Acute Afterload Stress Induced by Phenylephrine Administration Reveals Ventricular Dysfunction in Myocardial Infarcted Female Rats Previously Exposed to Cigarette Smoke

Background/Objective: This study investigated the hemodynamic responses to acute pressure overload in female rats with myocardial infarction (MI) previously exposed to cigarette smoke (CS).

Methods

Female Wistar rats were allocated into four groups: sham (S, n = 10), Smoker (SS, n = 8), myocardial infarction (MI, n = 9), and smoker with myocardial infarction (SMI, n = 10). The S and MI groups were housed under standard conditions for 16 weeks, whereas the SS and SMI groups were exposed to CS for 16 weeks. Subsequently, MI was induced by coronary artery occlusion (CAO), while sham-operated animals underwent the corresponding surgical procedure without coronary occlusion. Left ventricular pressure was measured using a micromanometer introduced through right common carotid artery catheterization, with the transducer positioned within the left ventricular cavity. Ascending aortic flow was simultaneously recorded. Hemodynamic signals were acquired using the AcqKnowledge® system to determine left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), heart rate, first derivative positive (+dP/dt) and negative (-dP/dt) of left ventricular pressure, cardiac output, stroke volume (SV), and systolic work (SW). Systolic work was calculated as SW = (LVSP − LVEDP) × SV × 0.0136.