Fletcher P J, Pfeffer J M, Pfeffer M A
Am Heart J. 1986 Jan;111(1):120-7. doi: 10.1016/0002-8703(86)90563-6.
Left ventricular dysfunction reduces the ability of the heart to maintain forward output when subjected to the additional stress of an increased vascular resistance. To determine the extent to which hearts from rats with both hypertension and myocardial infarction are sensitive to increases in vascular resistance, spontaneously hypertensive rats (SHR) and normotensive Wistar rats (NWR) with and without myocardial infarction (coronary artery ligation) were infused with methoxamine (0.08 to 1.6 mg/kg/min). Mean arterial pressure during methoxamine infusion was significantly lower in infarcted rats than in noninfarcted rats in each strain, due largely to a lower cardiac output in infarcted rats. When compared at equal pressures, the infarcted groups of each strain generated a lower cardiac output than did the respective noninfarcted groups, as a result of both a lower stroke volume and heart rate. During the methoxamine infusion, absolute pressure levels in SHR with large infarcts were similar to those in NWR. Thus, infarcted hearts from both hypertensive and normotensive rats, when subjected to the stress of an increase in vascular resistance, demonstrated an impairment of pumping ability that was related to the extent of left ventricular damage. Impaired pressure-generating capacity was most pronounced in SHR with large infarcts, which were unable to generate hypertensive levels of blood pressure.
