Biomedical subjects

F Bellemare

Publications and source records attributed to F Bellemare.

At least 37 records · Page 2Linked to original sources

PubMed1994

Diaphragmatic and abdominal muscle activity after endoscopic cholecystectomy.

We studied diaphragmatic and abdominal muscle activity immediately and 16 h after laparoscopic cholecystectomy (LAPC). Tidal volumes (VT), partitioning of VT between the rib cage and the abdomen, and esophageal, gastric, and transdiaphragmatic pressures were recorded for 5 min every 15 min up to 90 min after the end of anesthesia in 10 young patients submitted to an elective LAPC. All had chest radiographs in full inspiration and expiration as well as lung function tests (LFTs) before and 16 h after surgery. In 5 of the 10 patients, thoracoabdominal patterns of breathing were also measured before both LFTs. After LAPC, VT did not change. There was no significant shift from abdominal to thoracic respiration. No paradoxical respiration developed. Functional residual capacity (FRC) and residual volume (RV) remained normal. However, all measures of LFTs requiring maximum inspiratory effort decreased up to 20%. Tonic and phasic activity of the abdominal muscle appeared early in the recovery period and disappeared after 75 min. The diaphragm adjusted to this additional load so that VT remained constant. These results indicate that diaphragm function is intact during quiet breathing after LAPC, but slightly reduced when maximum effort is needed. However, this represents a net gain over the changes previously described after classic "open" cholecystectomy (OC).

Abdominal Muscles↗

PubMed1993

Effects of fatigue on the length-tetanic force relationship of the rat diaphragm.

It has been established that the in vivo operating length of the diaphragm corresponds to a wide range of the ascending limb of its length-tetanic force relationship. To investigate the length-dependent effects of fatigue on maximum force production, we constructed length-tetanic force relationships of rat costal diaphragm strips in vitro before and after fatigue induced by repetitive supramaximal electrical field stimulations at optimal length. Two levels of fatigue were studied (i.e., force reductions of 40 and 65% at optimal length). Results indicate that fatigue, when evaluated with high-frequency stimulations, causes a proportionately larger decrease in tetanic force at short muscle lengths as seen by a smaller control force-to-fatigue force ratio and an apparent shift in the length at which active force is zero. A possible explanation for the results obtained is failure of propagation of membrane depolarization into the t-tubule system at short muscle lengths, which is aggravated by fatigue evaluated by high-frequency stimulation.

Animals↗

PubMed1993

Assessment of diaphragm function using mouth pressure twitches in chronic obstructive pulmonary disease patients.

The relative invasiveness of the balloon catheter technique in measuring twitch transdiaphragmatic pressure (Pdit) limits its clinical use. By phrenic stimulation we obtained swings in mouth pressure (Pmt) in six COPD patients (age 50 to 72, FEV1 18 to 48% of predicted) at relaxed FRC (rFRC) and during graded inspiratory efforts (IE; twitch occlusion, TO). At rFRC, Pmt was damped and time lagged relative to the esophageal pressure twitch (Pes(t)), as if pressure had equilibrated through an RC system. Pmt was not correlated with Pdit. Conversely, Pmt and Pes(t) were always well matched during IE [Pmt = 0.971 (SEM +/- 0.028) Pes(t), r > 0.89], possibly in relation to a decrease in upper airway compliance or more uniform pleural pressure swings. Pmt decreased with the level of voluntary diaphragmatic contraction (Pdivol) in proportion to Pdit, reflecting a progressive increase in the level of diaphragm activation. During IE, Pmt was closely related to the voluntary mouth pressure in five subjects but not in the remaining subject, indicating intersubject variability in the level of diaphragmatic recruitment relative to other inspiratory muscles. We submit that measuring Pm during inspiratory efforts upon which bilateral phrenic stimulation is superimposed offers a relatively simple method for the assessment of diaphragm activation, potentially applicable in the clinical field.

Aged↗

PubMed1993

Force-frequency relationships of in vivo human and in vitro rat diaphragm using paired stimuli.

Supramaximal stimuli, with time intervals of 100 ms (10 Hz) to 10 ms (100 Hz), were delivered in pairs to the phrenic nerves, bilaterally, in five seated normal subjects, while transdiaphragmatic pressure swings (Pdi,s) were recorded at relaxed end-expiratory lung volume with airways closed. In fresh diaphragms, Pdi,s increased between 10-20 Hz and reached a plateau between 20-30 Hz. Diaphragmatic fatigue decreased Pdi,s at all frequencies. Pdi,s was assumed to be the sum of two successive responses (T1+T2), T1 being constant at any frequency and equal to a single twitch, T2 being obtained by subtraction. We found that T2 amplitude, which was significantly reduced after fatigue, was fully returned to normal after 15 min rest at high, not at low, stimulation frequencies. The ratio of T2 at 10 Hz over 100 Hz (T2(10/100)) thus decreased from 1.33 +/- 0.05 before fatigue to 0.97 +/- 0.12 after fatigue, and to 0.81 +/- 0.06 after 15 min rest. Similar results were obtained in isolated rat diaphragmatic strips stimulated and fatigued in vitro, from which we found a highly linear relationship (r = 0.94, p < 0.001) between the ratio of T2(10/100) and that of tetanic force at 10 Hz over 100 Hz (P10/100). We conclude that phrenic nerve paired twitches provide similar information when obtained from phrenic tetanic stimulation in terms of diaphragmatic contractility, and the decrease in T2(10/100) ratio indicates diaphragm low frequency fatigue.

Animals↗

PubMed1993

Evaluation of human diaphragm function.

When single supramaximal shocks are delivered during relaxation to both phrenic nerves simultaneously, the resulting transdiaphragmatic pressure twitch (PdiT) or mouth pressure twitch (PmT) are found to decrease linearly with increasing lung volume thereby reflecting changes in diaphragm contractility. Whereas fatigue decreases PdiT at any given lung volume, chronic lung hyperinflation tends to increase PdiT at any given lung volume. When the phrenic nerve shocks are delivered during ongoing voluntary contractions, PdiT decreases with increasing level of diaphragm activation. Its amplitude thus detects the reverse left for full activation of the diaphragm by the voluntary motor drive. The ability to maximally activate the diaphragm decreases with fatigue but is retained in patients with chronic lung hyperinflation.

Diaphragm↗

PubMed1992

Incorporation into a planar lipid bilayer of K channels from the luminal membrane of rabbit proximal tubule.

The presence of ionic channels at the apical membrane of rabbit proximal tubule cells was investigated by fusion of brush-border membrane vesicles (BBMV) with a planar lipid bilayer (PE/PC, 1:1). The BBMV obtained from native membranes showed poor fusogenic properties. The probability of vesicles fusion with a planar bilayer was, however, enhanced by preincubating the BBMV with liposomes made of azolectin. We report here the presence in BBMV preparations of two K(+)-selective channels of 65 pS and 40 pS, respectively, in asymmetrical 200 parallel 50 mM KCl solutions. The channel of 65 pS appeared highly selective to K+ over Na+ and Cl- ions, while the 40 pS channel discriminated poorly between K+ and Na+ with a permeability ratio PK/PNa = 4. The open probability Po of both channels was found to be voltage-independent within the potential range -60 mV to +60 mV. These K+ channels may be related to channels identified using other methods.

Animals↗

PubMed1992

Effect of fatigue on diaphragmatic function at different lung volumes.

The transdiaphragmatic pressure twitches (PdiT) in response to single maximal shocks delivered bilaterally to the phrenic nerves were recorded as a function of lung volume when the diaphragm was fresh and when fatigued. All relationships were linear and negatively sloped (all r greater than 0.85). From these relationships PdiT was found to decrease with fatigue more rapidly and to recover more quickly at high than at low lung volumes. Complete recovery of PdiT at all lung volumes was greater than 1 h. Contraction and relaxation rate constants of PdiT did not change significantly with fatigue. We conclude that fatigue affects diaphragm contractility more at high than at low lung volumes and that changes in diaphragm contractility are best reflected in the measurement of PdiT as a function of lung volume.

Adult↗

PubMed1992

Evaluation of human diaphragm contractility using mouth pressure twitches.

Mouth (PmT), esophageal (PesT), and transdiaphragmatic pressure twitches (PdiT) in response to single supramaximal bilateral phrenic nerve shocks were recorded during relaxation between total lung capacity (TLC) and functional residual capacity (FRC) in five normal volunteers. The PmT versus PesT or PmT versus PdiT relationships, which were linearly correlated (all r greater than 0.76), were not affected by diaphragm fatigue and were reproducible on repeated determinations over a period exceeding 1 yr. The PmT versus lung volume relationship was also linear (all r greater than 0.72) and reproducible, and its changes following diaphragm fatigue reliably reflected the changes in diaphragm contractility. We conclude that PmT is a reliable measure of diaphragm pressure-generating capacity in normal individuals and has the potential of providing similar information in patients.

Adult↗

PubMed1991

Improved stability of rabbit and rat intestinal brush border membrane vesicles using phospholipase inhibitors.

The initial rates of Na(+)-dependent D-aspartate and D-glucose uptakes were shown to decline from the time of resuspension of brush border membrane vesicles isolated from rabbit and rat jejunum by standard divalent cation precipitation procedures. The former were however more stable than the latter and followed quite closely the decrease in the intravesicular volume, thus suggesting that the loss of transport activity may involve both nonspecific opening of the vesicles and either direct or indirect specific inactivation of the transporters. Uptake rates for both substrates did tend to stabilize at 6-24 h from resuspension, however this final 'next day' uptake activity was too low to be of practical use in kinetic studies. Freezing aliquots of rabbit jejunal vesicles in liquid N2 until the time of assay resulted in complete stabilization of D-glucose uptake. A modified homogenate buffer designed to inhibit a broad spectrum of phospholipase activities resulted in a partial stabilization of glucose transport by rabbit jejunal vesicles with, on average, an over 6-fold enrichment in the 'next day' stable specific activity of uptake as compared to unfrozen vesicles. The modified homogenate buffer also improved the stability and the 'next day' specific activities of D-glucose uptake in rat jejunal brush border vesicles and D-aspartic acid uptake in rabbit jejunal vesicles. It also completely stabilized the intravesicular volume in the latter preparation. An evaluation of the kinetic parameters of Na(+)-dependent D-glucose transport in rabbit vesicles prepared from either the standard homogenate media and frozen in liquid N2 or the modified media and allowed to stabilize overnight, revealed a single transport system with a Km of 0.31-0.32 mM as the best model to fit the data. As such the modifications to the homogenate media do not appear to effect the functional properties of D-glucose transport in the membrane. While being less efficient in stabilizing the vesicles than the rapid freezing protocol, it is shown that the modified homogenate should however be preferred when dealing with slowly permeant ions like choline since it provides in this case the only alternative to reliable measurement of uptake rates across a stable and equilibrated vesicle preparation.

Animals↗

PubMed1991

Contractile properties of the human diaphragm during chronic hyperinflation.

BACKGROUND: In patients with chronic obstructive pulmonary disease (COPD) and hyperinflation of the lungs, dysfunction of the diaphragm may contribute to respiratory decompensation. We evaluated the contractile function of the diaphragm in well-nourished patients with stable COPD, using supramaximal, bilateral phrenic-nerve stimulation, which provides information about the strength and inspiratory action of the diaphragm. METHODS: In eight patients with COPD and five control subjects of similar age, the transdiaphragmatic pressure generated by the twitch response to phrenic-nerve stimulation was recorded at various base-line lung volumes, from functional residual capacity to total lung capacity, and during relaxation and graded voluntary efforts at functional residual capacity (twitch occlusion). RESULTS: At functional residual capacity, the twitch transdiaphragmatic pressure ranged from 10.9 to 26.6 cm of water (1.07 to 2.60 kPa) in the patients and from 19.8 to 37.1 cm of water (1.94 to 3.64 kPa) in the controls, indicating considerable overlap between the two groups. The ratio of esophageal pressure to twitch transdiaphragmatic pressure, an index of the inspiratory action of the diaphragm, was -0.50 +/- 0.05 in the patients, as compared with -0.43 +/- 0.02 in the controls (indicating more efficient inspiratory action in the patients than in the controls). At comparable volumes, the twitch transdiaphragmatic pressure and esophageal-to-transdiaphragmatic pressure ratio were higher in the patients than in normal subjects, indicating that the strength and inspiratory action of the diaphragm in the patients were actually better than in the controls. Twitch occlusion (a measure of the maximal activation of the diaphragm) indicated near-maximal activation in the patients with COPD, and the maximal transdiaphragmatic pressure was 106.9 +/- 13.8 cm of water (10.48 +/- 1.35 kPa). CONCLUSIONS: The functioning of the diaphragms of the patients with stable COPD is as good as in normal subjects at the same lung volume. Compensatory phenomena appear to counterbalance the deleterious effects of hyperinflation on the contractility and inspiratory action of the diaphragm in patients with COPD. Our findings cast doubt on the existence of chronic fatigue of the diaphragm in such patients and therefore on the need for therapeutic interventions aimed at improving diaphragm function.

Aged↗

PubMed1991

Electrical and mechanical output of the expiratory muscles in anesthetized dogs.

In anesthetized intact and vagotomized dogs chest wall diameters, expiratory muscles' (EM) electrical activity, work, mean pressure and volume displacement contributed by EM contraction were assessed in the supine and upright posture during rebreathing, and during continuous positive pressure breathing (CPAP) in the supine posture. Corresponding inspiratory mechanical output variables were related to diaphragm activity. During resting breathing triangularis sterni and internal interosseous were more easily recruited than transversus abdominis and external oblique. EM activity increased with tilting, CPAP and rebreathing. Vagotomy depressed or abolished abdominal EM activity, with lesser effects on rib cage EM. Expiratory mechanical output grossly paralleled EM activity: it markedly depended on rib cage and abdominal EM coactivation, besides lung inflation and chest wall shape. Upper rib cage configuration at end-expiration never departed from the relaxation one, suggesting trivial effects of the triangularis sterni contraction. Lower chest wall distortion occurred almost regularly, so that much of EM activity was not converted into external work. In contrast with expiratory electromechanical relations, those for the diaphragm were always highly significant and independent of EM activation.

Animals↗

PubMed1990

Electrical and mechanical output of the inspiratory muscles in anesthetized dogs.

In anesthetized dogs with progressive hypercapnia, the relationships between tidal volume (VT) or occluded inspiratory esophageal pressure swings (Pes) and diaphragm (Edi) or thoracic inspiratory muscle (Etm) peak electrical activity were determined after either cordotomy at C7-T1 or bilateral phrenicotomy, and used together with the Etm vs Edi relationships established in intact and vagotomized dogs to estimate the contribution of each muscle group to VT and Pes observed under the latter conditions. Etm was obtained as the mean of scalene, 2nd and 5th parasternal peak activity, the relationships between these activities being the same under all conditions. In supine and head-up phrenicotomized dogs, VT and Pes increased linearly with Etm and were unaffected by body position. After cordotomy, VT and Pes increased progressively less with increasing Edi and at any Edi were smaller in the head-up posture. Diaphragm relative contribution to VT and Pes was greater when supine than head-up and greater after than before vagotomy, but in all cases it decreased with increasing chemical drive. That of the thoracic inspiratory muscles increased with chemical drive and eventually became equal to (supine) or larger than (head-up) diaphragm contribution.

Anesthesia↗

PubMed1990

Aminophylline and human diaphragm strength in vivo.

The transdiaphragmatic pressure (Pdi) twitch response to single shocks from supramaximal bilateral phrenic nerve stimulation was studied before and after acute intravenous infusions of aminophylline [14.9 +/- 3.1 (SD) micrograms/ml] in nine normal subjects. Stimulation was performed with subjects in the sitting position against an occluded airway from end expiration. Baseline gastric pressure and abdominal and rib cage configuration were kept constant. There was no significant difference in peak twitch Pdi from the relaxed diaphragm between control (38.8 +/- 3.3 cmH2O) and aminophylline (40.2 +/- 5.2 cmH2O) experiments. Other twitch characteristics including contraction time, half-relaxation time, and maximum relaxation rate were also unchanged. The Pdi-twitch amplitude at different levels of voluntary Pdi was measured with the twitch occlusion technique, and this relationship was found to be similar under control conditions and after aminophylline. With this technique, maximum Pdi (Pdimax) was calculated as the Pdi at which stimulation would result in no Pdi twitch because all motor units are already maximally activated. No significant change was found in mean calculated Pdimax between control (146.9 +/- 27.0 cmH2O) and aminophylline (149.2 +/- 26.0 cmH2O) experiments. We conclude from this study that the acute administration of aminophylline at therapeutic concentrations does not significantly affect contractility or maximum strength of the normal human diaphragm in vivo.

Adult↗

PubMed1989

Cardiovascular failure and apnea in shock.

A model of shock was developed in anesthetized dogs by limiting venous return with a balloon inflated in the right atrium. The change in ventilation (VE) in response to a sustained decrease in arterial pressure (Pa) to 50-60 Torr was studied by recording transdiaphragmatic pressure (Pdi) and diaphragm (Edi) and parasternal intercostal (Eic) electrical activity. Four dogs died of cardiac arrest after 20-60 min. In 11 dogs, VE, after an initial increase, decreased progressively until apnea occurred after 103 +/- 24 min, after 60% reductions in breathing frequency, Pdi, and Eic and a 30% fall in Edi. No decrease in diaphragm contractility was found in response to artificial phrenic nerve stimulation. The cardiocirculatory function deteriorated during shock until it became irreversible at apneic time. No recovery from apnea occurred without a recovery of Pa. We conclude that the fall in VE and ensuing apnea in this model resulted from a decrease in central respiratory neural output associated with a progressive deterioration of the cardiocirculatory function.

Animals↗

PubMed1988

Inspiratory muscle activity during unloaded and obstructed rebreathing in dogs.

Moving-average electromyogram (EMG) of the diaphragm (DI), scalenes, and cranial and caudal parasternals was assessed in anesthetized, supine, and head-up dogs during rebreathing. The shape of EMG trajectory was similar for all muscles and conditions; activation of different muscles could be thus compared on the basis of changes in peak activity. In intact dogs changes in peak activity were greater for the scalenes and cranial parasternals than for the caudal parasternals and greater for the inspiratory thoracic muscles (ITM) than for the DI. Posture, vagotomy, and cordotomy at C7-T1 did not affect the rate of rise of DI activity. The relations between peak activity of ITM did not change because of posture, vagotomy, and phrenicotomy. Vagotomy selectively depressed the rate of rise of ITM activity, but relative changes in peak ITM activity for a given change in peak DI activity were independent of intact vagi. Differences in the pattern of activation between inspiratory muscles with rebreathing are largely independent of proprioceptive inputs and likely reflect properties of central control mechanisms. However, airway occlusion at end expiration caused a reflex fall of DI activity and reflex increase of ITM activity in intact and vagotomized dogs. Cordotomy at C7-T1 did not change DI response, whereas reduction of ITM activity occurred after phrenicotomy, indicating that both facilitatory and inhibitory segmental inputs are involved in ITM response to loading.

Airway Obstruction↗

PubMed1988

Failure of neuromuscular propagation during human maximal voluntary contraction.

The mechanism for fatigue of the adductor pollicis was studied in normal subjects during maximal voluntary contractions (MVC) sustained for 90-100 s, by comparing the force and electrical response of this muscle to voluntary motor drive with that obtainable with artificial stimulation of the ulnar nerve. The adequacy of nerve stimulation was checked by recording simultaneously the electrical response of a nonfatiguing muscle, the abductor of the small finger. The decrease in force and in the natural electrical activity with fatigue was accompanied by a parallel decrease in the amplitude of synchronous muscle action potentials (M waves) evoked by artificial stimulation of the ulnar nerve at different frequencies. The decline in M-wave amplitude in the adductor pollicis was not due to a submaximal nerve stimulation, since the amplitudes recorded simultaneously from the nonfatiguing abductor digiti minimi remained unchanged. The force and the electrical responses from the adductor pollicis recovered in parallel with a half time of approximately 1 min. These results suggest that the loss of force of the adductor pollicis with fatigue and its subsequent recovery are largely determined by the extent of neuromuscular propagation failure. The slow recovery of the M-wave amplitude during repetitive stimulation suggests that it may be related to some aspect of muscle metabolism.

Action Potentials↗

PubMed1988

Respiratory sensation and pattern of respiratory muscle activation during diaphragm fatigue.

We have examined the relationship between respiratory effort sensation (modified Borg scale) and amplitude of the integrated surface electromyogram of the diaphragm (Edi, esophageal electrode), rib cage muscles (Erc), and sternomastoid muscle (Esm) during the development of diaphragm fatigue in five normal subjects. Three conditions were studied: run A: transdiaphragmatic pressure (Pdi), 65% Pdimax; esophageal pressure (Pes), 60% Pesmax; run B: Pdi, 50% Pdimax; Pes, 60% Pesmax; and run C: Pdi, 50% Pdimax; Pes, 20% Pesmax. During all runs there was a progressive rise in sensation, which was greater in runs A and B than in run C (P less than 0.05, analysis of variance). There was no difference between runs A and B. At the end of run C subjects did not report a maximal Borg score despite their inability to generate the target Pdi. The increase in sensory score with fatigue correlated highly with Esm/Esmmax and with Erc/Ercmax. There was no correlation between sensory score and Edi/Edimax. We conclude that the increase in respiratory effort sensation that accompanies diaphragm fatigue is not due to perception of increased diaphragmatic activation. It may reflect increased overall respiratory motor output not directed to the diaphragm.

Adult↗

PubMed1987

Central components of diaphragmatic fatigue assessed by phrenic nerve stimulation.

The extent to which diaphragmatic fatigue results from failure of neural drive has been investigated using twitch occlusion. Fatigue was induced by repeatedly generating transdiaphragmatic pressures (Pdi) of either 50 or 75% maximum Pdi (Pdimax) until approximately 10 min after the target Pdi could no longer be reached (Tlim). Maximal bilateral shocks delivered periodically to the phrenic nerves elicited Pdi twitches between breaths (Tr) and superimposed on the voluntary contractions (Ts). The ratio [1 - Ts/Tr], which provides an index of the degree of central nervous system muscle activation, increased as fatigue developed. However, superimposed twitches were still detectable at and beyond Tlim when all contractions involved maximal efforts. They were not seen in maximal contractions of the unfatigued muscle. Initially, the diaphragm electromyogram increased, but then declined. No impairment of neuromuscular transmission was seen. We conclude that at and beyond Tlim about one-half of the reduction in Pdimax resulted from reduced central motor drive; the remainder resulted from peripheral muscle contractile failure. No fatigue was evident during 50% Pdimax dynamic contractions.

Adult↗