PubMed · 6454409
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J E Murtagh. 1981. Exercises for your back.. https://pubmed.ncbi.nlm.nih.gov/6454409/
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OBJECTIVE: A thick endothelial glycocalyx provides the endothelial surface with a nonadherent shield. Oxidized LDL (Ox-LDL) degrades the endothelial glycocalyx. We hypothesized that glycocalyx degradation stimulates leukocyte-endothelial cell adhesion, whereas intravascular supplementation with sulfated polysaccharides reconstitutes the endothelial glycocalyx and attenuates Ox-LDL-induced leukocyte-endothelial cell adhesion. METHODS AND RESULTS: Degradation of the endothelial glycocalyx by local microinjection of heparitinase (10 to 50 U/mL) into mouse cremaster venules dose-dependently increased the number of adherent leukocytes. Systemic administration of Ox-LDL (0.4 mg/100 g body weight) induced 10.1+/-0.9 adherent leukocytes/100 microm at 60 minutes. In the venules perfused with 500-kDa dextran sulfate (1 mg/mL), the number of adherent leukocytes at 60 minutes after Ox-LDL bolus application was not influenced (9.2+/-1.0 leukocytes/100 microm). However, the venules locally perfused with heparan sulfate (10 mg/mL) or heparin (1 mg/mL) displayed a significantly lower number of adherent leukocytes induced by Ox-LDL: 5.1+/-0.7 and 5.4+/-0.9 leukocytes/100 microm, respectively (P<0.05). Fluorescently labeled heparan sulfate and heparin, but not dextran sulfate, attached to the venule luminal surface after Ox-LDL administration. CONCLUSIONS: Endothelial glycocalyx degradation stimulates leukocyte immobilization at the endothelial surface. Circulating heparan sulfate and heparin attach to the venule wall and attenuate Ox-LDL-induced leukocyte immobilization.
In prior experiments that employed the transneuronal transport of isogenic recombinants of pseudorabies virus (PRV), we demonstrated that neurons located ventrally in the medial medullary reticular formation (MRF) of the ferret provide collateralized projections to both diaphragm and abdominal muscle motoneurons as well as to multiple abdominal muscle motoneuron pools. The goal of the present study was to determine whether single MRF neurons also furnish inputs to diaphragm motoneurons and those innervating an airway muscle with inspiratory-related activity: the tongue protruder genioglossus. For this purpose, PRV recombinants expressing unique reporters (beta-galactosidase or enhanced green fluorescent protein) were injected into either the diaphragm or the genioglossal muscle. The virus injections produced transneuronal infection of overlapping populations of MRF neurons. A small proportion of these neurons (<15%) was infected by both PRV recombinants, which indicated that they provide collateralized inputs to genioglossal and diaphragm motoneurons. These findings show that, whereas some MRF neurons simultaneously influence the activity of upper airway and respiratory pump muscles, other cells in this brain stem region independently contribute to diaphragm and genioglossal muscle contraction regulation.
Inspiratory muscle weakness due to lung hyperinflation and muscle wasting may occur in cystic fibrosis. We therefore measured diaphragm function and bulk in 18 stable patients with cystic fibrosis and 15 matched control subjects; the abdominal and quadriceps muscles were studied for comparison. We assessed diaphragm mass, abdominal muscle thickness, twitch transdiaphragmatic and gastric pressures, quadriceps cross-section and isokinetic strength, and lean body mass. Lean body mass, quadriceps strength, and quadriceps cross-section were lower in patients with cystic fibrosis. Twitch transdiaphragmatic pressure was 23% lower and twitch gastric pressure was 22% greater in patients with cystic fibrosis than in control subjects, but diaphragm mass and abdominal muscle thickness were similar in the two groups. For any given lean body mass and quadriceps cross-section, patients with cystic fibrosis had greater diaphragm mass and abdominal muscle thickness. Diaphragm mass had greater intersubject variability in patients with cystic fibrosis than in control subjects. We conclude that diaphragm strength is decreased but abdominal muscle strength is increased in patients with cystic fibrosis. Diaphragm and abdominal muscle bulk are not affected by the general muscle wasting, which suggests that there may be a training effect of cystic fibrosis on respiratory muscles. However, the variability of diaphragm mass indicates that this beneficial response does not occur in all patients with cystic fibrosis.