Biomedical subjects

D Murciano

Publications and source records attributed to D Murciano.

At least 37 records · Page 2Linked to original sources

PubMed1988

Effects of Ca2+ withdrawal on diaphragmatic fiber tension generation.

The effects of extracellular Ca2+ withdrawal were studied on isolated diaphragmatic muscle fibers and compared with the effects on the papillary, soleus, and extensor digitorum longus (EDL) contractility, using the same in vitro model. Diaphragmatic fibers were obtained from 15 rats, and papillary muscles, soleus, and EDL were obtained from 10 animals. Isometric force generated in response to 1-Hz supramaximal electrical stimulation was measured with a highly sensitive photoelectric transducer. After control measurements, perfusion with a Krebs solution depleted of calcium (0 Ca2+) was started while the fibers were continuously stimulated (4 times/min) and twitches recorded. For the papillary fibers, perfusion with zero Ca2+ was followed by an immediate decrease in twitch tension, complete twitch abolition occurring within 3 +/- 1 min after zero-Ca2+ exposure. Diaphragmatic fibers behaved similarly, although twitch abolition was delayed (10 +/- 3 min after 0-Ca2+ exposure). For the soleus fibers, the twitch amplitude amounted to 38 +/- 10% of control (62% decrease on the average) after 30 min of zero-Ca2+ exposure, no twitch abolition being noted even after 1 h of Ca2+-free exposure. The twitch amplitude of the EDL fibers amounted to 75 +/- 7% of control (25% decrease) after 30 min of zero-Ca2+ exposure. The recovery kinetics for the four fiber types after reexposure to Ca2+-containing solution were also different, with papillary and diaphragmatic fibers recovering completely within 2.5 +/- 0.5 and 4 +/- 0.5 min, respectively. By contrast, neither the soleus nor the EDL showed complete recovery after 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Effects of sepsis on diaphragmatic function in rats.

The effects of a 3-day pneumococcal infection on diaphragmatic strength and endurance capacity were studied in an in vivo rat model. Thirty-four rats were divided into a control (C) (n = 17) or a septic (S) group (n = 17). Animals were inoculated subcutaneously with 10(11) Streptococcus pneumoniae (S), or sterile culture media (C). All rats were studied 3 days after inoculation. Diaphragmatic strength and endurance capacity were studied in 11 animals of each group. Diaphragmatic strength was assessed by measuring transdiaphragmatic pressure (Pdi) generated during electrical stimulation of the phrenic nerves at different frequencies (0.5, 10, 20, 30, 50, and 100 Hz). Endurance index was calculated as the ratio of Pdi generated after 30 s of phrenic nerve stimulation at 10 Hz divided by the initial force. Measurements of lung weights and lung histologic examinations were performed in the 6 remaining rats from each group. S animals were hyperthermic (39 to 40 degrees C rectal temperature). There was no evidence of pneumonia at histologic examination in Group S. No differences in wet weight of the lung and in the dry-to-wet weight ratio were noted in Group S as compared with Group C. However, S. pneumoniae was isolated from blood and lungs of S animals. Diaphragmatic weight was not different between S and C groups, whereas the weights of the extensor digitorium longus (EDL), tibialis anterior (TA), and soleus muscles were significantly reduced in Group S as compared to Group C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Tracheal occlusion pressure: a simple index to monitor respiratory muscle fatigue during acute respiratory failure in patients with chronic obstructive pulmonary disease.

STUDY OBJECTIVE: To assess respiratory muscle fatigue in acute respiratory failure in patients with chronic obstructive pulmonary disease and evaluate its influence on weaning patients from mechanical ventilation. DESIGN AND PATIENTS: We studied the time course of tracheal occlusion pressure (P0.1) and high-to-low ratio of the diaphragmatic electromyogram in 16 patients in acute respiratory failure with chronic obstructive pulmonary disease. METHODS: All patients were intubated and studied during a 15-minute weaning period from ventilation. Minute ventilation (VE), arterial blood gases, P0.1 and high-to-low ratio of the diaphragm were measured every day from the onset to the end of acute failure (before extubation) at 5 and 15 minutes into the weaning period. The diaphragmatic electromyogram was recorded with an esophageal electrode and the high-to-low ratio of the electrical signal analyzed to assess diaphragmatic fatigue. MEASUREMENTS AND MAIN RESULTS: In all patients P0.1 was markedly increased (7.1 +/- 2.4 cm H2O, mean +/- SE) on the first day of acute failure and did not change during weaning. In 11 patients, P0.1 had decreased to 4.7 +/- 1.8 cm H2O (P less than or equal to 0.002) before extubation (which was done after 5 to 9 days). In these patients, the high-to-low ratio of the diaphragm decreased rapidly-during the first minutes of weaning on the first day of acute failure and remained low throughout weaning, whereas before extubation no decrease in high-to-low ratio was seen during weaning. In 5 patients, P0.1 did not change significantly from the onset of acute failure and the high-to-low ratio remained low before extubation. These 5 patients had to be reintubated within 2 to 6 days. In both groups of patients, VE did not change significantly from the first to last day of acute failure (10.3 +/- 3 compared with 10.7 +/- 2.1 min-1), whereas blood gases during room air breathing improved significantly from the first to last day of acute failure, respectively, in each group (arterial oxygen pressure [PaO2], 33.5 +/- 1.5 compared with 44 +/- 9 mm Hg (P less than or equal to 0.05) and PaO2 56 +/- 2.3 compared with 49 +/- 2 mm Hg (P less than 0.005). CONCLUSIONS: Extubation should not be done in patients with respiratory muscle fatigue despite improvement in arterial blood gases and clinical status; and P0.1 provides a valid and simple index to assess the likelihood of respiratory muscle fatigue.

Acute Disease↗

PubMed1987

[Action of aminophylline on the strength of contraction of the diaphragm in patients with chronic obstructive respiratory insufficiency].

The effect of a sustained-release aminophylline preparation on diaphragmatic contractility was investigated in patients with stable chronic obstructive lung disease (FEV1 = 22.6% of predicted value). Ten such patients were tested before (control) and after a week's course of oral aminophylline. Diaphragmatic contractility was evaluated by measuring the transdiaphragmatic pressure generated at residual functional capacity by bilateral electrical stimulation of the phrenic nerves. The nerves were stimulated supramaximally at 1 Hz, using needle electrodes. Plasma aminophylline levels (12.5 +/- 0.9 mg/l) were within therapeutic range in all patients. After treatment with aminophylline, for each stimulation the transdiaphragmatic pressure increased significantly from 14 +/- 1.3 to 17 +/- 1.3 cm H2O (+21%; P less than 0.005). These results confirm that aminophylline increases the force of contraction of the diaphragmatic fibres electively tested by the technique used. Long-term treatment with theophylline in therapeutic doses may be of interest in such patients, as it might improve their diaphragmatic contractility and result in better control of both respiratory muscle fatigue and episodes of acute respiratory failure.

Aged↗

PubMed1987

Effects of theophylline and enprofylline on diaphragmatic contractility.

Experimental data suggest that theophylline (T) enhances diaphragmatic contractility by increasing the influx of calcium at the cell membrane level through an inhibition of adenosine receptors (Aubier et al., J. Appl. Physiol. 54: 460-4, 1983). Enprofylline (E) is a xanthine drug that has poor ability to antagonize physiological actions of adenosine. The aim of this study was to compare the effects on diaphragmatic contractility of T and E in order to determine whether antagonism of adenosine receptors was the underlying mechanism of the inotropic effect of T on diaphragmatic contractility. Ten normal subjects were studied in the sitting position. The contractile properties of the diaphragm were assessed by measuring the transdiaphragmatic pressure (Pdi) generated at functional residual capacity during bilateral electrical stimulation of the phrenic nerves. The subjects were randomized, and after control measurements were performed, they received T or E. This was a double-blind crossover study, the measurements being repeated with the second drug after one week. Both drugs were administered intravenously with a loading dose of 6 and 2 mg/kg administered in 30 min for T and E and a maintenance dose of 0.9 and 0.075 mg.kg-1 X h-1 for T and E, respectively. Measurements were performed before and 60 min after T or E administration. Plasmatic levels of both drugs were also analyzed. In all the subjects, therapeutic levels of T or E were reached (14.8 +/- 0.6 and 3.9 +/- 0.42 mg/l for T and E, respectively, at 30 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Effects of digoxin on diaphragmatic strength generation in patients with chronic obstructive pulmonary disease during acute respiratory failure.

We studied the effects of digoxin, a compound that has an inotropic effect on the myocardium, on diaphragmatic function in 8 patients with chronic obstructive pulmonary disease. All the patients were in acute respiratory failure and were artificially ventilated. Diaphragmatic strength was assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. The latter were stimulated before and at 45 and 90 min after administration of digoxin (0.02 mg/kg infused for 10 min). In all the patients, cardiac output was measured by the thermodilution technique using a Swan-Ganz catheter placed in the pulmonary artery. Arterial blood gases and pH were maintained within normal range by mechanical ventilation. In all the patients, digoxin plasma levels reached the therapeutic range (mean values, 2.82 +/- 0.17 and 2.90 +/- 0.20 nmol/L at 45 and 90 min, respectively) after digoxin administration. Diaphragmatic strength improves significantly after digoxin administration, the transdiaphragmatic pressure for an identical phrenic stimulation increasing by 19.5% (p less than 0.001) on the average. This increase was noted 45 and 90 min after digoxin administration. We conclude that digoxin has a potent effect on diaphragmatic strength generation that may be beneficial in patients with chronic obstructive pulmonary disease during acute respiratory failure. Furthermore, this inotropic positive effect of digoxin on the diaphragm, as previously observed for the myocardium, emphasizes the similarities between these 2 contractile tissues.

Action Potentials↗

PubMed1986

Effects of digoxin on diaphragmatic strength generation.

Contrary to hindlimb muscle, extracellular calcium plays an important role in diaphragmatic strength generation (J. Appl. Physiol. 58: 2054-61, 1985). Since the inotropic effect of digitalis appears to be related to cell membrane transport of calcium, we studied the effect of digoxin on diaphragmatic contractility in 20 anesthetized dogs. The diaphragm was electrically stimulated with intramuscular electrodes. The transdiaphragmatic pressure (Pdi) during supramaximal (50 V) 2-s stimulations applied over a frequency range of 10-100 Hz was measured with balloon catheters at functional residual capacity. Cardiac output was measured with a Swan-Ganz catheter and diaphragmatic blood flow (Qdi) by timed volume collections of left inferior venous effluent. The force generated by the sartorius muscle during electrical stimulations was studied concomitantly to Pdi. In 10 dogs (group A) 0.04 mg/kg of digoxin was infused in 10 min. In 10 other dogs (group B) 0.2 mg/kg was administered. All measurements were performed during control and 30, 60, 90, and 120 min after digoxin administration. In group A, digoxin plasmatic level at 60 min reached a therapeutic range in all dogs (1.8 +/- 0.3 ng/ml), whereas in group B, digoxin plasmatic level was higher (8 +/- 1.3 ng/ml). No significant change in cardiac output and Qdi was noted after administration of digoxin, either in the dogs of group A or those of group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Effects of theophylline on isolated diaphragmatic fibers. A model for pharmacologic studies on diaphragmatic contractility.

An in vitro model of isolated diaphragmatic muscle fibers was developed to study the effects of theophylline on diaphragmatic contractility. The effects of theophylline on this model were compared for each dose with the effects of the drugs on a "classic" hemidiaphragmatic muscle preparation. Diaphragmatic strips obtained from 20 rats were placed into an open topped channel of a plexiglass tissue chamber and perfused with continuously flowing Krebs solution heated to 37 degrees and bubbled with a 95% O2 and 5% CO2 gas mixture so as to maintain pH, PO2, PCO2 constant (7.4, 100, and 35 mmHg, respectively). Isometric force generated in response to 1 Hz supramaximal electrical stimulation was measured with a highly sensitive photoelectric transducer. Graded doses of aminophylline (15 to 75 mg/L) were administered and their effect assessed on diaphragmatic peak twitch tension. On the single diaphragmatic muscle fibers preparation, theophylline produced a dose dependent increase in peak twitch tension, which, at a concentration of theophylline of 15 mg/L, a therapeutic dose, amounted to 111 +/- 1.5% of control (p less than 0.05). At a concentration of 60 mg/L the increase in peak twitch tension averaged 35 +/- 2.5% of control, (p less than 0.001). On the other hand, theophylline had no effect on the hemidiaphragm preparation until a dose of 250 mg/L. These findings suggest that the effects of theophylline on diaphragmatic contractility are due to a direct action of the drug on the contractile properties of the diaphragmatic fibers and also validate the presented in vitro model as a promising one for future pharmacologic studies on diaphragmatic contractility.

Animals↗

PubMed1986

[Evaluation of the efficacy of the surgical treatment of panlobular emphysema].

26 patients presenting with panlobular emphysema between 1978 and 1984 were submitted to a thoracotomy for surgical resection of their bullae. Pre-operative and post-operative evaluations of the following were made: The level of dyspnoea in 5 grades. The FEV1 (VEMS) the forced vital capacity (CVF) the functional residual capacity (CRF) measured plethysmographically, the residual volume (VR), the total lung capacity (CPT). Arterial blood gases. The presence of radiological signs of compression on pulmonary angiography and on plain chest radiographs: an index of compression rated 0 to 6 was defined at the outset. The subjects were split into 3 groups based on their post-operative respiratory function: Group 1: no improvement (n = 7). Group 2: moderate improvement of dyspnoea (n = 11). Group 3: a big improvement in dyspnoea (n = 7). These three groups were homogenous as regards their preoperative respiratory function. On the other hand, the compression caused by the bullae based on the pre-operative radiological data was much greater (p 0.01) in the group of patients who improved. In addition when the index of compression was equal or superior to 3 (n = 14) all the patients were improved (n = 6). The comparison of pre- and post-operative values shows the following results: The change in blood gases was very limited in all groups; the ventilatory parameters were unchanged in group 1; on the other hand in group 2 and 3 one notes an overall improvement in pulmonary function. The size of the improvement however, was very variable from one individual to another.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure.

We studied the effects of hypophosphatemia on diaphragmatic function in eight patients with acute respiratory failure who were artificially ventilated. Their mean serum phosphorus level was 0.55 +/- 0.18 mmol per liter (normal value, 1.20 +/- 0.10). The contractile properties of the diaphragm were assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. Diaphragmatic function was evaluated in each patient before and after correction of hypophosphatemia, which was achieved by administration of 10 mmol of phosphorus (as KH2PO4) as a continuous infusion for four hours. After phosphate infusion, the mean serum phosphorus level increased significantly (1.33 +/- 0.21 mmol per liter, P less than 0.0001). The increase in serum phosphorus was accompanied by a marked increase in the transdiaphragmatic pressure after phrenic stimulation (17.25 +/- 6.5 cm H2O as compared with 9.75 +/- 3.8 before phosphate infusion, P less than 0.001). Changes in the serum phosphorus level and transdiaphragmatic pressure were well correlated (r = 0.73). These results strongly suggest that hypophosphatemia impairs the contractile properties of the diaphragm during acute respiratory failure, and they emphasize the importance of maintaining normal serum inorganic phosphate levels in such patients.

Acute Disease↗

PubMed1985

[Hypophosphoremia during mechanical ventilation for chronic obstructive bronchopathies].

Hypophosphoremia may interfere with respiratory function in chronic obstructive pulmonary diseases (COPD) through different mechanisms: muscular exhaustion and weakness. Accordingly, the frequency and magnitude of hypophosphoremia was studied in 36 consecutive patients with acute respiratory failure and mechanical ventilation. Initial phosphoremia was normal (1,32 +/- 0,12 mmol/l) but often and rapidly decreased in all patients after mechanical ventilation had been started (0,54 +/- 0,14 mmol/l after 24 h). After this, phosphoremia remained low, slowly increasing with continued enteral nutrition (2000 Kcal, 276 g of glucides, 33 mmol/l of phosphorus). Four patients had severe hypophosphoremia after 24 h of mechanical ventilation (less than 0,30 mmol/l). Phosphoremia returned to a normal level 36 h after extubation. Hypophosphoremia was closely linked to pH improvement (r = + 0,67, P less than 0,001) and was paralleled by a drop in phosphaturia, suggesting intra-cellular penetration of phosphorus.

Acidosis↗

PubMed1985

[Function of the respiratory muscles in acute cardiac decompensation].

In anesthetized dogs the performance of the respiratory muscles during cardiogenic shock and their influence on its outcome was studied. Shock was induced by cardiac tamponade. Cardiac output during shock amounted to 25-35% of control and was kept constant. Minute ventilation (VE) initially increased and then progressively decreased until respiratory arrest. The latter was due to impairment of respiratory muscle contractility, the pressure generated by the diaphragm (Pdi) decreasing despite a marked increase in the diaphragmatic electromyogram and of the phrenogram. Mechanical ventilation during shock prolonged survival for the same decrease in cardiac output, and also decreased substantially the severity of lactic acidosis. Furthermore, blood flow to the respiratory muscles during shock was different in the animals breathing spontaneously (SB) from that in mechanically ventilated animals (MV). The fraction of cardiac output distributed to the respiratory muscles during control amounted to 1.85% in MV and 2.79% in SB. With shock this decreased to 1.55% in MV while in SB it decreased by 21%, which suggests that mechanical ventilation during shock preserves a large portion of cardiac output used by the respiratory muscles during spontaneous breathing, thus making it available to other organs.

Animals↗

PubMed1985

Bilateral phrenic stimulation: a simple technique to assess diaphragmatic fatigue in humans.

Transdiaphragmatic pressure (Pdi) and the rate of relaxation of the diaphragm (tau) were measured at functional residual capacity (FRC) in six normal seated subjects during single-twitch stimulation of both phrenic nerves. The latter were stimulated supramaximally with needle electrodes with square-wave impulses of 0.1-ms duration at 1 Hz before and after diaphragmatic fatigue produced by resistive loaded breathing. Constancy of chest wall configuration was achieved by monitoring the diameter of the abdomen and the rib cage with a respiratory inductive plethysmograph system. During control the peak Pdi generated during the phrenic stimulation amounted to 34.4 +/- 4.2 (SE) cmH2O and represented in each subject a fixed fraction (17%) of its maximal transdiaphragmatic pressure. After diaphragmatic fatigue the peak Pdi decreased by an average of 45%, amounting to 18.1 +/- 2.7 cmH2O 5 min after the fatigue run, and tau increased from 55.2 +/- 9 ms during control to 77 +/- 8 ms 5 min after the fatigue run. The decrease in peak Pdi and the increase in tau observed after the fatigue run persisted throughout the 30 min of the recovery period studied, the peak Pdi amounting to 18.4 +/- 2.8 and 18.9 +/- 3.3 cmH2O and tau to 81.3 +/- 5.7 and 88.7 +/- 10 ms at 15 and 30 min after the end of the fatigue run, respectively. It is concluded that diaphragmatic fatigue can be detected in man by bilateral phrenic stimulation with needle electrodes without any discomfort for the subject and that the decrease in diaphragmatic strength after fatigue is long lasting.

Action Potentials↗

PubMed1985

Effects of hypocalcemia on diaphragmatic strength generation.

We studied the effects of hypocalcemia on diaphragmatic force and diaphragm blood flow (Qdi) in 12 anesthetized dogs. The diaphragm was electrically stimulated with intramuscular electrodes surgically implanted in the ventral surface of each hemidiaphragm. The transdiaphragmatic pressure (Pdi) during supramaximal (50 V) 2-s stimulations applied over a frequency range of 10-100 Hz was measured with balloon catheters during tracheal occlusion at functional residual capacity. A catheter was placed via the femoral vein into the left inferior phrenic vein, and Qdi was measured by timed volume collections of left inferior venous effluent. A catheter was introduced in a femoral artery to monitor blood pressure (BP). In five additional dogs, the force generated by the sartorius muscle during electrical stimulation was also studied concomitantly to diaphragmatic force. The animals were mechanically ventilated throughout the experiment, and the arterial blood gases and pH were maintained constant. Hypocalcemia was induced by a continuous infusion of EGTA (70 mg X kg-1 X h-1), which led to a progressive decrease (P less than 0.0001) of ionized calcium plasmatic level from 2.21 +/- 0.4 meq/1 during control to 1.69 +/- 0.06, 1.25 +/- 0.5, and 1.07 +/- 0.5 meq/1 after 30, 60, and 120 min, respectively. Hypocalcemia decreased progressively Pdi, which amounted to 84 +/- 3 (P less than 0.001) and 98 +/- 2% of control values for the low frequencies (10 and 20 Hz) and the high frequencies (50 and 100 Hz), respectively, after 30 min of EGTA infusion and to 74 +/- 5 and 79 +/- 6% for the low and high frequencies, respectively, after 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Work of breathing in patients with chronic obstructive pulmonary disease in acute respiratory failure.

In 11 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) in acute ventilatory failure, we measured the total inspiratory (WItot) and total resistive (WI + Eres) work rate of breathing, together with lung mechanics (dynamic pulmonary elastance and inspiratory and expiratory pulmonary flow resistance). All variables were markedly increased compared with those in normal subjects. No significant correlation was found between WItot and WI + Eres with lung mechanics data. However, when WItot and WI + Eres were expressed per liter of ventilation, a significant positive correlation was found with all lung mechanics data. These results indicate that although in patients acutely ill with COPD, work rate and work per liter of ventilation are increased, only the latter is related to the severity of pulmonary mechanical impairment, and it could be used as one of the criteria for extubation. In addition, our results indicate that at end-expiration the alveolar pressure was positive (range, 6 to 13 cm H2O) in all patients (intrinsic PEEP), a fact that must necessarily affect hemodynamics; furthermore, it imposes an extra burden on the inspiratory muscles.

Acute Disease↗

PubMed1984

Effects of theophylline on diaphragmatic strength and fatigue in patients with chronic obstructive pulmonary disease.

We studied the effects of theophylline on diaphragmatic strength and fatigue in 15 patients with severe chronic obstructive pulmonary disease. Diaphragmatic strength was assessed by measurement of the transdiaphragmatic pressure generated at functional residual capacity during a maximal inspiratory effort against closed airways. Diaphragmatic fatigue was induced by resistive loaded breathing. The electrical activity of the diaphragm was recorded with an esophageal electrode during the fatigue runs, and the high-low ratio of the electrical signal was analyzed to assess diaphragmatic fatigue. Studies were performed before and after 7 and 30 days of theophylline administration (mean plasma level, 13 +/- 2 mg per liter). A control group received a placebo instead of theophylline. Theophylline increased maximal transdiaphragmatic pressure by 16 per cent after 7 days of administration (P less than 0.01), and this increase persisted after 30 days. No significant change in maximal transdiaphragmatic pressure was observed in the group given the placebo. Theophylline also suppressed diaphragmatic fatigue in all patients who received it. We conclude that theophylline has a potent and long-lasting effect on diaphragmatic strength and fatigue in patients with fixed airway obstruction.

Diaphragm↗

PubMed1984

Effects and mechanism of action of terbutaline on diaphragmatic contractility and fatigue.

We studied the effects of intravenously administered terbutaline on diaphragmatic force and fatigue during electrical stimulation of the diaphragm in 17 anesthetized dogs. The diaphragm was stimulated indirectly through the phrenic nerves with electrodes placed around the fifth roots and directly with electrodes surgically implanted in the abdominal side of each hemidiaphragm. Transdiaphragmatic pressure (Pdi) during direct or indirect supramaximal 2-s stimulation applied over a frequency range of 10-100 Hz was measured with balloon catheters during tracheal occlusion at functional residual capacity. In seven dogs the administration of terbutaline (0.5 mg) had no effect on Pdi at any stimulation frequency applied directly or indirectly. The effect of terbutaline (0.5 mg) on diaphragmatic fatigue was then tested in 10 other dogs. Diaphragmatic fatigue was produced by continuous 20-Hz electrical supramaxial stimulation of the phrenic nerves during 30 min. At the end of the fatigue procedure Pdi decreased by 50 +/- 5 and 30 +/- 8% of control values at 10 and 100 Hz, respectively, for either direct or indirect stimulation. The decrease in Pdi for low frequencies of stimulation (10 and 20 Hz) lasted 100 +/- 18 min, whereas it lasted only 40 +/- 10 min for the high frequencies (50 and 100 Hz). When terbutaline (0.5 mg) was administered after the fatiguing procedure, Pdi increased within 15 min by 20 +/- 4% at 10 Hz and by 12 +/- 3% at 100 Hz for either direct or indirect stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Effects of aminophylline on diaphragmatic fatigue during acute respiratory failure.

The effects of aminophylline on diaphragmatic fatigue and recovery in the face of hypoxemia and hypercapnic acidosis were studied in anesthetized, spontaneously breathing, dogs. The phrenic nerves were stimulated supramaximally at 10, 20, 50, and 100 Hz during 2 s with electrodes placed around the fifth roots, and the resulting transdiaphragmatic pressure (Pdi) was measured with balloon catheters. The dogs were occluded before the stimulations at functional residual capacity. The latter was monitored by measuring the end-expiratory transpulmonary pressure, which remained constant throughout the experiment. Diaphragmatic fatigue was produced by resistive loaded breathing. At the end of the runs, which lasted 15 +/- 2 min, all the dogs were severely hypoxemic (30 +/- 5 mmHg), hypercapnic (65 +/- 4 mmHg), and acidotic (7.1 +/- 0.05). During the fatigue runs, phrenic stimulation resulted in a marked decrease in Pdi, which amounted at 20 Hz to 70 +/- 8% and 45 +/- 12% of the control values 5 min after the onset of the fatigue runs and at the end, respectively. After recovery (3 h), Pdi and arterial blood gas determinations returned to control values. Identical fatigue runs were repeated with aminophylline infusion (loading dose, 6 mg/kg in 10 min and maintenance dose, 1 mg/kg/h), leading to a plasmatic concentration of 16.4 +/- 2 mg/l. Aminophylline protected the diaphragm against fatigue, and despite the presence of hypoxemia and hypercapnic acidosis, the Pdi generated for a 20 Hz stimulation of the phrenic nerves at identical times of the preceding run amounting to 100 +/- 15% and 85 +/- 10% of control values, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗