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Cigarette smoking acutely increases aortic stiffness and BP in male smokers with hypertension, and the effects persist longer than in male smokers without hypertension.

Abstract-The mechanism of myocardial stunning has been studied extensively in rodents and is thought to involve a decrease in Ca 2ϩ responsiveness of the myofilaments, degradation of Troponin I (TnI), and no change in Ca 2ϩ handling. We studied the mechanism of stunning in isolated myocytes from chronically instrumented pigs. Myocytes were isolated from the ischemic (stunned) and nonischemic (normal) regions after 90-minute coronary stenosis followed by 60-minute reperfusion. Baseline myocyte contraction was reduced, PϽ0.01, in stunned myocytes (6.3Ϯ0.4%) compared with normal myocytes (8.8Ϯ0.4%). The time for 70% relaxation was prolonged, PϽ0.01, in stunned myocytes (131Ϯ8 ms) compared with normal myocytes (105Ϯ5 ms). The impaired contractile function was associated with decreased Ca 2ϩ transients (stunned, 0.33Ϯ0.04 versus normal, 0.49Ϯ0.05, PϽ0.01). Action potential measurements in stunned myocytes demonstrated a decrease in plateau potential without a change in resting membrane potential. These changes were associated with decreased L-type Ca 2ϩ -current density (stunned, Ϫ4.8Ϯ0.4 versus normal, Ϫ6.6Ϯ0.4 pA/pF, PϽ0.01). There were no differences in TnI, sarcoplasmic reticulum Ca 2ϩ ATPase (SERCA2a), and phospholamban protein quantities. However, the fraction of phosphorylated phospholamban monomer was reduced in stunned myocardium. In rats, stunned myocytes demonstrated reduced systolic contraction but actually accelerated relaxation and no change in Ca 2ϩ transients. Thus, mechanisms of stunning in the pig are radically different from the widely held concepts derived from studies in rodents and involve impaired Ca 2ϩ handling and dephosphorylation of phospholamban, but not TnI degradation.

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