{'fraction_non_alphanumeric': 0.06547619047619048, 'fraction_numerical': 0.03741496598639456, 'mean_word_length': 4.051502145922747, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Effects of hypoxia and reoxygenation on maximum rate of early left ventricular filling.

Left ventricular early filling during hypoxia and reoxygenation was examined in isolated working rat hearts that contracted 300 times/min when perfused with Krebs-Henseleit solution at 37 degrees C. Left ventricular short-axial diameter (LVD = D) was measured with a pair of ultrasonic crystals. The maximum lengthening velocity of LVD [(dD/dt)max] decreased with hypoxia and recovered after reoxygenation (from a control of 20.3 +/- 6.7 to 7.3 +/- 1.7 mm/s after 15 min of hypoxia and to 16.3 +/- 8.1 mm/s after 15 min of reoxygenation; n = 7). However, (dD/dt)max/delta D (where delta D is systolic shortening) showed no significant change with either hypoxia or reoxygenation (from a control of 21.0 +/- 2.9 l/s to 22.2 +/- 2.7 l/s after 15 min of hypoxia and to 22.5 +/- 3.7 l/s after 15 min of reoxygenation; n = 7). Therefore, we concluded that the changes of (dD/dt)max with hypoxia and reoxygenation were caused by the changed systolic shortening and that left ventricular myocardial recoil, expressed by (dD/dt)max/delta D, showed no change with either hypoxia or reoxygenation.