Diaphragmatic fatigue may play an important role in precipitating acute respiratory failure. Pharmacologically, theophylline and beta-2 agonists have been used to improve diaphragmatic contractility. We designed experiments to study the effects of albuterol, a beta-2 agonist, on diaphragmatic fatigue in humans. In 5 normal subjects, fatigue was induced by breathing through an inspiratory resistance. Studies were done at 2 levels of diaphragmatic tension-time index (TTdi) of 0.25 and 0.30. At each TTdi, either placebo or albuterol (4 mg three times daily) was taken for 3 days. All subjects experienced side effects of sympathetic stimulation. Albuterol did not significantly increase the strength of the fresh diaphragm. With a TTdi of 0.25, values for mean endurance time were 649 +/- 250 (mean +/- SE) and 552 +/- 161 s, respectively, in placebo and albuterol runs. Respective values for TTdi of 0.30 were 109 +/- 14 and 143 +/- 27 s. During recovery, the mean values for the time needed for maximal transdiaphragmatic pressure (Pdimax) to reach 90% of the prefatigue Pdimax were 891 +/- 370 and 1043 +/- 394 s, respectively, for placebo and albuterol runs (TTdi = 0.25). Respective values for TTdi of 0.30 were 219 +/- 57 and 231 +/- 108 s. We conclude that, in humans, albuterol has no significant effect on the strength of the fresh or fatigued diaphragm, diaphragm endurance time, or the recovery of Pdimax from fatigue.
Seven children with neuromuscular disease were placed on mechanical ventilation before the age of 2 years. The outcome for these patients was variable and did not correlate with primary diagnosis. There appeared to be a high correlation between the incidence of electrocardiogram changes and death. Our experience demonstrates that there was a high mortality rate (57%) in neuromuscular patients supported by mechanical ventilation before the age of 2 years.
Because aspirin (ASA) is often reported to have an adverse effect on pulmonary function in children with chronic asthma, acetaminophen is commonly used as an ASA substitute in these children. To study acetaminophen effects on pulmonary functions, double-blind, oral challenges of ASA (600 mg), acetaminophen (600 mg), or lactose were administered on separate days to 25 chronic asthmatics, ten boys and 15 girls, ranging in age from 8 to 18 years (mean age ± 1 SD: 12.5 ± 2.8 years). No patient had a past history of adverse reactions to either drug. Forced expiratory volume in 1 second (FEV1), peak expiratory flow rate (PEFR), maximal mid-expiratory flow rate (FEF25-75), forced vital capacity (FVC), maximal voluntary ventilation (MVV), and flow volume curves were measured at base line and ½, 1, 2, 3, and 4 hours after ingestion of drug or placebo. Persistent decreases from base line FEV1 (> 20%) or FEF25-75 (> 30%) occurred in four ASA- and two acetaminophen-challenged patients. One ASA-sensitive patient was placebo intolerant; another reacted to acetaminophen. The acetaminophen responses were of less intensity than the ASA responses. Analysis of group mean pulmonary function responses to ASA, acetaminophen, and lactose showed no significant difference among the three agents at any time. Aspirin should be used cautiously in asthmatic children. Acetaminophen appears to be an adequate, although not completely, innocuous ASA substitute.
a-Thrombin, a serine protease with potent procoagulant activity, has the capacity to stimulate the proliferation of fibroblasts, vascular endothelial cells and macrophages. However, for the latter cell type, esterolytically intact enzyme is not required and, in fact, the mitogenic potency of the molecule appears to reside in a limited unique region of thrombin termed the 8-loop peptide (B-LP). In an attempt to determine the mechanism by which B-LP mediates mitogenesis, B-LP sensitive 5774.1 macrophage cells were fixed in paraformaldehyde and incubated for 1 hr with lZ51 BzLP in the presence and absence of exogenous unlabeled ligand (10 'O-l0-~)(n=5).The data show that the 5744.1 cells possess a specific, saturable B-LP receptor that exhibits a Kd of -1.12 nM; a value that coincides with the concentration of peptide necessary to optimally elicit a mitogenic response in these cells. Native a-thrombin, inactivated DIPthrombin and unlabeled B-LP displace bound lZ5-labeled B-LP from 5774 cells at equimolar concentrations suggesting that all the 3 peptides interact with a common receptor site on macrophages.Scatchard analysis indicates that -4000 such receptors are present per cell. We suggest that ligand activation of these receptors is responsible for triggering the biological response associated with thrombin-stimulated macrophages, and therefore, is likely pivotal in promoting the accumulation of these cells during the processes of inflammation and wound healing. Table). IOSS OF HEPATITlSEvidence of HBsAb (n=37) or exposure to hepatitis vaccine (n=10) was found in 87% of HTLV-111 positive patients at some time during their care i n our clinic. However, 17% demonstrated subsequent antibody loss and/or did not respond to hepatitis vaccine. This unusual HBsAb response was restricted to patients < 17 years of age (63% of all patients). This result contrastFd to only a 2% loss of HBsAb or vaccine non-response in the HTLV-111 negative patients who had previously been positive for HBsAb (n=24) or were given the hepatitis vaccine (n=16). This result suggests that loss or a1 teration of hepatitis B immunity in children occurs as a result of HTLV-I11 infection or exposure. The hematologic manifestations of 100 pediatric patients with AIDSIARC were reviewed. Acute or chronic anemia was present in 94% of all patients. Two patients had autoimmune hemolytic anemia and 1 patient had an aplastic anemia. A positive Coombs test was detected in 40% of all patients. Leukopenia and neutropenia occurred in 50% and 40% of patients respectively. Antineutrophil antibodies were detected in 2 patients. Ten of 13 children developed neutropenia on Bactrim. Forty percent of all children were lymphopenic. Monocytosis and eosinophilia occurred in 66% and 40% of patients respectively. Thrombocytopenia was seen in 33% and of these 25% developed a persistent thrombocytopenia. Platelet antibodies were detected in 10 of 11 patients. Pancytopenia occurred in 20% of children with opportunistic infection (0.1.).Acquired Von Willebrands disease and auto...
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