摘要:

Previous studies have shown that rabbit hearts subjected to in vivo left ventricular myocardial infarction and subsequent ex vivo perfusion respond to A'-formylmethionyl-leucylphenylalanine (fMLP) with enhanced eicosanoid synthesis. This synthetic response occurs primarily in the right cardiac atrium, a site distant from the injury, and is not the result of increased enzymatic capacity for arachidonate metabolism. To further investigate the mechanism of this enhanced synthetic response, [3H]fMLP binding was characterized and binding sites were localized autoradiographically in intact tissue sections prepared from control hearts and hearts subjected to left ventricular myocardial infarction (1, 2, and 4 days postinfarction). Analysis of binding isotherms revealed a saturable high affinity (KD∼l nM) fMLP binding site in the right cardiac atrium. After myocardial infarction specific binding in right atria (2 day) increased 12-fold (B=14.8 ± 2.4 fmol/cm2) compared with normal controls (Bnu=1.2 ± 0.1 finol/cm2). Specific binding of fMLP also increased in the infarcted zone of left ventricle, but B-u was only 30–50% that of right atria. Light microscopic autoradiography studies revealed that atrial fMLP binding sites were highly concentrated in small morphologically undifferentiated cells located in interstitial and perivascular spaces. These results demonstrate the existence of a formylated peptide receptor on a nonleukocytic cell and illustrate its regulation following left ventricular injury. {Circulation Research 1989;65:215–223)

ISSN:0009-7330    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Coronary pressure-flow relations during autoregulated and vasodilated flow states were compared between eight dogs with renovascular hypertension and left ventricular hypertrophy and 12 normal dogs. Each relation was constructed from serial steady-state measurements of end-diastolic coronary pressure and flow during perfusion of the circumflex artery by an extracorporeal circuit at controlled diastolic pressures of 20–200 mm Hg. Autoregulated pressure-flow relations were compared at three levels of myocardial oxygen demand: resting, high (dobutamine 10 /μ/kg/min), and low (propranolol 2.5 /μ/kg/min). Autoregulatory capacity was assessed by calculation of closed-loop flow gain. At each level of myocardial oxygen demand, the lower limit of autoregulation occurred at higher perfusion pressures in the hypertrophy group (rest 65 ± 3, high 92 ± 4, low 66 ± 4 mm Hg) than in the normal group (rest 53 ± 2, p<0.05; high 75 ± 5, p<0.05; low 51 ± 3 mm Hg) (p<0.05). Maximum autoregulatory gain was similar in the normal and hypertrophy groups during resting and low myocardial oxygen demand but was reduced in the hypertrophy group during dobutamine studies. When coronary flow decreased below the lower limit of autoregulation, systolic shortening was reduced in both normal and hypertrophy groups. However, as the autoregulatory limits were at higher pressures in the hypertrophy group, shortening in this group deteriorated at perfusion pressures that did not affect the normal heart. Coronary pressure-flow relations during physiological (peak hyperemia after 15-second flow occlusion) and pharmacological (intracoronary adenosine 400 /μ/min) vasodilation was curvilinear and fitted by quadratic regression. During hyperemic vasodilation, maximal conductance per unit mass of myocardium was less in the hypertrophy group over a wide range of perfusion pressures. At a diastolic perfusion pressure of 80 mm Hg, maximum conductance was 4.6 ± 0.5 ml/min/100 g/mm Hg in the normal group and 3.4 ± 0.4 ml/min/100 g/mm Hg (p<0.05) in the hypertrophy group. Intracoronary adenosine elicited further vasodilation in bom groups, but maximum conductance remained less in the hypertrophy group (8.5 ± 1.7 ml/min/100 g/mm Hg at a perfusion pressure of 80 mm Hg) than in the normal group (13.5 ± 2.0 ml/min/100 g/mm Hg) (p<0.05). Maximal coronary flow reserve is reduced in left ventricular hypertrophy, with a consequent shift of the lower limit of autoregulation to higher perfusion pressures. Thus, as coronary perfusion pressure is decreased, coronary flow and myocardial shortening become unpaired at higher pressures in the hypertrophied heart than in the normal heart.

ISSN:0009-7330    

出版商:OVID    

年代:1989

数据来源: OVID