Direct measurement of myocadial hardness (Journal article)
Sideris, D. A./ Harocopos, F. S./ Karamitsos, C. B./ Moulopoulos, S. D.
Myocardial hardness, defined as resistance to a pitting force, was measured on several sites of the myocardium in 20 anesthetized dogs. The durometer used for hardness measurements consisted of an indentor, 4 mm in diameter, pressed perpendicularly on the myocardium by a calibrated spring (elastic modulus 325 N/m). Hardness changes during the cardiac cycle caused movement of the indentor which interrupted a light beam falling on a photoresistance. Changes in illumination of the photoresistance resulted in resistance changes, which were recorded using a Wheatstone bridge and a DC amplifier. Hardness was expressed in mm of spring shortenings. Balanced in (zero hardness), the indentor protruded 7.2 mm beyond the foot. Thus hardness adequate to press the indentor level with the foot defined as 7.2 mm. The left ventricular pressure (LVP) rise followed slightly the hardness rise (from 29.5 +/- 3.6 msec--mean +/- SEM--for the basal area at the right ventricle to 35.8 +/- 5.9 msec for the basal area of the left ventricle. Apical areas were significantly harder in systole than corresponding basal areas and left ventricular areas had a significantly higher systolic hardness (SH) than corresponding right ventricular areas. Changes in LVP by transfusion bleeding caused almost proportional changes in SH. While using a constant pressure reservoir in left atrium and another in aorta, adrenaline caused a significant increase in SH, decrease in diastolic hardness (DH) and increase in hardness width (WH); calcium chloride caused a nonsignificant increase in SH and WH and a significant decrease in DH; practolol caused a nonsignificant decrease in SH and a significant increase in DH and decrease in WH. Ligation of 3--5 branches of the anterior descending coronary artery resulted in a significant increase in DH and reduction in the WH distally to the ligation during the first 11 min. The WH was significantly reduced as a function of time in both areas (healthy and infarcted) taken collectively. The WH was significantly higher over the healthy area than over the infarcted one at corresponding times.
|Institution and School/Department of submitter:||Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής|
|Keywords:||Animals,Calcium Chloride/pharmacology,Coronary Disease/physiopathology,Dogs,Epinephrine/pharmacology,*Hardness Tests/methods,Heart/drug effects/*physiology,*Myocardial Contraction,Practolol/pharmacology|
|Appears in Collections:||Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)|
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