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1 Author(s): Louis D Alecy, D.M.D., Ph.D., 2009 License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Non-commercial Share Alike 3.0 License: We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact open.michigan@umich.edu with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers.
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3 M2 Mini Review August 2008 Physiology/Pathophysiology Of Coronary Blood Flow Louis G. D Alecy, Professor of Physiology 3
4 Coronary Blood Flow Outline 1) Myocardial Ischemia Supply Demand 2) Coronary Flow Reserve 3) Determinants of Coronary Blood Flow 4) Neural (autonomic) Mechanisms 5) Endothelial Factors (Mechanisms) 6) NOS, NO and ADMA 4
5 Myocardial Ischemia ( MI ) - blood flow to a tissue or organ (heart) that is inadequate to maintain function. 5
6 Heart statistics 300g / 70,000g = or < 0.5% Body Weight. Heart consumes more energy than any other organ. Coronary flow = 4% of cardiac output. Resting flow 30X flow/g tissue of skeletal muscle. Highest oxygen consumption per g of tissue in body. (arterial oxygen 20 Vol % to coronary sinus 8 Vol %) (typical mixed venous oxygen higher at 17 Vol %) ***SEE SLIDE 37 & 38 FOR SUMMARY OF OTHER TISSUES **Must increase coronary blood flow to increase oxygen delivery. Vol % = ml O 2 / 100mL blood 6
7 1 2 Arterial F IO2 & Hct (or Hb) Thus an enlarged heart has greater demand. r = radius Source Undetermined Pressure X Rate Product 7
8 How can coronary flow remain relatively constant with an 80% lesion?? Fig. 6.3 Source Undetermined Occlusion proximal arterial stenosis 8
9 Series Resistance Network Compensatory Vasodilation here. Therefore series resistance and flow stays the same. Pi Lesion here 6.3 MH 9 Source Undetermined
10 With the same perfusion pressure, the same measured flow means the overall (series) resistance is the same regardless of a focal lesion BUT *** You have used up vasodilator reserve e.g.. exercise Fig /10/11 10 Source Undetermined
11 LOST RESERVE Lesion upstream and down stream vasodilation used up. LOST RESERVE Source Undetermined Lesion down stream and large vessel vasodilation used up even with no upstream lesion. Papaverine inhibits breakdown of cgmp & camp by PDE 11
12 DETERMINANTS OF CORONARY BLOOD FLOW (PERFUSION) 1 DIASTOLIC PERFUSION PRESSURE P 2 SYSTOLIC COMPRESSION ( Resistance ) 3 METABOLIC CONTROL (Resistance) O 2 & adenosine 4 NEURAL CONTROL (Resistance) Sympathetic & Parasysmpathetic 12
13 Anterior view Source Undetermined Posterior view But where is the origin of perfusion pressure? 13
14 Highest pressure Origin of left coronary artery Lowest pressure Venous end is at coronary venous sinus right atrium. 3/10/11 14 Source Undetermined
15 120 mmhg Systolic Pressure Systolic compression Left coronary flow ml/min 0 Time Right Coronary flow ml/min 3/10/11 15 Source Undetermined
16 DETERMINANTS OF CORONARY BLOOD FLOW 1 PERFUSION PRESSURE 2 SYSTOLIC COMPRESSION 3 METABOLIC CONTROL 4 NEURAL CONTROL 16
17 TISSUE VASCULAR RESISTANCE (***Assume Perfusion Pressure is Constant ***) Vasoconstriction " # r " $ R tissue " # F tissue Vasodilation % " $ r " # R tissue " $ F tissue F tissue = Perfusion Pressure = Coronary flow R tissue 17
18 Flow vs. Perfusion Angiography Large surface Focal Fixed diameter Bypass Stent Nuc. Imaging Arteriolar Vasodilator reserve Functional flow Distributed resistance Collateral channels 18
19 Intrinsic Regulation of Coronary Blood Flow Thus any additional oxygen requirement must be met by an increase in blood flow. P 143 Lilly You must use vasodilator reserve --- assuming you have any left 19
20 Source Undetermined 20
21 Isolated Vascular Effects (vessel strips or rings in bath) - Sympathetic alpha adrenergic & 1 vasoconstriction - Sympathetic beta adrenergic vasodilation ' 1 (evidence for innervated VSM) % % %' 2 non-innervated VSM - Parasympathetic cholinergic vasodilation 21
22 BUT HOW DOES IT WORK IN VIVO???? Parasympathetic Activation Stimulate parasympathetic to heart >> Ach >>SA node >> (( HR >>(( metabolism >> (( Coronary Blood flow BUT PACE heart (i.e. fixed heart rate) >> no change in HR >>% no change metabolism Therefore Stimulate parasympathetic to paced heart >> >> Ach vasodilation >> )) coronary blood flow 22
23 BUT HOW DOES IT WORK IN VIVO???? Sympathetic Activation Stimulate sympathetic nerves to heart >> )) Norepi >>% >> )) HR + )) inotropism >> )) metabolism >> >> % % % % )) )) Coronary Blood flow BUT Block ' 1&2 receptors and Stimulate sympathetics to heart >> )) Norepi (stress) >> no change in HR >> >> no change inotropism >> >> no change in metabolism >> potential for % % % >> (( Coronary Blood flow by unmasked & 1 adrenergic vasoconstriction Can Metabolic control still dominate?? 23
24 Source Undetermined 24
25 Sheer or Flow Mediated Dilation * FMD * Box 6.1 Page 144 3/10/11 25 Source Undetermined
26 Source Undetermined 26
27 Source Undetermined Fig
28 Page , Inappropriate Vasoconstriction. Lilly Source Undetermined unmasked & 1% 28
29 Source Undetermined ++ Drug effects ++ Endothelial Dysfunction 29
30 Asymmetrical Dimethylarginine (ADMA is a NOS Inhibitor) (-) Sheer or flow mediated vasodilation 3/10/11 Page Source Undetermined
31 ADMA (NOS Inhibitor) Sheer or flow mediated vasodilation (-) X X 3/10/11 31 Source Undetermined
32 Does ADMA Cause Endothelial Dysfunction? John P. Cooke (Arterioscler Thromb Vasc Biol. 2000;20: ) THEN LATER 2004 Circulation 2004; 109:
33 Asymmetrical Dimethylarginine Predicts Progression to Dialysis and Death in Patients with Chronic Kidney Disease: The Mild to Moderate Kidney Disease Study. Danilo Fliser, et al. J Am Soc Nephrol 16: , 2005 ADMA independent risk marker for progression...mortality Elevation of asymmetric dimethylarginine in patients with Unstable angina and recurrent cardiovascular events. Tanja K. Krempl et al. European Heart Journal (2005) 26, ADMA significantly elevate reduction may indicate decreased risk. 33
34 Tanja K. Krempl et al. European Heart Journal (2005) 26, Percutaneous Coronary Intervention (previously called Angioplasty) After PCI Pts with decreased ADMA had greater survival Tanja K. Krempl et al. European Heart Journal (2005) 26,
35 2008 3/10/11 35 Arterioscler Thromb Vasc Biol 2008; 28:
36 ADMA-NOS-NO Pathway the newest drug target? + - PRMT DDAH all in blood *** my laboratory interest PRMT = Protein arginine methyltransferase DDAH = Dimethylarginine dimethylaminohydrolase Source Undetermined 36
37 Published interest in ADMA 84 Publications In 2003 Atherosclerosis Supplements 4 (2003)1 3 Source Undetermined 111 Publications In 6 MONTHS of
38 Source Undetermined Look out for Limits to Compensatory VD and EC Dysfunction 38
39 McGraw-Hill 39
40 Source Undetermined 40
41 Arterioscler Thromb Vasc Biol 2008; 28:
42 Additional Source Information for more information see: Slide 7: Source Undetermined Slide 8: Source Undetermined Slide 9: Source Undetermined Slide 10: Source Undetermined Slide 11:Source Undetermined Slide 13: Source Undetermined Slide 14: Source Undetermined Slide 15: Source Undetermined Slide 20: Source Undetermined Slide 24: Source Undetermined Slide 25: Source Undetermined Slide 26: Source Undetermined Slide 27: Source Undetermined Slide 28: Source Undetermined Slide 29: Source Undetermined Slide 30: Source Undetermined Slide 31: Source Undetermined Slide 32: Circulation 2004; 109: Slide 34: Source Undetermined Slide 35: Arterioscler Thromb Vasc Biol 2008; 28: Slide 36: Source Undetermined Slide 37: Source Undetermined Slide 38: Source Undetermined Slide 39: McGraw-Hill Slide 40: McGraw-Hill Slide 41: Arterioscler Thromb Vasc Biol 2008; 28:
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