Simultaneous counting of 85Kr in lung and myocardium during measurement of coronary blood flow

1975 ◽  
Vol 39 (5) ◽  
pp. 788-795
Author(s):  
F. L. Belloni ◽  
D. E. Mohrman ◽  
H. V. Sparks

Coronary blood flow rate (ml-min-1–100 g-1) was estimated by a) measuring pump flow into the cannulated circumflex branch of the left coronary artery and dividing by the weight of perfused myocardium and b) measuring the clearance of 85Kr following intra-arterial injection (detection with a 2-in. crystal with cylindrical collimation). Although the correlation between the two measurements was relatively high (r equals 0.90), the line best fitting the data was 85Kr flow equals 0.55 pump flow + 25.6. We tested the possibility that the discrepancy between the two methods was primarily due to the counting of 85Kr removed from myocardium and delivered to lung. Relative efficiency of lung counting versus myocardial counting was determined as well as clearance pattern of 85Kr from lung in each dog. A simple mathematical model which assumes no recirculation of 85Kr to heart allowed correction of coronary clearance curves using this information. When corrected 85Kr flow equals 1.00 pump flow + 4.1 (r equals 0.90). Thus, the major systematic cause for the discrepancy between the two measurements under the conditions of this experiment appears to be simultaneous counting of 85Kr in lung and in myocardium.

1963 ◽  
Vol 204 (2) ◽  
pp. 317-322 ◽  
Author(s):  
Robert M. Berne

Experiments were performed on isolated cat hearts perfused with Tyrode's solution and intact hearts of open-chest dogs. Cardiac hypoxia resulted in a decrease in coronary vascular resistance and a release of significant amounts of inosine and hypoxanthine from the myocardium. From 3 to 27 times more inosine and hypoxanthine were released from the heart during myocardial hypoxia than were required to double the coronary blood flow when infused as adenosine into the left coronary artery. Based on the assumption that with hypoxia the nucleotide derivatives leave the myocardial cell as adenosine, an hypothesis is proposed for the metabolic regulation of coronary blood flow.


Author(s):  
Soroush Nobari ◽  
Rosaire Mongrain ◽  
Richard Leask ◽  
Raymond Cartier

Coronary artery disease (CAD) is considered to be a major cause of mortality and morbidity in the developing world. It has recently been shown that aortic root pathologies such as aortic stiffening and calcific aortic stenosis can contribute to the initiation and progression of this disease by affecting coronary blood flow [1,2]. Such pathologies influence the distensibility of the aortic root and therefore the hemodynamics of the entire region. As a consequence the coronary blood flow and velocity profiles will be altered [3,4,5] which could accelerate the development of an existing coronary artery disease. However, it would be very interesting to see if an occluded coronary artery would have a mutual impact on valvular dynamics and aortic root pathologies. This bi-directionality could aggravate and contribute to the progression of both the coronary and aortic root pathology.


Author(s):  
Valentina Magagnin ◽  
Maurizio Turiel ◽  
Sergio Cerutti ◽  
Luigi Delfino ◽  
Enrico Caiani

The coronary flow reserve (CFR) represents an important functional parameter to assess epicardial coronary stenosis and to evaluate the integrity of coronary microcirculation (Kern, 2000; Sadamatsu, Tashiro, Maehira, & Yamamoto, 2000). CFR can be measured, during adenosine or dipyridamole infusion, as the ratio of maximal (pharmacologically stimulated) to baseline (resting) diastolic coronary blood flow peak. Even in absence of stenosis in epicardial coronary artery, the CFR may be decreased when coronary microvascular circulation is compromised by arterial hypertension with or without left ventricular hypertrophy, diabetes mellitus, hypercholesterolemia, syndrome X, hypertrophic cardiomyopathy, and connective tissue diseases (Dimitrow, 2003; Strauer, Motz, Vogt, & Schwartzkopff, 1997). Several methods have been established for measuring CFR: invasive (intracoronary Doppler flow wire) (Caiati, Montaldo, Zedda, Bina, & Iliceto, 1999b; Lethen, Tries, Brechtken, Kersting, & Lambertz, 2003a; Lethen, Tries, Kersting, & Lambertz, 2003b), semi-invasive and scarcely feasible (transesophageal Doppler echocardiography) (Hirabayashi, Morita, Mizushige, Yamada, Ohmori, & Tanimoto, 1991; Iliceto, Marangelli, Memmola, & Rizzon, 1991; Lethen, Tries, Michel, & Lambertz, 2002; Redberg, Sobol, Chou, Malloy, Kumar, & Botvinick, 1995), or extremely expensive and scarcely available methods (PET, SPECT, MRI) (Caiati, Cioglia, Montaldo, Zedda, Rubini, & Pirisi, 1999a; Daimon, Watanabe, Yamagishi, Muro, Akioka, & Hirata, 2001; Koskenvuo, Saraste, Niemi, Knuuti, Sakuma, & Toikka, 2003; Laubenbacher, Rothley, Sitomer, Beanlands, Sawada, & Sutor, 1993; Picano, Parodi, Lattanzi, Sambuceti, Andrade, & Marzullo, 1994; Saraste, Koskenvuo, Knuuti, Toikka, Laine, & Niemi, 2001; Williams, Mullani, Jansen, & Anderson, 1994), thus their clinical use is limited (Dimitrow, 2003). In addition, PET and intracoronary Doppler flow wire involve radiation exposure, with inherent risk, environmental impact, and biohazard connected with use of ionizing testing (Picano, 2003a). In the last decade, the development of new ultrasound equipments and probes has made possible the noninvasive evaluation of coronary blood velocity by Doppler echocardiography, using a transthoracic approach. In this way, the peak diastolic coronary flow velocity reserve (CFVR) can be estimated as the ratio of the maximal (pharmacologically stimulated) to baseline (resting) diastolic coronary blood flow velocity peak measured from the Doppler tracings. Several studies have shown that peak diastolic CFVR, computed in the distal portion of the left anterior descending (LAD) coronary artery, correlates with CFR obtained by more invasive techniques. This provided a reliable and non invasive tool for the diagnosis of LAD coronary artery disease (Caiati et al., 1999b; Caiati, Montaldo, Zedda, Montisci, Ruscazio, & Lai, 1999c; Hozumi, Yoshida, Akasaka, Asami, Ogata, & Takagi, 1998; Koskenvuo et al., 2003; Saraste et al., 2001).


1996 ◽  
Vol 26 (5) ◽  
pp. 968
Author(s):  
Seung-Jea Tahk ◽  
Won Kim ◽  
Jing-Song Shen ◽  
Joon-Han Shin ◽  
Han-Soo Kim ◽  
...  

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