The septal artery and its collaterals in dogs with and without circumflex occlusion

1980 ◽  
Vol 238 (4) ◽  
pp. H504-H514 ◽  
Author(s):  
K. W. Scheel ◽  
J. L. Wilson ◽  
L. A. Ingram ◽  
L. McGehee
Keyword(s):  
Myocardial Perfusion ◽  
Collateral Circulation ◽  
Time Course ◽  
Isolated Heart ◽  
Coronary Vessels ◽  
Collateral Development ◽  
Physiological Conditions ◽  
Vascular Bed ◽  
Collateral Growth ◽  
Heart Preparation

The purpose of this investigation was to study myocardial perfusion and the collateral circulation of the septal artery in dogs without occlusion and to determine the magnitude and time course of septal collateral development with gradual circumflex occlusion. After the dogs with circumflex occlusion for 1 and 3 mo were allowed to develop a prolific collateral circulation under normal physiological conditions, coronary and collateral resistances were determined on an isolated heart preparation with maximal vasodilation. It was found that the septal artery contributes about 25% to the collateral circulation of the major coronary arteries (right, circumflex, and anterior descending). Septal collateral growth increased up to 15 times with circumflex occlusion. Due to the anatomic location of the septal artery, this collateral growth was intramyocardial in contrast to epicardial collaterals. Although there was collateral proliferation to all major coronary vessels, the most significant growth was toward the circumflex, the ischemic vascular bed. Although primary collateralization in the dog is via epicardial collaterals, the septal artery participates in collateral development.

Hypertrophy and coronary and collateral vascularity in dogs with severe chronic anemia

1985 ◽  
Vol 249 (5) ◽  
pp. H1031-H1037 ◽  
Author(s):  
K. W. Scheel ◽  
S. E. Williams
Keyword(s):  
Body Weight ◽  
Coronary Flow ◽  
Collateral Circulation ◽  
Isolated Heart ◽  
Normal Donor ◽  
Coronary Resistance ◽  
Chronic Anemia ◽  
Volume Load ◽  
Heart Preparation ◽  
The Right

The purpose of this study was to determine 1) whether a severe hypoxic stimulus could produce an increase in coronary and collateral vascularization and 2) whether minimal coronary resistance, which increases with hypertension-induced hypertrophy, decreases when hypoxia is superimposed on volume load hypertrophy. Data were obtained on 11 dogs rendered anemic to a hematocrit of 11 +/- 0.2 vol% and maintained at this level for 4 wk. Eighteen dogs with a hematocrit of 42 +/- 0.02 vol% were used as controls. After chronic anemia the coronary and collateral flows were quantitated in a beating, vasodilated, isolated heart preparation perfused solely with blood from two normal donor dogs. The following variables were significantly increased in anemia-exposed hearts compared with controls: coronary flow per gram myocardium for the left anterior descending, the circumflex, the right, and the septal arteries; ratio of total coronary flow of each vessel to body weight; and the collateral flows to each coronary vessel. Both the right and left ventricles were hypertrophied. We conclude that severe chronic anemia produces a dissociation between hypertrophy and increased minimal coronary resistance. Severe chronic anemia appears to increase vascularization of both coronary and collateral circulation probably due to tissue hypoxia. In this model coronary collateral vascularity seems to increase in the absence of a pressure difference across collaterals.

Coronary and myocardial adaptations to high altitude in dogs

1990 ◽  
Vol 259 (6) ◽  
pp. H1667-H1673
Author(s):  
K. W. Scheel ◽  
E. Seavey ◽  
J. F. Gaugl ◽  
S. E. Williams
Keyword(s):  
High Altitude ◽  
Myocardial Hypertrophy ◽  
Isolated Heart ◽  
Ambient Pressure ◽  
Right Heart ◽  
Vascular Growth ◽  
Heart Chamber ◽  
Collateral Growth ◽  
Heart Preparation ◽  
Different Color

The objective of this study was to determine whether exposure to high altitude (hypoxic hypoxemia) induces coronary and/or collateral growth. Fourteen mongrel dogs were maintained at a simulated altitude of 18,000 ft for 1 mo and 7 dogs maintained for 3 mo. Within 2 days after their sojourn, the following data were obtained at ambient pressure: pulmonary, right heart chamber, and wedge pressures as well as cardiac output. On an isolated heart preparation, coronary and collateral flows were determined; each vessel was injected with a different color tracer; and the heart was sliced, separated by perfusion territories, and examined for myocardial hypertrophy. We found that pulmonary artery pressures in altitude-adapted animals were higher compared with controls, and coronary flow per gram was increased after 1 mo of exposure but not different from control after 3 mo. Collateral flows were not significantly different from that of control animals, and biventricular hypertrophy occurred with right ventricular dominance. Comparing these results with those that we obtained previously from anemic animals, we favor the hypothesis that oxygen availability rather than blood flow velocity is most likely linked to vascular growth.

Influence of stable iodine on the uptake of the thyroid – model vs. experiment

2001 ◽  
Vol 40 (01) ◽  
pp. 31-37 ◽  
Author(s):  
U. Wellner ◽  
E. Voth ◽  
H. Schicha ◽  
K. Weber
Keyword(s):  
Time Course ◽  
Compartment Model ◽  
The Body ◽  
Iodine Uptake ◽  
Model Calculations ◽  
Physiological Conditions ◽  
Iodine Supply ◽  
Predicted Values ◽  
The Individual ◽  
Stable Iodine

Summary Aim: The influence of physiological and pharmacological amounts of iodine on the uptake of radioiodine in the thyroid was examined in a 4-compartment model. This model allows equations to be derived describing the distribution of tracer iodine as a function of time. The aim of the study was to compare the predictions of the model with experimental data. Methods: Five euthyroid persons received stable iodine (200 μg, 10 mg). 1-123-uptake into the thyroid was measured with the Nal (Tl)-detector of a body counter under physiological conditions and after application of each dose of additional iodine. Actual measurements and predicted values were compared, taking into account the individual iodine supply as estimated from the thyroid uptake under physiological conditions and data from the literature. Results: Thyroid iodine uptake decreased from 80% under physiological conditions to 50% in individuals with very low iodine supply (15 μg/d) (n = 2). The uptake calculated from the model was 36%. Iodine uptake into the thyroid did not decrease in individuals with typical iodine supply, i.e. for Cologne 65-85 μg/d (n = 3). After application of 10 mg of stable iodine, uptake into the thyroid decreased in all individuals to about 5%, in accordance with the model calculations. Conclusion: Comparison of theoretical predictions with the measured values demonstrated that the model tested is well suited for describing the time course of iodine distribution and uptake within the body. It can now be used to study aspects of iodine metabolism relevant to the pharmacological administration of iodine which cannot be investigated experimentally in humans for ethical and technical reasons.

Differential uptake of endothelin-1 by the coronary and pulmonary circulations

1992 ◽  
Vol 73 (2) ◽  
pp. 557-562 ◽  
Author(s):  
S. Rimar ◽  
C. N. Gillis
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Pulmonary Circulation ◽  
Enzyme Inhibitor ◽  
Isolated Heart ◽  
Mean Transit Time ◽  
Converting Enzyme ◽  
Endothelin 1 ◽  
Multiple Indicator Dilution ◽  
Multiple Indicator ◽  
Heart Preparation

Substantial removal of the vasoconstrictor peptide endothelin-1 (ET-1) by the pulmonary circulation has been reported to occur in perfused guinea pig and rat lungs. We examined the uptake of ET-1 by coronary and pulmonary circulations of the rabbit by measuring single-pass extraction of ET-1 in the isolated heart and lung. In separate experiments, each organ was perfused at 30 ml/min with Krebs-albumin (3%) solution. A bolus of 125I-ET-1 and [14C]dextran in 0.3 ml Krebs-albumin solution was injected, and extraction of endothelin (EET), relative to that of an intravascular reference indicator, [14C]dextran, was determined by multiple indicator-dilution technique. EET was 5 +/- 2% (SE) in the heart and 49 +/- 4% in the lung. Increasing flow rate in the lung preparation to approximate the mean transit time in the heart preparation did not significantly alter EET. Despite insignificant uptake of ET-1, the coronary circulation extracted an angiotensin-converting enzyme inhibitor (351A) and metabolized a synthetic angiotensin-converting enzyme substrate (benzoyl-phenyl-alanyl-proline), both properties of the normal pulmonary circulation. We therefore conclude that there is no significant ET-1 uptake in the coronary vascular bed.

Effects of exercise on collateral development in myocardial ischemia in pigs

1984 ◽  
Vol 56 (3) ◽  
pp. 656-665 ◽  
Author(s):  
C. M. Bloor ◽  
F. C. White ◽  
T. M. Sanders
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Exercise Training ◽  
Collateral Circulation ◽  
Coronary Artery Stenosis ◽  
Arterial Stenosis ◽  
Collateral Flow ◽  
Circumflex Coronary Artery ◽  
Complete Occlusion ◽  
Collateral Development

To study the effects of exercise on collateral development in myocardial ischemia, we induced coronary arterial stenosis of the left circumflex coronary artery (LCCA) in 18 of 30 pigs. During that surgery, we identified the coronary bed at risk. Nine of these pigs were then subjected to 5 mo of exercise training on a treadmill. After exercise training, we determined regional collateral and myocardial blood flow using radiolabeled microspheres. At autopsy, all animals had complete occlusion of the LCCA. Infarct size in the exercise-trained pigs was significantly less than in the sedentary pigs (5.9 +/- 1.0 vs. 11.7 +/- 1.0% of the left ventricle). The exercise-trained animals had a greater increase in collateral flow, 35.1 +/- 3.0 vs. 28.7 +/- 4.1 ml X min-1 X 100 g-1, in the noninfarcted jeopardized zone of the LCCA bed. The major findings of the study were the following: 1) chronic coronary artery stenosis progressing to occlusion stimulated development of the collateral circulation and salvaged tissue in the jeopardized myocardium of an animal model with sparse collaterals; 2) development of the collateral circulation and tissue salvage is increased by exercise training; 3) collaterals develop primarily in or near the ischemic zone; and 4) all collateral beds develop a circumferential flow gradient following occlusion.

Isolated Heart Preparation

2018 ◽  
pp. 185-193
Author(s):  
H. Hwang ◽  
R.A. Kloner ◽  
W. Dai ◽  
M.T. Kleinman ◽  
W.K. Poole ◽  
...  
Keyword(s):  
Isolated Heart ◽  
Heart Preparation

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

2002 ◽  
Vol 282 (6) ◽  
pp. H2031-H2038 ◽  
Author(s):  
Christine Barbé ◽  
Eric Dubuis ◽  
Annie Rochetaing ◽  
Paul Kreher ◽  
Pierre Bonnet ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Isolated Heart ◽  
Physiological Role ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Heart Preparation ◽  
Intracellular Microelectrodes

A physiological role of carbon monoxide has been suggested for coronary myocytes; however, direct evidence is lacking. The objective of this study was to test the effect of chronic carbon monoxide exposure on the K+ currents of the coronary myocytes. The effect of 3-wk chronic exposure to carbon monoxide was assessed on K+ currents in isolated rat left coronary myocytes by the use of the patch-clamp technique in the whole cell configuration. Moreover, membrane potential studies were performed on coronary artery rings using intracellular microelectrodes, and coronary blood flow in isolated heart preparation was recorded. Carbon monoxide did not change the amplitude of global whole cell K+ current, but it did increase the component sensitive to 1 mM 4-aminopyridine. Carbon monoxide exposure hyperpolarized coronary artery segments by ∼10 mV and, therefore, increased their sensitivity to 4-aminopyridine. This effect was associated with an enhancement of coronary blood flow. We conclude that chronic carbon monoxide increases a 4-aminopyridine-sensitive current in isolated coronary myocytes. This mechanism could, in part, contribute to hyperpolarization and to increased coronary blood flow observed with carbon monoxide.

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