Biomedical subjects

N Viirès

Publications and source records attributed to N Viirès.

7 recordsLinked 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↗

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

Different effects of halothane on diaphragm and hindlimb muscle in rats.

The effects of halothane administration on diaphragm and tibialis anterior (TA) muscle were investigated in 30 anesthetized mechanically ventilated rats. Diaphragmatic strength was assessed in 17 rats by measuring the abdominal pressure (Pab) generated during supramaximal stimulation of the intramuscular phrenic nerve endings at frequencies of 0.5, 30, and 100 Hz. Halothane was administered during 30 min at a constant minimum alveolar concentration (MAC): 0.5, 1, and 1.5 MAC in three groups of five rats. For each MAC, Pab was significantly reduced for all frequencies of stimulation except at 100 Hz during 0.5 MAC halothane exposure. The effects of halothane (0.5, 1, and 1.5 MAC) on diaphragmatic neuromuscular transmission were assessed in five other rats by measuring the integrated electrical activity of the diaphragm (Edi) during electrical stimulation of the phrenic nerve. No change in Edi was observed during halothane exposure. In five other rats TA contraction was studied by measuring the strength of isometric contraction of the muscle during electrical stimulation of its nerve supply at different frequencies (0.5, 30, and 100 Hz). Muscle function was unchanged during administration of halothane in a cumulative fashion from 0.5 to 1.5 MAC. These results demonstrate that halothane does not affect hindlimb muscle function, whereas it had a direct negative inotropic effect on rat diaphragmatic muscle.

Animals↗

PubMed1987

Effects of phrenic nerve cooling on diaphragmatic function.

The effects of phrenic nerve cooling at 0 degrees C on the nerve and diaphragmatic function were evaluated in dogs. Eleven dogs, anesthetized and mechanically ventilated, were studied. Left diaphragmatic function was assessed by recording the transdiaphragmatic pressure (Pdi) generated during electrical stimulation of the left phrenic nerve at different frequencies (0.5, 30, and 100 Hz). Phrenic nerve stimulations were achieved either directly by electrodes placed around the phrenic nerve above its pericardial course or by intramuscular electrodes placed close to the phrenic nerve endings. Electrical activity of the hemidiaphragm (Edi) was recorded and phrenic nerve conduction time (PNCT) was measured during direct phrenic stimulation. A transpericardial cooling of the nerve, at 0 degrees C, on a length of 1 cm, was performed during 30 min (group A, n = 7) or 5 min (group B, n = 4). After the cooling period, phrenic and diaphragmatic functions were assessed hourly for 4 h (H1-H4). Cooling the phrenic nerve produced a complete phrenic nerve conduction block in all dogs, 100 +/- 10 s after the onset of cold exposure. Conduction recovery time was longer in group A (11 +/- 7 min) than in group B (2 +/- 0.5 min) and PNCT remained increased throughout the study in group A. Furthermore, in group A, Pdi and Edi during direct phrenic stimulation were markedly depressed from H1 to H4. No change in these parameters was noted until H3 during intramuscular stimulation, time at which a significant decrease occurred. By contrast, Pdi and Edi from direct and intramuscular stimulations remained unchanged throughout the study in group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

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

Diaphragmatic contractility after upper abdominal surgery.

Postoperative dysfunction of the diaphragm has been reported after upper abdominal surgery. This study was designed to determine whether an impairment in diaphragmatic contractility was involved in the genesis of the diaphragmatic dysfunction observed after upper abdominal surgery. Five patients undergoing upper abdominal surgery were studied. The following measurements were performed before and 4 h after surgery: vital capacity (VC), functional residual capacity (FRC), and forced expiratory volume in 1 s. Diaphragmatic function was also assessed using the ratio of changes in gastric pressure (delta Pga) over changes in transdiaphragmatic pressure (delta Pdi). Finally contractility of the diaphragm was determined by measuring the change in delta Pdi generated during bilateral electrical stimulation of the phrenic nerves (Pdi stim). Diaphragmatic dysfunction occurred in all the patients after upper abdominal surgery as assessed by a marked decrease in delta Pga/delta Pdi from 0.480 +/- 0.040 to -0.097 +/- 0.152 (P less than 0.01) 4 h after surgery compared with preoperative values. VC also markedly decreased after upper abdominal surgery from 3,900 +/- 630 to 2,060 +/- 520 ml (P less than 0.01) 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after upper abdominal surgery compared with the preoperative values. We conclude that contractility of the diaphragm is not altered after upper abdominal surgery, and diaphragmatic dysfunction is secondary to other mechanisms such as possible reflexes arising from the periphery (chest wall and/or peritoneum), which could inhibit the phrenic nerve output.

Abdomen↗