Diminished Myocardial Function Precedes Tissue Acidosis during Coronary Hypoperf usion

Abstract

The current study sought to elucidate the relationship between myocardial pH and function during a significant but not absolute reduction in coronary flow. In a canine model, a partial coronary arterial stenosis was created, with the left anterior descending coronary artery (LAD) flow reduced by 50% compared to prestenosis levels, and maintained at that level for the duration of the study. During the experiment, interstitial myocardial pH and regional myocardial function, as assessed by the regional preload recruitable work area (PRWA), were measured. PRWA was depressed to 60% of baseline values, on average, for the entire period of reduced LAD flow. In contrast to the pattern observed with myocardial blood flow and systolic function, metabolic evidence of myocardial ischemia, that is, reduced myocardial pH did not become significantly different from baseline levels until after LAD flow had been reduced for 15 min. Thus, measurable changes in myocardial pH appeared slowly over time despite the fact that regional myocardial blood flow was decreased immediately. Therefore, myocardial pH cannot be used to anticipate alterations in myocardial contractile function.

Multiparameter Fiber Optic Sensor for the Assessment of Intramyocardial Perfusion

“…Since the PO 2 levels are highly responsive to blood flow, they may be useful in assessing improvement in coronary blood flow as a measure of graft patency. While we did not study partial occlusions in this experiment, we and others have measured reduced myocardial pH values during partial occlusion of the LAD 23 , 30 . Based on the observed rates of change of PO 2 and pH in response to occlusion, we suspect that myocardial PO 2 may be a more sensitive indicator of reduced myocardial contractility than myocardial pH.…”

Mechanisms of blood pressure variability-induced cardiac hypertrophy and dysfunction in mice with impaired baroreflex

“…1, top, right shaded area) add to it. In fact, low blood pressure episodes may reduce organ perfusion and add to organ damage elicited by high blood pressure variability (32,40). Therefore, we propose that the greater number of high blood pressure episodes associated with elevated blood pressure variability causes activation of mechanosensitive (p125 FAK and p38 MAPK) and autocrine (cardiac renin and TGF-␤1) pathways that ultimately lead to cardiac hypertrophy, fibrosis, and dysfunction.…”

“…The greater number of low and high blood pressure episodes will not alter the average of arterial blood pressure. Rather than protecting the heart, the lowpressure episodes may be detrimental due to coronary hypoperfusion (32,40). Furthermore, the greater number of highpressure episodes may activate mechanosensitive and autocrine pathways that lead to cardiac hypertrophy and myocardial dysfunction.…”

Release and effects of calcitonin gene-related peptide in myocardial ischaemia

“…Ischaemia-induced metabolic disturbances correlate well with ischaemia-induced myocardial acidosis (Ichihara and Abiko, 1982;Khuri et al, 1985). In a canine model, 50% reduction of left anterior descending coronary artery (LAD) flow caused a significant fall in myocardial pH within 15 minutes (Shortt et al, 1997). In a pig model myocardial pH already started falling after 10 s occlusion of the LAD, and after 50 min of LAD ischaemia pH was 5.5 (Hirche et al, 1980).…”