{'fraction_non_alphanumeric': 0.030721966205837174, 'fraction_numerical': 0.01152073732718894, 'mean_word_length': 5.14622641509434, '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}}
Cardiovascular shunts and oxygen transport in lower vertebrates.

O2 transport in animals with normal or abnormal cardiovascular shunts is analyzed using a two-compartment model. This analysis reveals that the O2 affinity of blood is a key factor determining the arterial, venous, and tissue O2 partial pressure (PO2) levels. Depending on the value of "critical" PO2, factors that decrease O2 affinity (e.g., increased temperature and reduced pH) should increase tissue PO2 and favor increased tissue oxygenation. Species comparisons suggest that O2 affinity is closely linked to critical PO2. In contrast to the model for environmental hypoxia, hypoxia due to shunting a right-shifted O2 dissociation curve is, at sea level, always adaptive. When hypoxia due to shunting is combined with external hypoxia, a decreasing O2 affinity causes increased blood and tissue PO2 values up to a "breaking point," which varies with shunt fraction, inspired PO2, lung PCO2, and respiratory properties of the blood. External hypoxia would cause ectotherms with high preferred body temperatures (e.g., lizards) to have blood and tissue PO2 values beyond the breaking point. This led to the hypothesis, now confirmed in several species, that external hypoxia would result in a reduction of preferred body temperature.