Klein L W, Askenase A D, Weintraub W S, Akaishi M, Mercier R J, Schneider R M, Agarwal J B, Helfant R H
Mid-Atlantic Heart and Vascular Institute, Presbyterian University of Pennsylvania Medical Center, Philadelphia 19104.
Cardiovasc Res. 1987 Feb;21(2):99-106. doi: 10.1093/cvr/21.2.99.
In a study to test the hypothesis that vascular reserve is exhausted in the setting of a resting blood flow deficit, the left anterior descending or circumflex artery was cannulated and perfused from the left carotid artery. After reactive hyperaemia had been assessed a stenosis was produced with a screw clamp. In the first experiment a moderate stenosis (diastolic perfusion pressure 40 mmHg) was produced in the left anterior descending artery (three dogs) or left circumflex artery (three dogs). Blood pressure was held constant with aortic constriction during intracoronary adenosine infusion (6 mumol.min-1). The stenosis was then adjusted to the preadenosine perfusion pressure. In the second experiment the anterior interventricular coronary vein was also isolated and segment length crystals were placed in the ischaemic and non-ischaemic zones. Severe stenosis (flow reduction of at least 50% and evidence of decreased segmental shortening) was produced in the cannulated left anterior descending artery (eight dogs). Intracoronary adenosine was given with aortic pressure held constant by transfusion and coronary venous drainage. In the first experiment resting coronary flow (ml.min-1) decreased from 41(3) to 29(6) (p less than 0.05) with stenosis. Coronary flow increased from 29(6) to 34(7) (p less than 0.05) with adenosine and to 50(10) (p less than 0.05) with stenosis adjustment. Subendocardial flow (ml.g-1.min-1) decreased from 0.89(0.26) to 0.78(0.23) (p less than 0.05) with adenosine and then increased from 0.94(0.49) with perfusion pressure adjustment. Subepicardial flow tended to increase with adenosine, and increased further with stenosis adjustment.(ABSTRACT TRUNCATED AT 250 WORDS)
在一项旨在检验静息血流不足时血管储备已耗尽这一假设的研究中,通过左颈动脉对左前降支或回旋支动脉进行插管和灌注。在评估反应性充血后,用螺旋夹造成狭窄。在第一个实验中,在左前降支动脉(三只狗)或左回旋支动脉(三只狗)造成中度狭窄(舒张期灌注压40 mmHg)。在冠状动脉内注入腺苷(6 μmol·min⁻¹)期间,通过主动脉缩窄使血压保持恒定。然后将狭窄调整至腺苷灌注前的压力。在第二个实验中,还分离了前室间冠状静脉,并在缺血区和非缺血区放置节段长度晶体。在插管的左前降支动脉(八只狗)造成严重狭窄(血流减少至少50%且有节段缩短减少的证据)。通过输血和冠状静脉引流使主动脉压力保持恒定时给予冠状动脉内腺苷。在第一个实验中,狭窄时静息冠状动脉血流(ml·min⁻¹)从41(3)降至29(6)(p<0.05)。腺苷使冠状动脉血流从29(6)增至34(7)(p<0.05),狭窄调整后增至50(10)(p<0.05)。腺苷使心内膜下血流(ml·g⁻¹·min⁻¹)从0.89(0.26)降至0.78(0.23)(p<0.05),然后灌注压调整后从0.94(0.49)增加。心外膜下血流腺苷时趋于增加,狭窄调整后进一步增加。(摘要截断于250字)