Range of effective PO2 and reversibility of the myocardial response: The spontaneously beating hearts reproducibly and reversibly reacted to a decreasing-increasing oxygen ramp within the range of 0 to 9.3 kPa (Figure 2). The progressive drop in PO2 provoked tachycardia, and a decrease in S and mCv. During reoxygenation, S and mCv reached a nadir associated with diastolic relaxation and then recovered totally when PO2 returned to its initial value of 9.3 kPa. It appears that the chronotropic and inotropic parameters started to be altered at PO2 levels lower than 4 kPa.
Embryonic ‘oxygen paradox’: Chronotropic and inotropic effects of a strictly controlled normoxia-anoxia-normoxia cycle on ventricular activity is illustrated in a representative recording in Figure 3. It should be stressed that myocardium reacted rapidly (less than 10 s) to the abrupt transitions of PO2. Under anoxia (N2), HR transiently almost doubled and then decreased progressively, shortening decreased slightly, relaxation became incomplete (contracture), and mCv and mRv decreased. You will always be glad to find ventolin inhalers and enjoy your online shopping.

Response of the embryonic heart to hypoxia and reoxygenation: An in vitro model

Figure 3 Representative time course of the response of the embryonic heart to an anoxia (N2) -reoxygenation (AIR) transition. Contractions (shortening), heart rate, shortening and maximal velocities of contraction and relaxation of the ventricle wall are reported on the same time scale. Anoxia leads to transient tachycardia, contracture and decline in inotropic parameters. Reoxygenation results in a sudden ventricular arrest of about 20 s (‘oxygen paradox’). Note that the heart reacts to PO2 variations within less than 5 s. Heart rate, shortening and velocities ofcontrac-tion and relaxation recover their preanoxic values within about 1 min