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PubMed1984

Effects of CO2 and bronchoconstriction on costal and crural diaphragm electromyograms.

To determine if neural control of the crural diaphragm is similar to that of the costal diaphragm, electrical activity was recorded from these two parts of the diaphragm in 10 anesthetized dogs during resting O2 breathing and during progressive hyperoxic hypercapnia. Within a breath, the onset of crural diaphragm inspiratory activity started significantly earlier than that of the costal diaphragm under both resting and CO2 stimulated conditions, although the relative delay in costal diaphragm activity was smaller during hypercapnia than during resting O2 breathing. Following hyperventilation to apnea, both parts of the diaphragm resumed activity on the same breath. During CO2 rebreathing, the maximal increase in crural diaphragm peak electrical activity was significantly greater than that of the costal diaphragm. We also examined the effects of histamine-induced bronchoconstriction on diaphragm activity. Following administration of histamine aerosol there was a transient of irregular breathing during which in three animals costal diaphragm activity became nearly quiet, although there was continued activity of the crural diaphragm. Once breathing became more regular, there was a significantly greater stimulation of crural diaphragm than costal diaphragm activity; this difference persisted for 15 min after histamine inhalation. These results support the concept that electrical activity can be distributed nonuniformly to the costal and crural diaphragm and demonstrate that the crural diaphragm has a greater gain with hypercapnia and bronchoconstriction than does the costal diaphragm.

Aerosols↗
PubMed1985

Catabolism of branched-chain amino acids by diaphragm muscles of fasted and diabetic rats.

In vitro catabolism of branched-chain amino acids, leucine and valine, was investigated using diaphragm muscles from normal, streptozotocin-diabetic and overnight fasted rats. Oxidation and transamination of [1-14C] branched-chain amino acids were both stimulated to a similar extent by diabetes or fasting, when diaphragms were incubated with glucose. Transamination of leucine and valine was increased when diaphragms were incubated with pyruvate; stimulation of transamination was greatest in diaphragms from diabetic rats. Leucine and valine oxidation by control diaphragms was inhibited by pyruvate while it was unchanged or slightly stimulated in diaphragms from fasted or diabetic rats. Thus diaphragms from diabetic rats oxidized two to threefold more branched-chain amino acids than controls when they were incubated with pyruvate. The specific radioactivity of extracellular alpha-ketoisocaproate (KIC; the product of leucine transamination) produced by diaphragms incubated with [14C]leucine was similar for all groups (fed, fasted, or diabetic) in the presence or absence of pyruvate. Oxidation of [1-14C]KIC by diaphragms from fasted or diabetic rats, incubated with glucose, was the same or less than KIC oxidation by control diaphragms. Incubation with pyruvate inhibited KIC oxidation by control diaphragms to a significantly greater degree than that by diaphragms from diabetic or fasted rats. These data suggest the following Flux through branched-chain amino acid transaminase is limited by the availability of amino group acceptors in diaphragms from normal and overnight fasted rats, and to a greater extent in diaphragms from diabetic rats. Flux through the transaminase may be a major determinant of accelerated branched-chain amino acid oxidation by diaphragms in fasting and diabetes. In diaphragms of fasted and diabetic rats, flux through the branched-chain alpha-ketoacid dehydrogenase complex is resistant to inhibition by pyruvate, which is normally observed in controls.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2002

Structural and oxidative enzyme characteristics of the diaphragm.

During exercise, the horse can achieve oxygen uptakes and ventilations in excess of 200 ml/kg/min and 1800 l/min, respectively. Whether the diaphragm has the capacity to contribute substantially to inspiratory effort in the exercising horse is not known. To investigate the potential for the horse diaphragm to generate tension, lung displacement and sustain ventilatory function, we measured diaphragm thickness, muscle length and oxidative enzyme activity (citrate synthase) within the ventral, medial and dorsal costal and crural diaphragm. In the diaphragms of 6 mature horses (5 Thoroughbreds, one Quarter Horse; body mass (mean +/- s.e.) 475 +/- 14 kg, age 4 +/- 1 years), the mass of the freshly-excised diaphragm was 4.54 +/- 0.19 kg of which 79% was the costal diaphragm, 17% the crural diaphragm and 4% the central tendon. The medial costal region (2.1 +/- 0.1 cm) was significantly thicker (P<0.05) than either the ventral (1.4 +/- 0.1 cm) or dorsal (1.2 +/- 0.2 cm) costal regions and the crural diaphragm was significantly thicker (>3.2 +/- 0.3 cm, P<0.05) than any costal diaphragm region. With respect to the costal diaphragm, excised muscle length was greatest (P<0.05) in the medial costal (17.2 +/- 1.0 cm) than either the ventral costal (<12.6 +/- 1.5 cm) or dorsal costal (<13.9 +/- 1.8 cm) regions and therefore the medial region would be expected to exhibit the greatest absolute length change on inspiration. Citrate synthase activity was high throughout the diaphragm (40.8 +/- 113 to 55.3 +/- 9.7 micromol/g/min), but was not significantly different among regions. These structural characteristics and the oxidative potential of the horse diaphragm are consistent with the diaphragm providing a significant and substantial contribution to the inspiratory effort during exercise in the horse. Consequently, clinical and physiological investigations of exercise performance should not ignore the potentially crucial importance of the diaphragm.

Animals↗
PubMed2004

Crural diaphragm inhibition during esophageal distension correlates with contraction of the esophageal longitudinal muscle in cats.

Esophageal distension causes simultaneous relaxation of the lower esophageal sphincter (LES) and crural diaphragm. The mechanism of crural diaphragm relaxation during esophageal distension is not well understood. We studied the motion of crural and costal diaphragm along with the motion of the distal esophagus during esophageal distension-induced relaxation of the LES and crural diaphragm. Wire electrodes were surgically implanted into the crural and costal diaphragm in five cats. In two additional cats, radiopaque markers were also sutured into the outer wall of the distal esophagus to monitor esophageal shortening. Under light anesthesia, animals were placed on an X-ray fluoroscope to monitor the motion of the diaphragm and the distal esophagus by tracking the radiopaque markers. Crural and costal diaphragm electromyograms (EMGs) were recorded along with the esophageal, LES, and gastric pressures. A 2-cm balloon placed 5 cm above the LES was used for esophageal distension. Effects of baclofen, a GABA(B) agonist, were also studied. Esophageal distension induced LES relaxation and selective inhibition of the crural diaphragm EMG. The crural diaphragm moved in a craniocaudal direction with expiration and inspiration, respectively. Esophageal distension-induced inhibition of the crural EMG was associated with sustained cranial motion of the crural diaphragm and esophagus. Baclofen blocked distension-induced LES relaxation and crural diaphragm EMG inhibition along with the cranial motion of the crural diaphragm and the distal esophagus. There is a close temporal correlation between esophageal distension-mediated LES relaxation and crural diaphragm inhibition with the sustained cranial motion of the crural diaphragm. Stretch caused by the longitudinal muscle contraction of the esophagus during distension of the esophagus may be important in causing LES relaxation and crural diaphragm inhibition.

Animals↗
PubMed2002

Treatment and prevention of diaphragm fatigue using low-dose dopamine.

There is increasing evidence that diaphragm fatigue is a major cause of failure in weaning patients from mechanical ventilation. Patients in intensive care units are often administered dopamine to improve renal blood flow without regard to its effect on diaphragm blood flow. The aim of this study was to investigate if intravenous low-dose dopamine, equivalent to the dose used in intensive care units, can treat and prevent diaphragm fatigue. Diaphragm fatigue was produced in anesthetized rats by inspiratory resistance loading (IRL). The effect on diaphragm shortening, diaphragm blood flow, and aortic blood flow was determined. When diaphragm fatigue was attained, group I was given saline for 30 min while maintaining IRL. At the time of diaphragm fatigue, group II was given low-dose dopamine (2 microg/kg/min) for 30 min while maintaining IRL. In group III, dopamine administration was started before and continued throughout the period of IRL. Administering dopamine after the development of diaphragm fatigue (group II) increased diaphragm performance as measured by increased diaphragm shortening and was accompanied by an increased diaphragm blood flow. Administering dopamine prior to and throughout IRL (group III) prevented diaphragm fatigue. Low-dose dopamine can prevent and/or reverse diaphragm fatigue in rats without a significant change in aortic blood flow. This effect of dopamine may be due to increased oxygen delivery associated with the increased diaphragm blood flow, resulting in less free radical formation and thus less muscle damage.

Animals↗
PubMed2002

Cervical cap versus diaphragm for contraception.

BACKGROUND: The cervical cap and the diaphragm are vaginal barrier contraceptive methods that prevent pregnancy by covering the cervix. The two devices also act as a reservoir for spermicide. The cervical cap is smaller and can remain in place longer than the diaphragm. Two types of cervical caps, the Prentif cap and the FemCap, have been compared to the diaphragm in randomized controlled trials. OBJECTIVES: The review seeks to evaluate the contraceptive efficacy, safety, discontinuation, and acceptability of the cervical cap with that of the diaphragm. SEARCH STRATEGY: We searched MEDLINE, Popline, Cochrane Controlled Trials Register, EMBASE, and LILACS for randomized controlled trials of cervical caps, and we reviewed the references of the included publications. Also, we wrote to the manufacturers and known investigators to request information about any other published or unpublished trials not found in our search. SELECTION CRITERIA: All randomized controlled trials in any language comparing a cervical cap with a diaphragm were eligible for inclusion. DATA COLLECTION AND ANALYSIS: All titles and abstracts located in the literature searches were assessed, and articles identified for inclusion were independently abstracted by two reviewers. Data were entered and analyzed with RevMan 4.1, and a second reviewer verified the data entered. Outcome measures include contraceptive efficacy, safety, discontinuation, and acceptability. Outcomes were calculated as Peto odds ratios with 95 percent confidence intervals using women as the denominators. Life-table and Kaplan-Meier cumulative rate ratios for selected measures were also presented in "Additional Tables." MAIN RESULTS: The Prentif cap was comparable to the diaphragm in preventing pregnancy, but the FemCap was not as effective in preventing pregnancy as its comparison diaphragm. The curves for the life-table cumulative pregnancy rates through 24 months for the Prentif cap and the diaphragm were not statistically significantly different (p-value of 0.39). However, the six-month Kaplan-Meier cumulative pregnancy rates for the FemCap and the diaphragm did not meet the a priori definition of clinical equivalence. The Prentif cap had a higher proportion of Class I to Class III cervical cytologic conversions at the three-month visit than the diaphragm; the odds ratio was 2.3 (95% CI, 1.0-5.1). The FemCap trial did not find differences in Papanicolaou smear results between the cap and diaphragm groups. Prentif cap users had a lower odds ratio of vaginal ulcerations or lacerations (0.3; 95% CI, 0.1-0.7) than diaphragm users. FemCap users had a higher odds ratio of blood in the device on removal (2.3; 95% CI, 1.3-4.1), but a lower odds ratio of urinary tract infections (0.6; 95% CI, 0.4-1.0) than those in the diaphragm group. In the FemCap trial, similar proportions of women reported liking their assigned device "somewhat" or "a lot" at the two-week interview. However, FemCap users were less likely than the diaphragm users to state that they were "probably" or "definitely" likely to use the device alone after completing the trial (odds ratio of 0.5; 95% CI, 0.3-0.7) or that they would recommend it to a friend (odds ratio of 0.5; 95% CI, 0.3-0.8). REVIEWER'S CONCLUSIONS: The Prentif cap was as effective as its comparison diaphragm in preventing pregnancy, but the FemCap was not. Both cervical caps appear to be medically safe.

Adult↗
PubMed1983

The synthesis and release of acetylcholine in normal and denervated rat diaphragms during incubation in vitro.

1. Normal and denervated rat diaphragms and neural (central) and aneural (peripheral) parts of normal diaphragms were incubated under several different conditions likely to affect the metabolism of acetylcholine (ACh), with the aim of discovering specific features of the control of neural and aneural ACh in the muscle. The concentrations of ACh in the tissue and the medium were measured at the end of the incubations using a radioenzymatic assay, and the amount of ACh synthesized during the incubations was calculated by subtracting the initial amount of ACh present in the tissue from that found in the tissue plus the medium at the end of the incubations.2. Confirming earlier results obtained with bioassays, it was found that, in a medium with 5 mM-K(+) and 2.5 mM-Ca(2+), denervated diaphragms released ACh into the medium at a rate equal to 47% of that observed in normal diaphragms; the amount of ACh released from aneural parts of normal diaphragms was 51% of that released from their neural parts. The release from normal diaphragms was increased (83%) in a Ca(2+)-dependent manner by raising the concentration of K(+) to 30 mM. In the denervated diaphragms, 30 mM-K(+) brought about a Ca(2+)-independent increase (67%) in the rate of ACh release. The elevation of K(+) was without effect on the release of ACh from aneural parts of normal diaphragms.3. The results indicate that a Ca(2+)-dependent mechanism of ACh release, known to function in the nerve terminals, is not likely to participate in the efflux of ACh from the muscle fibres. The K(+)-induced but Ca(2+)-independent enhancement of ACh release from the denervated diaphragms probably occurs by diffusion of ACh along the altered electrochemical gradient. It is suggested that the surface membranes of the muscle fibres become more permeable to ACh after denervation.4. During incubations with 30 mM-K(+) and 10 muM-hemicholinium-3 (HC-3), an inhibitor of the carrier-mediated transport of choline, the rates of ACh release and synthesis in normal diaphragms were diminished to the levels found in the denervated diaphragms, in which the concentration, release and synthesis of ACh were not affected by HC-3. The synthesis of aneural ACh thus appears to be independent of the carrier-mediated supply of choline across cell membranes.5. The release of ACh from normal diaphragms incubated with 5 mM-K(+) was increased in the presence of 100 muM-ouabain, whereas the release from denervated diaphragms was not affected. This finding suggests that the mechanism of ACh release that is activated by ouabain in the nerve cells involves, in addition to the inhibition of Na(+)-K(+)-ATPase, some other steps which are not operative in the muscle fibres.6. The results corroborate earlier evidence indicating that aneural ACh is produced, stored and released in the diaphragms. They fit the view that the aneural ACh is located in the cytoplasm of the muscle fibres and that it leaves the muscle fibres by molecular ;leakage' rather than by a specialized release mechanism. The efflux of ACh from the muscle fibres is likely to constitute about 50% of the total resting efflux (release) of ACh from normal diaphragms.

Acetylcholine↗
PubMed1998

Effects of lung volume on diaphragm EMG signal strength during voluntary contractions.

The use of esophageal recordings of the diaphragm electromyogram (EMG) signal strength to evaluate diaphragm activation during voluntary contractions in humans has recently been criticized because of a possible artifact created by changes in lung volume. Therefore, the first aim of this study was to evaluate whether there is an artifactual influence of lung volume on the strength of the diaphragm EMG during voluntary contractions. The second aim was to measure the required changes in activation for changes in lung volume at a given tension, i.e., the volume-activation relationship of the diaphragm. Healthy subjects (n = 6) performed contractions of the diaphragm at different transdiaphragmatic pressure (Pdi) targets (range 20-160 cmH2O) while maintaining chest wall configuration constant at different lung volumes. The diaphragm EMG was recorded with a multiple-array esophageal electrode, with control of signal contamination and electrode positioning. The effects of lung volume on the EMG were studied by comparing the crural diaphragm EMG root mean square (RMS), an index of crural diaphragm activation, with an index of global diaphragm activation obtained by normalizing Pdi to the maximum Pdi at the given muscle length (Pdi/Pdimax@L) at the different lung volumes. We observed a direct relationship between RMS and Pdi/Pdimax@L independent of diaphragm length. The volume-activation relationship of the diaphragm was equally affected by changes in lung volume as the volume-Pdi relationship (60% change from functional residual capacity to total lung capacity). We conclude that the RMS of the diaphragm EMG is not artifactually influenced by lung volume and can be used as a reliable index of diaphragm activation. The volume-activation relationship can be used to infer changes in the length-tension relationship of the diaphragm at submaximal activation/contraction levels.

Adult↗