{'fraction_non_alphanumeric': 0.01622002820874471, 'fraction_numerical': 0.013399153737658674, 'mean_word_length': 5.1965065502183405, '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}}
Central haemodynamic and forearm vascular effects of morphine in patients after open heart surgery.

Central haemodynamic and forearm vascular changes following administration of morphine i.v. were studied in patients 24--30 h after open heart surgery. Right atrial pressure, heart rate, mean arterial pressure, cardiac output and stroke volume were measured before and after morphine 5 and 10 mg per 70 kg in 14 subjects. In a further group of eight subjects, forearm blood flow was measured after morphine 10 mg per 70 kg. Total systemic and forearm vascular resistance were derived from these measurements. In spite of wide individual variations, significant decreases in mean arterial pressure occurred in most of the patients and appeared to be dose related. Significant decreases in mean cardiac index were noted only after morphine 10 mg per 70 kg. Forearm blood flow increased consistently and significantly and there was a corresponding decrease in vascular resistance. The decrease in mean arterial pressure and the change in forearm vascular resistance indicated that vasodilatation was probably the principle cause of the decrease in arterial pressure, whereas the sustained decrease in cardiac output seemed to indicate an effect on venous capacitance. The predominant action of morphine appears to be peripheral, causing a decrease in vascular resistance and, possibly, an increase in venous capacitance.