), pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac output, and cerebrospinal fluid (CSF) pressure were measured. The regional tissue blood flow was determined with radioactive microspheres labeled with four different nuclides. High ICP (80% of MAP) was induced by infusion of artificial CSF into the cisterna magna. The response to rapid arterial bleeding of 25% of blood volume was measured. The decrease in blood flow to the intestine, skeletal muscle, and the kidneys after blood loss was significantly greater during high ICP. The decrease in blood flow to the spleen and pancreas tended to be greater during high ICP, whereas the changes in blood flow to the liver, adrenal glands, and heart muscle showed no such tendency. The fall in cardiac output and heart stroke volume after blood loss were more pronounced when the ICP was high, and the increase in systemic vascular resistance was considerably greater. These observations suggest that during high ICP the physiological protective mechanisms against blood loss are impaired in the systemic circulation, and a loss of 25% of the blood volume, normally well compensated for, may induce a state of shock.


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