PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Diaphragmatic function”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1988

Phrenic nerve function in patients with diaphragmatic weakness and systemic lupus erythematosus.

Diaphragmatic weakness has been identified as one of the pulmonary manifestations of systemic lupus erythematosus. Whether this weakness results from a neuropathic or myopathic process has not been established. Thirty patients with SLE were screened for the presence of inspiratory muscle (IM) weakness. Detailed studies were performed in nine with IM weakness. All nine were found to have diaphragmatic weakness (mean +/- SD, maximal transdiaphragmatic pressure 50 +/- 12 cmH2O). Phrenic nerve latencies, evaluated using transcutaneous stimulation, were normal in all individuals excluding a demyelinating neuropathy. Compound diaphragm action potential (CDAP) with phrenic nerve stimulation was normal in six of these nine patients. Reduced CDAP in three of nine patients was consistent either with axonal degeneration of the phrenic nerve or diaphragm myopathy. Nerve conduction and electromyographic studies on peripheral nerves and muscles respectively failed to demonstrate an associated generalized neuropathy or myopathy. We conclude that diaphragmatic weakness in patients with SLE is both common and is very unlikely to be caused by a phrenic neuropathy.

Action Potentials↗
PubMed2000

[Experimental study on anti-fatigue effect of shenfu injection on diaphragmatic muscle].

OBJECTIVE: To study the effect of Shenfu injection (SFI) on function of diaphragmatic muscle in rabbits. METHODS: Taking the transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi) and diaphragmatic evoked potential (DEP) as criteria for observation, the diaphragmatic fatigue (DiF) was induced by stimulating bilateral phrenic nerve for 30 minutes. Pdi, EMGdi and DEP induced by stimulation with different frequency (Fc) were recorded before and after treatment. Then the high/low (H/L) frequency ratio and central Fc were calculated and analysed by variance analysis and q test. RESULTS: After administration of 2 ml/kg of SFI, the Pdi, H/L, Fc and amplitude of DEP were markedly increased and latent phase of DEP was shortened by the drug, in comparing with those before treatment, P < 0.05. CONCLUSION: SFI has the effect in antagonizing diaphragmatic fatigue.

Animals↗
PubMedDate not supplied

The effect of preventive use of alanyl-glutamine on diaphragm muscle function in cecal ligation and puncture-induced sepsis model.

BACKGROUND: Low muscle glutamine levels during sepsis are associated with reduced protein synthesis and elevated protein breakdown, in particular myofibrillar protein breakdown. Thus, in a cecal ligation and puncture (CLP)-induced sepsis model in the rat, we hypothesized that glutamine pretreatment would protect the diaphragm muscle function. METHODS: Eighty-four male Wistar rats weighing between 180 g and 200 g received standard amino acid solution 1.2 g kg(-1) per day intraperitoneally (IP) or standard amino acid solution 1.2 g kg(-1) per day plus alanyl-glutamine (GLN) 0.25 g kg(-1) per day (IP) during the first 6 days of the experiment. On the seventh day, CLP or sham procedures were applied. The sham and CLP groups were equally divided into 3 subgroups according to the termination of the experiment, which took place at either the 24th hour, 48th hour, or 72nd hour. After the compound muscle action potentials (CMAP) were recorded from the diaphragms of the rats at these selected times, they were decapitated under ketamine/xylazine anesthesia, and diaphragms were harvested for biochemical and histopathological examination. RESULTS: The mean area and amplitude of CMAP were significantly larger in sham+GLN groups when compared with CLP and CLP+GLN groups at all times (p < .05). Diaphragm Ca+2 -ATPase levels were found to be significantly decreased in CLP group at all times compared to sham groups (p < .05). Diaphragm reduced glutathione levels were significantly higher in sham+GLN groups when compared with CLP and CLP+GLN groups at all times (p < .05). In histopathologic assessment, moderate neutrophil infiltration, which was observed in CLP48, was significantly reduced with alanyl-glutamine supplementation in CLP+GLN48 group (p < .05). CONCLUSIONS: This study showed that glutamine pretreatment did not improve diaphragm muscle function, but prevented the biochemical and histopathological changes in diaphragmatic muscle in CLP-induced sepsis. However, further studies are needed to clarify whether a higher dose of glutamine supplementation might protect the diaphragmatic muscle functions.

Action Potentials↗
PubMed1993

Diaphragmatic dysfunction in neuralgic amyotrophy: an electrophysiologic evaluation of 16 patients presenting with dyspnea.

We report 16 adult men (age, 41 to 75 yr) with neuralgic amyotrophy (NA) who presented with dyspnea due to involvement of the diaphragm. All patients developed breathlessness after a prodrome of acute severe neck and shoulder pain. Bilateral diaphragm paralysis (BDP) was confirmed in 12 patients and unilateral diaphragm paralysis (UDP) in four by the absence of electrical and mechanical responses to percutaneous phrenic nerve stimulation. Global expiratory muscle strength was well preserved in all patients, but inspiratory muscle strength was reduced in proportion to the extent of diaphragmatic involvement. Lung function showed low lung volumes with preservation of carbon monoxide transfer coefficient in all patients. Two BDP patients were hypoxic (PaO2 = 67 and 54 mm Hg, respectively) on daytime arterial blood gas analysis; the latter patient with pre-existing chronic obstructive pulmonary disease and marked obesity also had borderline hypercapnia (PaO2 = 49 mm Hg). Overnight sleep studies in three BDP and two UDP patients showed frequent intermittent arterial oxygen desaturations apparently caused by obstructive sleep apneas, but there was no evidence of alveolar hypoventilation. Follow-up muscle studies in five BDP and four UDP patients between 2 and 4 yr after initial referral showed complete recovery of diaphragmatic function in only two UDP patients, one of whom relapsed a year later. We postulate that NA may be an important but underrecognized cause of diaphragmatic paralysis in otherwise normal patients. Diaphragmatic strength returns very slowly, if at all.

Action Potentials↗
PubMed1992

Age-related decrease in respiratory muscle mitochondrial function in rats.

The purpose of this study was to elucidate the effects of aging on diaphragmatic mitochondrial function. Diaphragm mitochondria were prepared from specific pathogen-free rats aged 7 wk (n = 7), 35 wk (n = 7), and 55 wk (n = 7). The activities of various portions of the mitochondrial electron transport chain, i.e., complexes I, II, III, and IV, were measured enzymatically. The specific activities of complex I decreased significantly (P less than 0.01) in 35-wk-old rats (726 +/- 90 nmol/min/mg protein) compared with 7-wk-old rats (1,018 +/- 121), and the decrease was more remarkable in 35-wk-old rats (565 +/- 64; P less than 0.01 versus 35-wk-old). The activities of complex IV also decreased significantly (P less than 0.01) in 55-wk-old rats (1,222 +/- 191) compared with 7-wk-old rats (1,797 +/- 208); however, no significant changes in complex IV activities between 7-wk-old rat and 35-wk-old rats were observed. In contrast, the activities of complex II and III were not affected by aging. Limb muscle, heart, and liver mitochondria were also prepared from the same rats. The same tendency was observed in limb muscle mitochondria; however, in heart and liver mitochondria, activities of all four complexes were not changed in rats of all age groups. These results indicate that vulnerability of mitochondrial electron transport chain to aging differs from organ to organ and that it also differs from portion to portion in the electron transport chain and the most vulnerable site was complex I.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1999

Propofol decreases diaphragmatic contractility in dogs.

UNLABELLED: Volatile anesthetics depress diaphragmatic muscle function; however, no data are available regarding the effect of propofol on diaphragmatic contractility. We therefore studied this effect in dogs. Pentobarbital-anesthetized animals were divided into three groups of 10 each. Group I received only maintenance fluid; Group II was infused with a subhypnotic dose of propofol (0.1-mg/kg initial dose plus 1.5-mg x kg(-1) x h(-1) maintenance dose); Group III was infused with an anesthetic dose of propofol (0.1-mg/kg initial dose plus 6.0-mg x kg(-1) x h(-1) maintenance dose). We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). With an infusion of propofol in Groups II and III, Pdi at low-frequency (20-Hz) stimulation decreased from the baseline values (P < 0.05), whereas Pdi at high-frequency (100-Hz) stimulation did not change. Compared with Group I, Pdi at 20-Hz stimulation decreased during propofol administration in Groups II and III (P < 0.05). The decrease in Pdi was more in Group III than in Group II (P < 0.05). We conclude that propofol is associated with a dose-related inhibitory effect on diaphragmatic contractility in dogs. IMPLICATIONS: Propofol is an effective IV anesthetic for the induction and maintenance of anesthesia. Subhypnotic and anesthetic doses of propofol decrease diaphragmatic contractility in dogs.

Anesthetics, Intravenous↗
PubMed1989

Mechanisms of postoperative pulmonary dysfunction.

Postoperative pulmonary complications are not uncommon, and the factors that contribute to lung dysfunction are well documented. Postoperative pain, spasm, and paralysis are all known to reduce lung function, although relief of pain does not completely restore function. Rather, diaphragmatic dysfunction has been found to persist even with adequate pain relief. Functional residual capacity is reduced both by the supine position and anesthesia. During anesthesia, the reduced FRC can contribute to airway closure during expiration and to a compression atelectasis that in turn precipitates hypoxemia and infection. Muscle paralysis can also create or contribute to atelectasis. Microthromboembolism impedes perfusion distribution, adding to the other causes of a ventilation-perfusion mismatch. Different anesthetic techniques and intraoperative management may help prevent or reduce the incidence of postoperative lung complications.

Anesthesia↗
PubMed1992

Halothane does not depress contractile function of fresh or fatigued diaphragm in pentobarbitone-anaesthetized dogs.

We have studied the effect of halothane on diaphragmatic contractile function by measuring transdiaphragmatic pressure (Pdi) and electromyogram of the diaphragm (Edi) during various stimulation frequencies in 15 pentobarbitone-anaesthetized dogs undergoing mechanical ventilation. We have examined also the effect of halothane on the fatigued diaphragm by repeating the measurements 5, 10, 15, 30, 60 and 90 min after 30 min of tetanic stimulation applied to the phrenic nerves. Administration of 1-2 MAC of halothane did not affect Pdi at any given stimulation frequency. Changes in the depth of halothane anaesthesia (0, 1 and 2 MAC) did not alter the force-frequency relationship of the diaphragm during recovery from fatigue. Edi was unaffected by halothane, except for a small decline during 100-Hz stimulation with 2 MAC. In contrast with the changes in Pdi, Edi during recovery from fatigue was the same as that determined before fatigue. It is concluded that halothane, in clinical concentrations, did not depress the contractile function of fresh or fatigued diaphragm in vivo.

Anesthesia, Intravenous↗
PubMed1993

Fetal upper respiratory tract function in cases of antenatally diagnosed congenital diaphragmatic hernia: preliminary observations.

Fetal upper respiratory tract function was studied in five cases of antenatally diagnosed congenital diaphragmatic hernia and in 16 cases of uncomplicated pregnancy at gestational ages ranging from 27 to 38 weeks. The evaluation of fetal upper respiratory tract function was performed using ultrasonography combined with color-flow and spectral Doppler analysis. In all cases with uncomplicated pregnancy, fetal breathing-related nasal and oropharyngeal fluid flow was seen at the level of the nose. The five cases with congenital diaphragmatic hernia all demonstrated fetal breathing activity by thoracic wall movement. In four of the fetuses, perinasal fluid flow was seen by the Doppler technique. The fetus with no demonstrated perinasal flow during breathing movements died in the early neonatal period and had pulmonary hypoplasia. Observation of the fetal breathing-related nasal and oropharyngeal fluid flow in cases of antenatally diagnosed congenital diaphragmatic hernia provides a rationale to hypothesize that the absence of this phenomenon is a useful marker for prenatal prediction of pulmonary hypoplasia.

Journal Article↗
PubMed2002

[Roles of diaphragmatic crural barrier and esophageal body clearance in patients with gastroesophageal reflux disease].

OBJECTIVE: Aim of this study was to investigate functions of lower esophageal sphincter (LES) barrier and esophageal clearance in fasting and postprandial stages in gastroesophageal reflux disease (GERD). METHODS: Eight patients with confirmed GERD and 8 healthy subjects (HS) were observed in the study. The esophageal pH and manometry were recorded simultaneously for 1 h during fasting and 2 h after a meal (1,675 kJ) using pneumohydrolic capillary perfusion system. RESULTS: (1) The esophageal pH monitoring showed that median of percentage of pH < 4 at postprandial in HS and patients with GERD was 0.45% and 11.2%, respectively (P < 0.05). (2) Pressure of lower esophageal sphincter (LESP) significantly decreased after a test meal in GERD (P < 0.001) and in HS (P < 0.001). (3) The amplitude of post-LES relaxation related to swallow (post-LESRA) in GERD was much lower than in HS either during fasting or postprandial stage (P < 0.05). (4) The tension of crural diaphragm at resting (Dia-A0) in GERD was lower than in HS during fasting and postprandial stage(P < 0.05). (5) The tension of crural diaphragm at deep inspiration (dia-AM) in GERD and HS increased 3 or 4 times at pressure at gastroesophageal junction (GEJ). (6) The peristaltic amplitude of the distal esophagus in GERD were much lower than that in HS in both pre- and postprandial periods. CONCLUSIONS: (1) Impaired clearance of Post-LESRA and esophageal body, function of diaphragmatic crural play an important role in development of GERD. (2) The tension of crural diaphragm at deep inspiration can increase the pressure at GEJ.

Adolescent↗
PubMed1977

Management of pulmonary insufficiency in diaphragmatic hernia using extracorporeal circulation with a membrane oxygenator (ECMO).

Persistent fetal circulation (PFC) causes severe pulmonary insufficiency in patients who have demonstrated adequate lung function following diaphragmatic hernia repair. Patent ductus arteriosus (PDA) ligation corrects this condition, but carries the risk of sudden right ventricular failure. Pharmacologic reversal of PFC may be attempted, and if unsuccessful, prolonged venoarterial bypass becomes necessary to provide effective pulmonary support. PDA ligation can then be performed safely and maturation of the pulmonary vasculature allowed to occur. Pulmonary artery pressure monitoring is essential.

Ductus Arteriosus, Patent↗
PubMed2001

Lung volume reduction surgery restores the normal diaphragmatic length-tension relationship in emphysematous rats.

OBJECTIVE: Improved respiratory muscle function is a major effect of a lung volume reduction surgery. We studied length adaptation in rat diaphragmatic muscle in an attempt to elucidate the mechanism by which diaphragmatic function improves after this controversial operation. METHODS: We developed a model of elastase-induced emphysema and bilateral volume reduction through median sternotomy in rats. Five months after emphysema induction, maximum exchangeable lung volume was determined in intubated and anesthetized control animals and animals with emphysema. Costal diaphragmatic length was measured in vivo, and the length at which maximal twitch force is generated was determined on muscle strips in vitro. Also 5 months after elastase administration, another cohort underwent volume reduction or sham sternotomy. Five months after the operation, these animals were similarly studied. RESULTS: Lung volume was increased in emphysematous rats versus control rats (50.9 +/- 1.7 vs 45.4 +/- 1.3 mL, P =.001). Lung volume was decreased in emphysematous animals that had undergone volume reduction versus sham sternotomy (44.7 +/- 0.60 vs 49.4 +/- 1.0 mL, P =.001). In situ diaphragm length (1.99 +/- 0.04 vs 2.24 +/- 0.07 cm, P =.001) and the length at which maximal twitch force is generated (2.25 +/- 0.06 vs 2.48 +/- 0.09 cm, P =.038) were shorter in emphysematous than control animals. After volume reduction, in situ diaphragm length (2.13 +/- 0.06 vs 1.83 +/- 0.02 cm, P <.001) and the length at which maximal twitch force is generated (2.50 +/- 0.08 vs 2.27 +/- 0.06 cm, P =.013) were longer than in animals undergoing sham sternotomy. CONCLUSIONS: In this experimental model of emphysema and lung volume reduction surgery, emphysema shortens the length at which maximal twitch force is generated and shifts the diaphragmatic length-tension curve to lower lengths; volume reduction returns the length at which maximal twitch force is generated toward normal and shifts the diaphragmatic length-tension curve back to longer lengths. This restoration toward normal physiology may enable the improvement in diaphragmatic function seen after lung volume reduction surgery. The mechanism by which these length adaptations occur merits further investigation.

Adaptation, Physiological↗
PubMed1990

Diaphragmatic plication for unilateral diaphragmatic paralysis: a 10-year experience.

Unilateral paralysis of the diaphragm due to nonmalignant disease is an uncommon disorder previously thought to have benign implications. Some patients, however, experience dyspnea and orthopnea with impairment of pulmonary function. Unilateral diaphragmatic plication was performed on 17 patients (16 men and 1 woman with a mean age of 53.7 years [range, 28 to 74 years]) during the last 10 years. Preoperatively each patient was shown to have paradoxical movement of the paralyzed diaphragm on sniffing and to have a reduction in forced vital capacity and lung volumes. These reductions were greater when the patient was in the supine position. All patients had moderate hypoxemia (mean arterial oxygen tension, 73.1 +/- 10.9 mm Hg). Plication was performed by imbricating the diaphragm in layers through a thoracotomy incision. After plication, all patients showed both subjective and objective improvement. Six patients were reassessed 5 or more years after plication (range, 5 to 7 years), and the improvement was maintained. Diaphragmatic plication is a safe and effective procedure for adult patients with dyspnea due to unilateral diaphragmatic paralysis; furthermore, the initial improvement is maintained.

Adult↗
PubMed1984

Diaphragmatic fatigue in unanesthetized adult sheep.

We studied diaphragmatic muscle function during inspiratory flow resistive (IFR) loaded breathing in unanesthetized sheep. We measured the change in transdiaphragmatic pressure (dPdi) and arterial blood gas tensions and recorded diaphragmatic electromyogram (EMG) from electrodes implanted on the muscle. We found that, with IFR loads less than 150 cmH2O X l-1 X s, dPdi and the integrated EMG increased, reached a plateau, and were maintained at high levels. The centroid frequency (fc) of the EMG power spectrum did not consistently change. With IFR loads greater than 150 cmH2O X l-1 X s, O2 was administered to prevent hypoxia, cyanosis, and agitation. With these loads, dPdi increased severalfold above base line, reached a plateau, and then started to decrease. Arterial PCO2 increased sharply at the time when dPdi decreased. The integrated EMG (iEMG) and fc started to decrease gradually 10-20 min before dPdi started to decrease. We conclude that 1) the diaphragm is capable of generating large pressures for prolonged periods with no evidence of fatigue; 2) with very high IFR loads, mechanical failure of the diaphragm can occur in the unanesthetized awake sheep; 3) diaphragmatic fatigue is associated with acute hypercapnia and therefore failure of the entire respiratory pump; and 4) a decrease in iEMG and a concommitant shift in the power spectrum density towards lower frequencies precede the mechanical failure of the diaphragm.

Animals↗