LVDP and +dP/[dt.sub.max] were monitored and used as the contractility indexes.
During the reperfusion, a dramatically elevated LVEDP and significant decreases in RPP (the product of HR and
LVDP) and [+ or -]dp/dt were observed in the I/RI group ( P = 0.036).
In control group,
LVDP was maintained constantly at 50-80 mmHg.
LVDP was calculated as the difference between the LVSP and the LVEDP.
The effects of treatment on
LVDP, [+ or -]dp/[dt.sub.max], CF, and HR during reperfusion in control group, I/R group, and treated hearts were shown in Figure 1.
Furthermore, experimental hypertension is associated with higher infarct size and probability of arrhythmia following ischemia reperfusion, (9) decreased recovery of
LVDP, (8) and higher coronary resistance.
However, hearts from the multipollutant-mixture group had lower baseline
LVDP (69.2 [+ or -] 16.0 cm[H.sub.2]O) compared with the FA group (146.4 [+ or -] 14.8 cm[H.sub.2]O; p < 0.05) although there was no significant difference between the FA- and [O.sub.3]-groups (134.2 [+ or -] 5.4 cm[H.sub.2]O) (Figure 1B).
LVDP (an index of cardiac contractility) was calculated as the difference between the systolic and the diastolic pressures, and this pressure was accepted as the contractile force.
However, coadministration of RD and high-fat diet was associated with an increase in the Blood pressure, LVSP, and
LVDP.
For the ischaemic control group, the end of the reperfusion was marked by a dramatic decrease of
LVDP, HR and coronary flow compared with the pre-ischaemic values (Table 1).
female's hearts displayed better recovery of
LVDP than the hearts
Left ventricle pressures (
LVDP, left ventricle developed pressure; LVEDP, left ventricle end-diastolic pressure) were measured with a pressure transducer (Statham Gould P23ID), and the rate of pressure development (+dp/dt) and relaxation (-dp/dt) were obtained using a PowerLab 8/30 data acquisition system and analyzed by LabChart 7.0 Pro software (ADInstruments, Colorado Springs, Colorado, USA).
