A Simple Radioactive Microsphere Method for Measuring Regional Flow and Cardiac Output

Systemic and regional hemodynamic changes were measured in restrained, conscious rhesus monkeys with indwelling arterial and venous catheters before and after clonidine (5 and 15 mug/kg) was slowly infused intravenously or smaller doses (2 mug/kg) were injected into a lateral cerebral ventricle. Dye-dilution cardiac outputs and the complete distribution of cardiac output were obtained intermittently with the use of the radioactive microsphere method. After the higher intravenous dose and the intraventricular injection, systemic arterial pressure was significantly lowered for 30-45 min. Both of these groups had similar changes in the redistribution of cardiac output and blood flow that outlasted the hypotensive period. Blood flow was maintained or increased in the hepatic and renal arteries at the expense of skin; flow to skeletal muscle and brain also decreased during the first hour. These data support previous studies that indicate that the primary action of clonidine is in the central nervous system and, in addition, add new information about the regional blood flow changes evoked by clonidine.

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The radioactive microsphere method for the assessment of regional myocardial blood flow after coronary artery occlusion

Pflügers Archiv - European Journal of Physiology ◽

10.1007/bf00587030 ◽

1975 ◽

Vol 353 (4) ◽

pp. 337-347 ◽

Cited By ~ 12

Author(s):

R. S. Reneman ◽

A. H. M. Jageneau ◽

W. van Gerven ◽

J. Dony ◽

P. Beirnaert

Keyword(s):

Blood Flow ◽

Coronary Artery ◽

Myocardial Blood Flow ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Regional Myocardial Blood Flow ◽

Radioactive Microsphere ◽

Microsphere Method ◽

Radioactive Microsphere Method ◽

Regional Myocardial Blood

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Canine gastric blood flow and its distribution

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1964.207.6.1195 ◽

1964 ◽

Vol 207 (6) ◽

pp. 1195-1202 ◽

Cited By ~ 96

Author(s):

John P. Delaney ◽

Eugene Grim

Keyword(s):

Blood Flow ◽

Gastric Blood Flow ◽

Total Flow ◽

Venous Outflow ◽

Radioactive Microsphere ◽

Venous Catheterization ◽

Microsphere Method ◽

Radioactive Microsphere Method ◽

Clearance Technique

Total gastric blood flow in the dog as estimated by the K42 clearance technique agreed within 5% with measured total venous outflow. Extraction of the isotope by the stomach was found to be such that 30–60 sec following injection the organ contained a fraction of the injected dose that was the same as the fraction of the cardiac output that perfused the organ. By comparison with the radioactive microsphere method, the K42 clearance technique was also found to be reasonably accurate for determination of the distribution of the total flow within the organ. Mean total gastric blood flow in intact dogs, unoperated upon except for femoral arterial and venous catheterization, was 49 ml/min per organ or 0.54 ml/min per gram. This was distributed 80% to corpus and 20% to antrum. The corpus flow was partitioned among the mural tissues: mucosa 72%, submucosa 13%, and muscle serosa 15%.

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Role of EDRF in splanchnic blood flow of normal and chronic portal hypertensive rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.2.g149 ◽

1992 ◽

Vol 263 (2) ◽

pp. G149-G154 ◽

Cited By ~ 1

Author(s):

F. Iwata ◽

T. Joh ◽

T. Kawai ◽

M. Itoh

Keyword(s):

Blood Flow ◽

Splanchnic Blood Flow ◽

Constant Infusion ◽

Relaxing Factor ◽

Radioactive Microsphere ◽

Blood Flow Reduction ◽

Microsphere Method ◽

Radioactive Microsphere Method ◽

Endothelium Derived Relaxing Factor

The role of endogenous endothelium-derived relaxing factor (EDRF) in splanchnic blood flow was assessed in normal and portal vein-stenosed rats (PSRs). Specific and maximal inhibition of EDRF was achieved by intravenous administration of NG-nitro-L-arginine (L-NOARG) as a 1.75 mumol/kg bolus, followed by constant infusion of 1.75 mumol/kg for 20 min. Pretreatment with L-arginine (175 mumol/kg iv) completely blocked both hypertension and the reduction in blood flow induced by L-NOARG. Pretreatment with D-arginine (175 mumol/kg iv) and prazosin (500 micrograms/kg iv) did not attenuate the pressor effect of L-NOARG. These results indicate that L-NOARG selectively blocks EDRF. The blood flow to the stomach, duodenum, jejunum, ileum, cecum, and colon in control rats was 81.1 +/- 8.7, 199.1 +/- 21.9, 153.3 +/- 20.0, 68.6 +/- 10.6, 79.4 +/- 11.8, and 59.3 +/- 7.8 ml.min-1.100 g-1, respectively, and in PSRs was 141.4 +/- 10.8, 244.0 +/- 10.4, 208.3 +/- 9.8, 126.8 +/- 13.0, 166.9 +/- 16.5, and 94.8 +/- 4.7 ml.min-1.100 g-1, respectively. Blood flow was measured using the radioactive microsphere method. L-NOARG significantly reduced blood flow to the stomach, duodenum, jejunum, ileum, cecum, and colon in control rats by 47, 44, 48, 55, 40, and 41%, respectively, and in PSRs by 30, 27, 36, 33, 28, and 23%, respectively. The magnitude of blood flow reduction in PSRs was lower than in normal rats. These results indicate that EDRF plays an important role in control of the splanchnic circulation, but its effect on the hyperdynamic circulation observed in PSRs is insignificant.

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A tool for balancing activity from isotopes used for the radioactive microsphere method

Computer Methods and Programs in Biomedicine ◽

10.1016/s0169-2607(97)01808-7 ◽

1997 ◽

Vol 53 (2) ◽

pp. 81-86 ◽

Cited By ~ 8

Author(s):

M. Kleen ◽

O. Habler ◽

K. Messmer

Keyword(s):

Radioactive Microsphere ◽

Microsphere Method ◽

Radioactive Microsphere Method

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At 2 Receptor-Mediated Vasodilation in the Heart: Effect of Myocardial Infarction.

Hypertension ◽

10.1161/hyp.36.suppl_1.704-c ◽

2000 ◽

Vol 36 (suppl_1) ◽

pp. 704-704

Author(s):

Martin P Schuijt ◽

Munesh Basdew ◽

Richard van Veghel ◽

Pramod R Saxena ◽

Regien G Schoemaker ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiac Output ◽

Receptor Antagonist ◽

Ang Ii ◽

Hemodynamic Effects ◽

Systemic Hemodynamic ◽

Renal Vasoconstriction ◽

Link Type ◽

Microsphere Method ◽

Radioactive Microsphere Method

P64 To investigate the functional consequences of the changes in AT 2 receptor density that have been reported following myocardial infarction (MI; Matsubara, Circ Res, 1998), three consecutive 10 min intravenous infusions of angiotensin (Ang) II (100, 300 and 1000 ng/kg/min) were given to 19 sham-operated and 16 coronary artery-ligated rats, at four weeks after surgery, pretreated with either saline, the AT 1 receptor antagonist irbesartan (100 μg/kg/min for 30 min), or the AT 2 receptor antagonist PD123319 (20 μg/kg/min for 30 min, followed by continuous infusion). Systemic and regional hemodynamic effects were studied using the radioactive microsphere method. Ang II induced comparable changes in sham and MI rats in mean arterial pressure (MAP; maximally +30±10% and +30±8%, resp., mean±SEM) and systemic vascular conductance (cardiac output/MAP, -27±8% and -32±5%, resp.). Cardiac output decreased in MI (-20±5%) but not in sham rats. Irbesartan decreased MAP by 34% (sham) and 22% (MI), increased SVC by 41% (sham) and 24% (MI), and blocked the Ang II-mediated systemic hemodynamic effects in both sham and MI rats, while PD123319 did not affect these parameters. Myocardial conductance at baseline was diminished in MI vs. sham rats (41±3 vs. 55±6 μl/min/mmHg, resp.), while renal conductance was comparable in both groups (168±9 vs. 156±18 μl/min/mmHg, resp.). Ang II increased myocardial conductance maximally to 56±3 (MI) and 72±3 (sham) μl/min/mmHg, and decreased renal conductance to 67±4 (MI) and 74±8 (sham) μl/min/mmHg. Irbesartan increased renal, but not myocardial, conductance in both groups and blocked the Ang II-mediated renal vasoconstriction. PD123319 did not affect renal or myocardial conductance and blocked the Ang II-mediated myocardial vasodilation in sham but not in MI rats. PD123319 did not affect the Ang II-mediated renal responses. In conclusion, Ang II increases myocardial, but not renal, conductance (i.e., induces vasodilation) via AT 2 receptor stimulation. The inability of PD123319 to block this response in MI rats suggests either an upregulation of AT 2 receptors or a role for non-AT 1 , non-AT 2 receptors in the infarcted heart.

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