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. Results: At baseline, significant differences were observed in dP/dt_max, with the highest values in SS rats (10610.00 ± 1160.00 mmHg/s), followed by S (8663.00 ± 767.50 mmHg/s), MI (6054.00 ± 1122.10 mmHg/s), and SMI rats (4611.00 ± 1100.50 mmHg/s). Similarly, stroke work index was reduced in infarcted animals, with the lowest values observed in the SMI (0.46 ± 0.3 gm.min−1/kg) compared to other groups (S:0.85 ± 0.17, SS: 0.84 ± 0.17, MI: 0.65 ± 0.14; gm.min−1/kg). Following acute pressure overload induced by phenylephrine, indexed stroke work index differed significantly among groups (S: 71.72 ± 6.49%; SS: 28.05 ± 25.02%; MI: -16.00 ± 29.47%; SMI: -50.00 ± 16.22%; p< 0.0001). These findings demonstrate that ventricular functional reserve is markedly impaired in rats with MI previously exposed to CS. Conclusions: Prior exposure to cigarette smoke appears to exacerbate the cardiac dysfunction associated with myocardial infarction, particularly under conditions of acute increases in ventricular afterload.