Regional Myocardial Function and Dimensions Early and Late after Myocardial Infarction in the Unanesthetized Dog

SUMMARY Pairs of ultrasonic dimension gauges and a micromanometer implanted in the subendocardium of the left ventricles of unanesthetized dogs were used to analyze serial changes in hemodynamic status and segmental function for up to 4 weeks after permanent circumflex coronary artery occlusion. Regional function was studied in control segments and in segments identified as marginal (hypokinetic) and ischemic. In three dogs, after transient regional dysfunction, no myocardial infarction developed, whereas in five dogs regional dysfunction at 3 hours after occlusion was followed by the development of persistent dysfunction and infarction. Left ventricular end-diastolic segment length (EDL) changes over time; EDL of the control segments increased progressively, but in marginal segments EDL was 12% below control and in the ischemic segments 30% below control by 4 weeks. Progressive increases in percent active shortening occurred in control segments, but holosystolic bulging was replaced by akinesia in ischemic segments, and persistent reduction in shortening was present in marginal segments at 4 weeks. Correlations were found between percent scar and reductions in percent shortening, EDL, and the ratio of change in diastolic length to change in diastolic pressure. These methods have detected hyperfunction in normal regions and variable segmental loss of contractile function, together with reduction of subendocardial dimensions and changes that may reflect decreased diastolic compliance in ischemic regions. We conclude that this model for the conscious animals may be useful for studying the influence of therapy on the extent of myocardial damage after experimental coronary occlusion.

[1]  J. Ross,et al.  Analysis of regional myocardial function, dimensions, and wall thickness in the characterization of myocardial ischemia and infarction. , 1976, Circulation.

[2]  W. Hood Experimental myocardial infarction. 3. Recovery of left ventricular function in the healing phase. Contribution of increased fiber shortening in noninfarcted myocardium. , 1970, American heart journal.

[3]  T. Regan,et al.  Left ventricular function during the early and late stages of scar formation following experimental myocardial infarction. , 1970, American heart journal.

[4]  J. Covell,et al.  Factors Influencing Infarct Size Following Experimental Coronary Artery Occlusions , 1971, Circulation.

[5]  D Franklin,et al.  Regional Myocardial Function during Acute Coronary Artery Occlusion and Its Modification by Pharmacologic Agents in the Dog , 1974, Circulation research.

[6]  Franklin De,et al.  Technique for radio telemetry of blood-flow velocity from unrestrained animals. , 1966 .

[7]  J. A. Richardson,et al.  Circulating epinephrine and norepinephrine in coronary occlusion , 1960 .

[8]  J. T. Shepherd,et al.  Role of Cardiac, Pulmonary, and Carotid Mechanoreceptors in the Control of Hind‐Limb and Renal Circulation in Dogs , 1975, Circulation research.

[9]  K. M. Hanson Escape of the Liver Vasculature From Adrenergic Vasoconstriction , 1972, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[10]  Y. Ito [Ischemic heart disease]. , 1966, Saishin igaku. Modern medicine.

[11]  G. Diamond,et al.  Dlastolic Pressure‐Volume Relationship in the Canine Left Ventricle , 1971 .

[12]  G. Diamond,et al.  Diastolic pressure-volume relationship in the canine left ventricle. , 1971, Circulation research.

[13]  J. Ross,et al.  Nature of Enhanced Performance of the Dilated Left Ventricle in the Dog during Chronic Volume Overloading , 1972, Circulation research.

[14]  R. V. Van citters,et al.  Technique for radio telemetry of blood-flow velocity from unrestrained animals. , 1966, The American journal of medical electronics.

[15]  S. Sarnoff,et al.  Ventricular Function: II. Quantitative Relationship between Coronary Flow and Ventricular Function with Observations on Unilateral Failure , 1954, Circulation research.

[16]  E. R. Smith,et al.  Coronary Artery Occlusion in the Conscious Dog: Effects of Alterations in Heart Rate and Arterial Pressure on the Degree of Myocardial Ischemia , 1972, Circulation.

[17]  E. Jones,et al.  Effect of controlled coronary occlusion on collateral circulation in conscious dogs. , 1971, The American journal of physiology.

[18]  J. Covell,et al.  Left Ventricular Dilatation and Diastolic Compliance Changes during Chronic Volume Overloading , 1972, Circulation.

[19]  H. Goldberg,et al.  Myocardial contractility in areas with chronic ischaemia: studies on isometric tension. , 1968, Cardiovascular research.

[20]  G. Mancia,et al.  Demonstration that the Atria, Ventricles, and Lungs Each Are Responsible for a Tonic Inhibition of the Vasomotor Center in the Dog , 1975, Circulation research.

[21]  R. Bing,et al.  Early Changes in Energy Metabolism in the Myocardium Following Acute Coronary Artery Occlusion in Anesthetized Dogs , 1968, Circulation research.

[22]  P. Hugenholtz,et al.  Quantification of function in normal and infarcted regions of the left ventricle. , 1972, Cardiovascular research.

[23]  B. Oberg,et al.  Studies on left ventricular receptors, signalling in non-medullated vagal afferents. , 1972, Acta physiologica Scandinavica.

[24]  J. Ross,et al.  Regional Myocardial Function in the Conscious Dog During Acute Coronary Occlusion and Responses to Morphine, Propranolol, Nitroglycerin, and Lidocaine , 1976, Circulation.

[25]  W. Hood,et al.  Experimental myocardial infarction. IV. Reduction of left ventricular compliance in the healing phase. , 1970, The Journal of clinical investigation.

[26]  H. Schelbert,et al.  Observations on Factors Affecting Local Forces in the Left Ventricular Wall during Acute Myocardial Ischemia , 1971, Circulation research.

[27]  W. Hood,et al.  Myocardial Infarction Following Coronary Ligation in Dogs: Hemodynamic Effects of Isoproterenol And Acetylstrophanthidin , 1967, Circulation research.

[28]  Cardiac function after embolization of coronaries with microspheres. , 1963, The American journal of physiology.

[29]  J. J. Stark,et al.  Improvement in myocardial function and coronary blood flow in ischemic myocardium after mannitol. , 1972, The Journal of clinical investigation.

[30]  J. C. Norman,et al.  Experimental myocardial infarction: II. Acute depression and subsequent recovery of left ventricular function: serial measurements in intact conscious dogs , 1970 .

[31]  S. Sasayama,et al.  Adaptations of the Left Ventricle to Chronic Pressure Overload , 1976, Circulation research.

[32]  A. E. Lawson,et al.  The effects of stimulation of the hepatic nerves, infusions of noradrenaline and occlusion of the carotid arteries on liver blood flow in the anaesthetized cat , 1967, The Journal of physiology.

[33]  J. T. Shepherd,et al.  Interplay among carotid sinus, cardiopulmonary, and carotid body reflexes in dogs. , 1976, The American journal of physiology.

[34]  C. Wiggers,et al.  THE EFFECT OF CORONARY OCCLUSION ON MYOCARDIAL CONTRACTION , 1935 .