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At least 19 recordsLinked to original sources
PubMed2001

Diaphragm versus diaphragm with spermicides for contraception.

BACKGROUND: The diaphragm is usually used with a spermicide. However, some practitioners have suggested that spermicides offer no additional contraceptive protection and have advocated alternative guidelines for the use of diaphragms. OBJECTIVES: The objective of this review was to compare the effectiveness, safety and acceptability of the diaphragm with and without spermicide. SEARCH STRATEGY: We searched MEDLINE, EMBASE, POPLINE, CINAHL, the Cochrane Controlled Trials Register, and reference lists of relevant articles. In addition, we contacted experts in the field to identify unpublished studies. SELECTION CRITERIA: Randomized controlled trials comparing women of reproductive age using the diaphragm with and without spermicide as the sole contraceptive method that reported clinical outcomes. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data on outcomes and trial characteristics and any discrepancies were resolved by consensus or by consultation with the third reviewer. The results of the one identified study are presented descriptively. MAIN RESULTS: We identified only one study. No significant difference was found in the pregnancy rates (with typical use or consistent use) or discontinuation rates between the diaphragm-with-spermicide and diaphragm-without-spermicide groups. There was a trend towards higher pregnancy rates in the diaphragm-without-spermicide group. However, this study failed to recruit the planned number of participants and was consequently underpowered. REVIEWER'S CONCLUSIONS: As only one underpowered study was identified, we cannot distinguish between the contraceptive effectiveness of the diaphragm with and without spermicide. We cannot draw any conclusion at this point, further research is needed.

Contraception↗
PubMed1999

Magnetic resonance navigator echo diaphragm monitoring in patients with suspected diaphragm paralysis.

Real-time magnetic resonance (MR) navigator echo (NE) monitoring of the diaphragm is now possible. Using this technique, temporal changes in diaphragm position can be analyzed in a non-invasive fashion, without x-ray exposure. In this preliminary study, we have optimized three NE parameters (the NE column area, the NE repeat time, and the location of the NE on the diaphragm surface), and demonstrated the clinical application of MR NE diaphragm monitoring in patients with suspected diaphragm paralysis. The NE parameters were defined in 10 healthy volunteers, and diaphragm traces were scored for variance in NE diaphragm position registration. Using the optimal NE column parameters, we investigated four patients with diaphragm paralysis, one of whom required positive pressure ventilation while in the MR scanner, to show the utility of this technique. The NE diaphragm position registration was significantly affected by the area of the NE column, with poor position registration for the smallest column area (2.25 cm2 vs. 4 cm2 vs. 6.25 cm2, variance 6.3 vs. 0.6 vs. 0.3, P = 0.006). Diaphragm position registration was also significantly affected by the NE repeat time, with misregistration for the shortest repeat time (250 msec vs. 500 msec vs. 1000 msec, variance 11.9 vs. 0.6 vs. 1.0, P = 0.02), and data clipping, with loss of end-expiratory and end-inspiratory position registration, for the longest repeat time. Finally, if the NE was positioned too anteriorly, the diaphragm traces were of poor quality (anterior vs. dome vs. posterior, variance 11.8vs. 0.6vs. 3.2, P < 0.001). Application of the technique confirmed diaphragm paralysis in all four patients. The technique can be applied during positive pressure ventilation if necessary. The optimal NE parameters for diaphragm monitoring at 0.5 T were: column area, 400 mm2; NE repeat time; 500 msec; NE column positioned on the diaphragm dome. MR NE diaphragm monitoring provides a safe, non-invasive method of assessing diaphragm motion in patients with suspected diaphragm paralysis and may prove useful for long-term follow-up and monitoring of therapeutic interventions in these subjects.

Adult↗
PubMedDate not supplied

The effect of dobutamine infusion on fractional diaphragm thickening and diaphragm blood flow during fatigue.

BACKGROUND: Diaphragm fatigue (DF) has been implicated in respiratory failure in diseases that increase inspiratory resistance loading (IRL) and may complicate weaning of patients from mechanical ventilation. OBJECTIVE: The purpose of this study was to examine the effects of dobutamine administration (10 micro g/kg/min) on DF and to identify the mechanisms by which dobutamine augments diaphragm shortening and diaphragm blood flow (DBF) during fatigue with a rat model. METHODS: The study had an experimental design with 3 groups of Sprague-Dawley rats (n = 38) with 4 experimental periods: period 1, control; period 2, application of IRL; period 3, treatment; and period 4, recovery. DF was produced via IRL. During period 3 treatment, normal saline solution was infused in group I, dobutamine in group II, and dobutamine plus butoxamine hydrochloride in group III. The percent change in fractional diaphragm thickness (FDT) during inspiration reflected diaphragm shortening. DBF and aortic blood flow were determined with fluorescent microspheres. Diaphragm vascular resistance and systemic vascular resistance were calculated on the basis of Poiseuille's equation. RESULTS: Results indicated infusion of dobutamine increased FDT (P =.01) and DBF (P =.009) with respect to fatigue levels. The effects of dobutamine on FDT and DBF were attenuated with infusion of butoxamine hydrochloride (a beta-2 adrenoceptor antagonist) with respect to fatigue. CONCLUSION: Administration of dobutamine at a rate similar to that used clinically increased diaphragm muscle contractility (FDT) and DBF in diaphragms fatigued by IRL. The dobutamine effect on FDT may be the result of restoration of the balance between diaphragm energy consumption and energy delivery to the diaphragm by increasing DBF. Butoxamine hydrochloride attenuated the dobutamine-induced increase in DBF, indicating dobutamine produced vasodilatation via beta-2 adrenoceptors. Thus, the administration of intravenous dobutamine may be a useful adjunct in the treatment of DF.

Animals↗
PubMed1999

Delayed diaphragm recovery in 12 patients after high cervical spinal cord injury. A retrospective review of the diaphragm status of 107 patients ventilated after acute spinal cord injury.

STUDY DESIGN: The functional outcome of the diaphragm after acute spinal cord injury was reviewed over a 16 year period for 107 patients who had required assisted ventilation in the acute phase. OBJECTIVES: To quantify the incidence of recovery of diaphragm function which occurred beyond the period of acute oedema; to produce a time-related profile of this as a guide to clinicians considering phrenic nerve pacing; and to assess the value of phrenic nerve testing in predicting recovery. SETTING: The Southport Regional Spinal Injuries Centre, Southport, England. METHODS: Bilateral phrenic nerve and diaphragm integrity was assessed clinically, by spirometry, and by fluoroscopy without and with phrenic nerve stimulation. RESULTS: Thirty-one per cent of all the ventilated patients (33 cases), with a level of injury between C1 and C4 (Scale A in ASIA Impairment Scale), had diaphragmatic paralysis at the time of respiratory failure. The subsequent diaphragm recovery which appeared in seven of these patients, between 40 and 393 days (mean 143), permitted weaning from ventilatory support at 93 to 430 days (mean 246) after the acute injury, with a vital capacity of over 15 ml kg(-1) at that stage. The diaphragm recovery in a further five patients, whose vital capacity remained below 10 ml kg(-1) and who could not be fully weaned, occurred significantly later, between 84 and 569 days (mean 290), P=0.053. Negative phrenic nerve tests were followed by weaning at a later interval in several cases. By contrast, one patient with an early positive phrenic stimulation test and subsequent diaphragm activity could not be weaned from the ventilator. CONCLUSION: Twenty-one per cent of the patients with initial diaphragm paralysis were ultimately able to breathe independently after 4 and 14 months, whilst a further 15% had some diaphragm recovery. Phrenic nerve testing should be repeated at 3 monthly intervals for the first year after high tetraplegia.

Acute Disease↗
PubMed1998

Delayed diaphragm injury and diaphragm force production.

The present study was designed to examine the effect of delayed diaphragm injury produced by inspiratory resistive loading (IRL) on diaphragm force production. On Day 1, three groups of anesthetized and intubated NZW rabbits (n = 7 in each group) were subjected to moderate IRL (Pao approximately 30 cm H2O), high IRL (Pao approximately 45 cm H2O), or no load for 1.5 h. On Day 3, the baseline twitch transdiaphragmatic pressure (Pdi) and Pdi at 10 to 80 Hz were measured during bilateral phrenic stimulation and these measurements were repeated after another IRL (high level) in all three groups. Diaphragm injury was assessed by the point-counting technique. Marked diaphragm injury was observed in the high-IRL group (p < 0.01), but no significant diaphragm injury was observed in the moderate-IRL or control groups. The baseline twitch Pdi was maintained in both IRL groups, whereas the baseline Pdi-frequency values in the high-IRL group were significantly reduced at most frequencies (p < 0.05). The decreases in twitch and Pdi at different frequencies were more pronounced after the IRL on Day 3 in the high-IRL group compared with controls. Moderate IRL did not decrease diaphragm force either before or after the high IRL on Day 3. We conclude that the diaphragm injury induced by high IRL has a significant impact on diaphragm force production and the attendant force loss produced by IRL is dependent on the intensity of inspiratory loading.

Adipose Tissue↗
PubMed2001

Changes in adenine nucleotide, SOD and MDA contents and mitochondria ulteractructure during diaphragm fatigue in dogs induced by diaphragm pacing.

OBJECTIVE: To explore the possible mechanisms for the occurrence of diaphragm fatigue induced by diaphragm pacing. METHODS: The phrenic nerve of 8 dogs were exposed and subjected to stimulation with electric pulses emitted by a diaphragm pacemaker to induce diaphragm fatigue models, and the contents of ATP, ADP, AMP and AXP in the diaphragm muscles before and after diaphragm pacing were determined by high-performance liquid chromatography (HPLC). The contents of SOD and MDA were also measured and the morphological alteration of the mitochondria observed with transmission electron microscope. RESULTS: The contents of ATP, ADP, AXP and SOD were found significantly lower but MDA was higher during fatigue than those in normal conditions, while AMP content manifested no obvious change. Some mitochondria in the diaphragm muscles swelled and in a few cases, vacuolar degeneration was observed. CONCLUSIONS: The exhaustion and synthesis disturbance of ATP may explain the generation of diaphragm fatigue, and the reduction of dynamophore and ultrastructural injuries of the cells induced by oxygen free radicals may also contribute to this result.

Journal Article↗
PubMed1999

An implantable impedance pneumograph monitor for detection of diaphragm contraction and airway obstruction during diaphragm pacing.

Impedance pneumography signals were characterised during diaphragm pacing using stimulating and recording electrodes placed on the abdominal surface of the diaphragm. These measurements were useful for the detection of muscle contraction without confounding effects from stimulus artifacts. Impedance pneumography signals were measured using 23 epimysial electrodes implanted in seven dogs with 1-5 experiments on each electrode. The polarity of the change in impedance associated with diaphragm pacing differed for each recording electrode and its configuration. Thirty-four of 57 cases produced increased impedance, 11 produced decreased impedance and the remaining 12 depended on the level of diaphragm activation. Impedance pneumography signals were useful for detecting complete airway obstruction. The mean difference between the impedance measured during open and obstructed airway conditions was 80% of the open airway impedance signal. The difference between open and obstructed airway impedance measurements was a mean of 2.3 times larger with a recording electrode on the same hemidiaphragm as the stimulating electrode, compared to an electrode placed on the opposite hemidiaphragm (p < 0.05, paired t test, four dogs). In addition, the differences between open and completely obstructed airways were a mean of 2.8 times larger when the second recording electrode was placed on the thorax at the fifth intercostal space, compared to the ninth intercostal space (p < 0.05, two-factor ANOVA, one dog, two replicates). It was concluded that impedance pneumograph circuitry could be incorporated into an existing diaphragm pacer using electrodes placed on the diaphragm to provide valuable measurements of the function of the device.

Airway Obstruction↗
PubMed1999

Thickening of the diaphragm: a new computed tomography sign of diaphragm injury.

Computed tomography examination is becoming a standard method of evaluating injury in blunt trauma. This report describes a previously unreported computed tomography sign of diaphragmatic injury. A retrospective review of imaging findings was performed on eight patients with surgically proven traumatic diaphragmatic rupture. Thickening of the diaphragm was present on computed tomography in six of eight patients with surgically proven diaphragm rupture. Two patients demonstrated previously established computed tomography signs of diaphragm rupture and two patients had no findings to suggest diaphragm injury. Diaphragm thickening is associated with diaphragm rupture and may be a useful diagnostic sign in the evaluation of patients with blunt trauma.

Adult↗
PubMed2005

Effect of increased diaphragm activation on diaphragm power spectrum center frequency.

Increased transdiaphragmatic pressure, reduced muscle blood flow, and increased duty cycle have all been associated with a reduction in the center frequency (CFdi) of the diaphragm's electrical activity (EAdi). However, the specific influence of diaphragm activation on CFdi is unknown. We evaluated whether increased diaphragm activation would result in a greater decline in the CFdi when pressure-time product (PTPdi) was kept constant. Five healthy subjects performed periods of intermittent quasi-static diaphragmatic contractions with a fixed duty cycle. In separate runs, subjects targeted transdiaphragmatic pressures (Pdi) by performing end-inspiratory holds with the glottis open and expulsive maneuvers at end-expiratory lung volume (EELV). Diaphragm activation and pressures were measured with an electrode array and balloons mounted on an esophago-gastric catheter, respectively. The EAdi, which was 25+/-8%(S.D.) of maximum at EELV, increased to 61+/-8% (P<0.001) when an identical Pdi (averaging 31+/-13 cmH2O) was generated at a higher lung volume (77% of inspiratory capacity). The latter was associated with a 17% greater decline in CFdi (P=0.012). In order to reproduce at EELV, the decrease in CFdi observed at the increased lung volume, a two-fold increase in PTPdi was required. We conclude that CFdi responds specifically to increased diaphragm activation when pressure-time product remains constant.

Action Potentials↗
PubMed2003

A significant reduction of the diaphragm in mdx:MyoD-/-(9th) embryos suggests a role for MyoD in the diaphragm development.

To further investigate the role of MyoD during skeletal myogenesis, we backcrossed mdx mutant mice (lacking dystrophin) with MyoD knock-out mice to obtain viable mice with MyoD allele on a pure mdx background. However, after nine generations of backcrossing, it was not possible to obtain a viable mdx:MyoD-/- phenotype (designated as: mdx:MyoD-/-(9th)). The compound-mutant embryos were examined just before birth. Essentially normal Myf5-dependent and most of the MyoD-dependent musculature was observed. By contrast, the skeletal muscle compartment of the diaphragm was significantly reduced. The mesenchymal compartment of the diaphragm was intact and no herniations were observed. Other examined organs (e.g., liver, kidney, brain, etc.) showed no histological abnormalities. Pulmonary hypoplasia was determined as the cause of neonatal death. Therefore, using a different approach, our new data supplement our previous findings and suggest an essential role for MyoD in development of skeletal muscle of the diaphragm. The failure of mdx:MyoD-/-(9th) diaphragm to develop normally is not caused by a reduced number of satellite cells, but from the inability of stem cells to progress through the myogenic program. Our data also suggest that functions of MyoD and Myf5 (and the respective muscle precursor cell sub-populations) are not entirely redundant by term, as previously suggested, since Myf5 is not capable of fully substituting for MyoD in the diaphragm development.

Animals↗
PubMed2001

Morphological and functional recovery from diaphragm injury: an in vivo rat diaphragm injury model.

Our objective was to develop an in vivo model to study the timing and mechanisms underlying diaphragm injury and repair. Diaphragm injury was induced in anesthetized rats by the application of a 100 mM caffeine solution for a 10-min period to the right abdominal diaphragm surface. Diaphragms were removed 1, 4, 6, 12, 24, 48, 72, and 96 h and 10 days after the injury, with contractile function being assessed in strips in vitro by force-frequency curves. The extent of caffeine-induced membrane injury was indicated by the percentage of fibers with a fluorescent cytoplasm revealed by inward leakage of the procion orange dye. One hour after caffeine exposure, 32.9 +/- 3.1 (SE) % of fibers showed membrane injury that resulted in 70% loss of muscle force. Within 72-96 h, the percentage of fluorescent cells decreased to control values. Muscle force, however, was still reduced by 30%. Complete muscle strength recovery was observed 10 days after the injury. Whereas diaphragmatic fiber repair occurred within 4 days after injury induction, force recovery took up to 10 days. We suggest that the caffeine-damaged rat diaphragm is a useful model to study the timing and mechanisms of muscle injury and repair.

Animals↗
PubMed1991

[Effects of diaphragm plication for phrenic nerve paralysis on respiratory mechanics and diaphragm function].

The purpose of this study is to examine the effects of unilateral diaphragm plication for phrenic nerve paralysis on the respiratory mechanics and diaphragm function. Study 1: We performed thoracotomy (BASELINE), left phrenicotomy (INJURY) and left diaphragm plication (PLICATION) in ten dogs. After chest was closed in each condition, measured were the tidal volume (TV), respiratory rate (f), esophageal and gastric pressure swing (delta Pes, delta Pga), dynamic compliance (Cdyn) the ratio of gastric to esophageal pressure swing (delta Pga/delta Pes) and the work of breathing per liter (WOB/L) under stable spontaneous breathing. Study 2: In eight other left-phrenicotomized dogs, Pdi and fractional shortening of the costal diaphragm during contralateral electrophrenic stimulation were measured before and after plication. After plication TV, delta Pga/delta Pes, Cdyn, Pdi and fractional shortening during stimulation increased significantly, whereas Pes and WOB/L decreased significantly compared with INJURY condition. In conclusion unilateral diaphragm plication after paralysis improves the intact hemidiaphragm contractility and diaphragmatic contribution to breathing.

Animals↗
PubMed1979

[Considerations on a pathology of the diaphragm. 1st Report: the pathology of the diaphragm as a part of a pathology of respiration (author's transl)].

The first part of this paper deals with the idea of a "pathology of the diaphragm" and its special relations to the respiration on phylogenetical and ontogenetical base. A pathology of diaphragm does not exist until now. The diaphragm represents an important respiration organ in orthological and pathological conditions. The function of this organ is described and derivated from its specific anatomical structure and topographical site. In this conception the pathology of the diaphragm is a part of the complex pathology of the respiration. A systematic presentation of diaphragm diseases will follow in a second part of this paper.

Animals↗
PubMed1998

[A case of rupture of the diaphragm caused by the plication for diaphragm eventration].

A 71-year-old woman, in whom the herniation of right-sided diaphragm was diagnosed, was admitted to our hospital on ambulance car complaining of increasing right-sided chest pain and worsening of dyspnea. She was given emergency laparotomy. The transverse colon and omentum pushed the liver backward. The tight adhesion between transverse colon and diaphragm was released by using thoracotomy additionally. In pleural cavity, there was prolapsing transverse colon which was not covered with peritonium and was caused by the rupture of right-sided diaphragm. The necrotic transverse colon was resected about 30 cm length. We considered that the rupture was caused not by external injury but by inflammation after plication for diaphragm eventration three years and ten months before.

Aged↗
PubMed1988

Experimental study on diaphragm fatigue during diaphragm pacing.

An experimental study was performed to determine the main site of fatigue associated with diaphragm pacing. Using 24 mature mongrel dogs, weighing 7.5 to 12.7 kg, direct phrenic nerve pacing was conducted from the right cervical area at three different respiration rates, 37 (Group 1, n = 6), 25 (Group 2, n = 6) and 12 (Group 3, n = 6) times per minute, under fixed stimulation conditions (pulse duration, 200 microseconds; frequency, 25 Hz; pulse train repetition time, 1.2 sec). Diaphragm fatigue was defined as the reduction in transdiaphragmatic pressure (Pdi) to less than or equal to 60% of the initial value. In each animal, tidal volume (Vt), induced muscle action potential (Edi), conduction time (CT) and electrical current (E) between two electrodes were examined at various periods until fatigue. In addition, after fatigue, aminophylline (10 mg/kg) was injected and each parameter was observed for an additional 45 min. In 10 animals, the polarity of stimulation was changed from anodal to cathodal current after fatigue and changes in Pdi and Edi were examined. The time to fatigue was 70 +/- 20 min for Group 1, 149 +/- 48 min for Group 2, and 371 +/- 97 min for Group 3, showing a significant stimulation rate dependency (P less than 0.05). Vt and Edi showed a significant decrease (P less than 0.05) at fatigue in all of the groups. However, no significant differences of CT and E were seen between pre- and postfatigue values. Pdi and Edi did not change even when polarity was changed after fatigue. Following administration of aminophylline, Pdi showed a significant (P less than 0.05) increase over time in all groups: 19.8 +/- 13.5% at 5 min, 23.0 +/- 13.5% at 15 min, and 16.2 +/- 14.9% at 30 min for Group 1; 23.6 +/- 11.6% at 5 min, 27.3 +/- 15.5% at 15 min, and 19.0 +/- 16.1% at 30 min for Group 2; and 29.9 +/- 21.1% at 5 min, 29.5 +/- 18.6% at 15 min, 22.3 +/- 13.8% at 30 min, and 15.5 +/- 13.4% at 45 min for Group 3. In contrast, administration of aminophylline caused no significant changes in Edi. Based upon the finding that aminophylline was significantly effective at the time of diaphragm fatigue, it is concluded that fatigue of the muscle itself constitutes one of the contributing factors for the fatigue phenomenon associated with diaphragm pacing.

Action Potentials↗
PubMed1996

The tension-time index of the diaphragm revisited in quadriplegic patients with diaphragm pacing.

The fatigue threshold of the human diaphragm, index of its endurance and fatigability, corresponds, during spontaneous breathing, to a tension-time index (TTdi = Pdi/Pdimax x T1/Ttot (i.e., the inspiratory time over the total breath duration) of 0.15 to 0.18. We studied three quadriplegic patients with diaphragm pacing in order to reassess this threshold in patients in whom the contribution of the other respiratory muscles is lacking. Transdiaphragmatic pressure (Pdi) was obtained from the difference between gastric (Pga) and esophageal (Pes) pressures while the electromyograms (EMG) of both hemidiaphragms were recorded with surface electrodes. Four runs at different TTdi were performed on different days in each subject, varying either the Pdi developed per breath, changing the frequency of stimulation, or the T1/Ttot. The time of fatigue was defined when Pdi decreased during the trials by 35% from baseline. No evidence of transmission fatigue (i.e., decline in action potential amplitude) was observed. The TTdi at which fatigue occurred in all the quadriplegic patients was around 0.10 to 0.12, well below the values previously described. After fatigue had occurred, the force recovery during the force-frequency curve was not complete after 2 h at low frequencies, whereas at high frequencies it was fully complete at 30 min. We conclude that when respiration is accomplished only by the diaphragm, without the contribution of the other respiratory muscles, the fatigue threshold is lower than previously reported.

Action Potentials↗
PubMed2004

Does the crural diaphragm share in the contractile activity of the costal diaphragm? The concept of an "autonomous esophageal crus" and its role in esophageal competence.

BACKGROUND: We investigated the hypothesis that the esophageal crus (EC, part of the crus surrounding the esophagus) is an "individual muscle" and does not share in the contractile activity of the costal diaphragm (CD). MATERIAL/METHODS: The electric activities of the EC and the costal diaphragm (CD) were recorded in 21 subjects (12 men, 9 women, aged 41.6+/-10.4 years) scheduled for laparotomy. One needle electrode was introduced into the EC, one into each vertebral crus (VC), and one in the CD. Recording was performed before and after diaphragmatic paralysis by curarization. While the diaphragm was paralyzed, the responses of the EC and the 2 VCs to CD stimulation were registered. RESULTS: The CD had significantly higher resting motor unit action potentials (MUAPs) than the EC and the 2 VCs (p<0.05), and the EC higher MUAPs than the 2 VCs (p<0.05). During diaphragmatic contraction on inspiration or by stimulation (5 square pulses, 1 ms apart, threshold 32.2+/-6.3 mA), the MUAPs of the CD increased significantly (p<0.01), while those of the EC or VCs exhibited no significant change (p<0.05). CONCLUSIONS: The current findings suggest that the EC is an autonomous muscle which does not share in the contractile activity of the CD. The EC seems to be essentially involved in the competent mechanism of the lower esophagus and has no role in respiratory function.

Abdominal Muscles↗