PubMed · 4396168
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K Donat. 1971. [Angina pectoris].. https://pubmed.ncbi.nlm.nih.gov/4396168/
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To study the rate and regulation of alveolar fluid clearance in acute pneumonia, we created a model of Pseudomonas aeruginosa pneumonia in rats. To measure alveolar liquid and protein clearance, we instilled into the airspaces a 5% bovine albumin solution with 1.5 microCi of 125I-human albumin, 24 h after intratracheal instillation of bacteria. The concentration of unlabeled and labeled protein in the distal airspaces over 1 h was used as an index of net alveolar fluid clearance. Since there was histologic evidence of alveolar epithelial injury, several methods were used to measure alveolar fluid clearance, including the use of experiments in rats with blood flow and the use of experiments in rats without blood flow, so that movement across the epithelial barrier would be minimized in the latter group. The results with each method were identical. We found that P. aeruginosa pneumonia increased alveolar liquid clearance over 1 h by 48% in studies with blood flow, and by 43% in rats without blood flow, compared with respective controls (P < 0.05). In both studies, this increase was inhibited with amiloride. However, propranolol had no inhibitory effect, thus ruling out a catecholamine-dependent mechanism to explain the increase in alveolar fluid clearance. An antitumor necrosis factor-alpha neutralizing antibody, instilled into the lung 5 min before bacteria, prevented the increase in alveolar liquid clearance in rats with pneumonia (P < 0.05). Also, TNFalpha (5 microg) instilled in normal rats increased alveolar liquid clearance by 43% over 1 h compared with control rats (P < 0.05). In normal rats instilled with TNFalpha, propranolol had no inhibitory effect. In conclusion, gram-negative pneumonia markedly upregulates net alveolar epithelial fluid clearance, in part by a TNFalpha-dependent mechanism. This finding provides a novel mechanism for the upregulation of alveolar epithelial sodium and fluid transport from the distal airspaces of the lung.
OBJECTIVES: To study determinants and adverse outcomes (mortality and rehospitalization) of beta-blocker underuse in elderly patients with myocardial infarction; and whether the relative risks (RRs) of survival associated with beta-blocker use were comparable to those reported in the large randomized controlled trials (RCTs). SETTING: New Jersey Medicare population. DESIGN: Retrospective cohort design using linked Medicare and drug claims data from 1987 to 1992. PATIENTS: Statewide cohort of 5332 elderly 30-day acute myocardial infarction (AMI) survivors with prescription drug coverage, of whom 3737 were eligible for beta-blockers. MAIN OUTCOME MEASURES: beta-Blocker and calcium channel blocker use in the first 90 days after discharge and mortality rates and cardiac hospital readmissions over the 2-year period after discharge, controlling for sociodemographic and baseline risk variables. RESULTS: Only 21% of eligible patients received beta-blocker therapy; this rate remained unchanged from 1987 to 1991. Patients were almost 3 times more likely to receive a new prescription for a calcium channel blocker than for a new beta-blocker after their AMIs. Advanced age and calcium channel blocker use predicted underuse of beta-blockers. Controlling for other predictors of survival, the mortality rate among beta-blocker recipients was 43% less than that for nonrecipients (RR=0.57; 95% confidence interval [CI], 0.47-0.69). Effects on mortality were substantial in all age strata (65-74 years, 75-84 years, and > or = 85 years) and consistent with the results for elderly subgroups of 2 large RCTs. beta-Blocker recipients were rehospitalized 22% less often than nonrecipients (RR=0.78; 95% CI, 0.67-0.90). Use of a calcium channel blocker instead of a beta-blocker was associated with a doubled risk of death (RR= 1.98; 95% CI, 1.44-2.72), not because calcium channel blockers had a demonstrable adverse effect, but because they were substitutes for beta-blockers. CONCLUSIONS: beta-Blockers are underused in elderly AMI survivors, leading to measurable adverse outcomes. These data suggest that the survival benefits of beta-blockade after an AMI may extend to eligible patients older than 75 years, a group that has been excluded from RCTs.
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