PubMed · 28579
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M J Halhuber. 1978. [Angina pectoris].. https://pubmed.ncbi.nlm.nih.gov/28579/
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Mice lacking catecholamines die before birth, some with cardiovascular abnormalities. To investigate the role of catecholamines in development, embryonic day 12.5 (E12.5) fetuses were cultured and heart rate monitored. Under optimal oxygenation, wild-type and catecholamine-deficient fetuses had the same initial heart rate (200-220 beats/min), which decreased by 15% in wild-type fetuses during 50 min of culture. During the same culture period, catecholamine-deficient fetuses dropped their heart rate by 35%. Hypoxia reduced heart rate of wild-type fetuses by 35-40% in culture and by 20% in utero, assessed by echocardiography. However, catecholamine-deficient fetuses exhibited greater hypoxia-induced bradycardia, reducing their heart rate by 70-75% in culture. Isoproterenol, a beta-adrenergic receptor (beta-AR) agonist, reversed this extreme bradycardia, restoring the rate of catecholamine-deficient fetuses to that of nonmutant siblings. Moreover, isoproterenol rescued 100% of catecholamine-deficient pups to birth in a dose-dependent, stereo-specific manner when administered in the dam's drinking water. An alpha-AR agonist was without effect. When wild-type fetuses were cultured with adrenoreceptor antagonists to create pharmacological nulls, blockade of alpha-ARs with 10 microM phentolamine or beta-ARs with 10 microM bupranolol alone or in combination did not reduce heart rate under optimal oxygenation. However, when combined with hypoxia, beta-AR blockade reduced heart rate by 35%. In contrast, the muscarinic blocker atropine and the alpha-AR antagonist phentolamine had no effect. These data suggest that beta-ARs mediate survival in vivo and regulate heart rate in culture. We hypothesize that norepinephrine, acting through beta-ARs, maintains fetal heart rate during periods of transient hypoxia that occur throughout gestation, and that catecholamine-deficient fetuses die because they cannot withstand hypoxia-induced bradycardia.
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BACKGROUND: Primary care organisations are faced with implementing a large number of guideline recommendations. We present methods by which the number of eligible patients requiring treatment, and the relative benefits to the whole population served by a general practice or Primary Care Trust, can be calculated to help prioritise between different guideline recommendations. METHODS: We have developed measures of population impact, "Number to be Treated in your Population (NTP)" and "Number of Events Prevented in your Population (NEPP)". Using literature-based estimates, we have applied these measures to guidelines for pharmacological methods of secondary prevention of myocardial infarction (MI) for a hypothetical general practice population of 10,000. RESULTS: Implementation of the NICE guidelines for the secondary prevention of MI will require 176 patients to be treated with aspirin, 147 patients with beta-blockers and with ACE-Inhibitors and 157 patients with statins (NTP). The benefit expressed as NEPP will range from 1.91 to 2.96 deaths prevented per year for aspirin and statins respectively. The drug cost per year varies from euro 1940 for aspirin to euro 60,525 for statins. Assuming incremental changes only (for those not already on treatment), aspirin post MI will be added for 37 patients and produce 0.40 of a death prevented per year at a drug cost of euro 410 and statins will be added for 120 patients and prevent 2.26 deaths per year at a drug cost of euro 46,150. An appropriate policy might be to reserve the use of statins until eligible patients have been established on aspirin, ACE-Inhibitors and beta blockers. CONCLUSIONS: The use of population impact measures could help the Primary Care Organisation to prioritise resource allocation, although the results will vary according to local conditions which should be taken into account before the measures are used in practice.