Changes In Transdiaphragmatic Pressure Research Articles

This Month in Anesthesiology

This Month in Anesthesiology

Poor Correlation between Diaphragm Thickening Fraction and Transdiaphragmatic Pressure in Mechanically Ventilated Patients and Healthy Subjects.

The relationship between the diaphragm thickening fraction and the transdiaphragmatic pressure, the reference method to evaluate the diaphragm function, has not been clearly established. This study investigated the global and intraindividual relationship between the thickening fraction of the diaphragm and the transdiaphragmatic pressure. The authors hypothesized that the diaphragm thickening fraction would be positively and significantly correlated to the transdiaphragmatic pressure, in both healthy participants and ventilated patients. Fourteen healthy individuals and 25 mechanically ventilated patients (enrolled in two previous physiologic investigations) participated in the current study. The zone of apposition of the right hemidiaphragm was imaged simultaneously to transdiaphragmatic pressure recording within different breathing conditions, i.e., external inspiratory threshold loading in healthy individuals and various pressure support settings in patients. A blinded offline breath-by-breath analysis synchronously computed the changes in transdiaphragmatic pressure, the diaphragm pressure-time product, and diaphragm thickening fraction. Global and intraindividual relationships between variables were assessed. In healthy subjects, both changes in transdiaphragmatic pressure and diaphragm pressure-time product were moderately correlated to diaphragm thickening fraction (repeated measures correlation = 0.40, P < 0.0001; and repeated measures correlation = 0.38, P < 0.0001, respectively). In mechanically ventilated patients, changes in transdiaphragmatic pressure and thickening fraction were weakly correlated (repeated measures correlation = 0.11, P = 0.008), while diaphragm pressure-time product and thickening fraction were not (repeated measures correlation = 0.04, P = 0.396). Individually, changes in transdiaphragmatic pressure and thickening fraction were significantly correlated in 8 of 14 healthy subjects (ρ = 0.30 to 0.85, all P < 0.05) and in 2 of 25 mechanically ventilated patients (ρ = 0.47 to 0.64, all P < 0.05). Diaphragm pressure-time product and thickening fraction correlated in 8 of 14 healthy subjects (ρ = 0.41 to 0.82, all P < 0.02) and in 2 of 25 mechanically ventilated patients (ρ = 0.63 to 0.66, all P < 0.01). Overall, diaphragm function as assessed with transdiaphragmatic pressure was weakly related to diaphragm thickening fraction. The diaphragm thickening fraction should not be used in healthy subjects or ventilated patients when changes in diaphragm function are evaluated.

Sex differences in diaphragmatic fatigue and the metaboreflex following inspiratory pressure-threshold loading.

Sex differences in diaphragmatic fatigue and the metaboreflex following inspiratory pressure-threshold loading.

Mechanics of the canine diaphragm in ascites: a CT study

Ascites causes an increase in the elastance of the abdomen and impairs the lung-expanding action of the diaphragm, but its overall effects on the pressure-generating ability of the muscle remain unclear. In the present study, radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm in five dogs, and the three-dimensional locations of the markers during relaxation and during phrenic nerve stimulation in the presence of increasing amounts of ascites were determined using a computed tomographic scanner. From these data, accurate measurements of muscle length and quantitative estimates of diaphragm curvature were obtained, and the changes in transdiaphragmatic pressure (Pdi) were analyzed as functions of muscle length and curvature. With increasing ascites, the resting length of the diaphragm increased progressively. In addition, the amount of muscle shortening during phrenic nerve stimulation decreased gradually. When ascites was 100 ml/kg body wt, therefore, the muscle during contraction was longer, leading to a 20-25% increase in Pdi. As ascites increased further to 200 ml/kg, however, muscle length during contraction continued to increase, but Pdi did not. This absence of additional increase in Pdi was well explained by the increase in the diameter of the ring of insertion of the diaphragm to the rib cage and the concomitant increase in the radius of diaphragm curvature. These observations indicate that the pressure-generating ability of the diaphragm is determined not only by muscle length as conventionally thought but also by muscle shape.

Effect of Lung Volume Reduction Surgery on Diaphragmatic Neuromechanical Coupling At 2 Years

We previously reported that patients with emphysema show an increase in diaphragmatic neuromechanical coupling at 3 months after lung volume reduction surgery. Diaphragmatic neuromechanical coupling was quantified as the quotient of tidal volume (normalized to total lung capacity) to tidal change in transdiaphragmatic pressure (normalized to maximal transdiaphragmatic pressure). As such, neuromechanical coupling estimates the fraction of diaphragmatic capacity used to generate tidal breathing. The present investigation was conducted to determine whether benefit is maintained at 2 years. Fifteen patients with severe COPD, 8 of whom completed the 2-year study. Lung volumes, exercise capacity (6-min walking distance), diaphragmatic function (maximal transdiaphragmatic pressure and twitch transdiaphragmatic pressure elicited by phrenic nerve stimulation), and diaphragmatic neuromechanical coupling were recorded before surgery, and at 3 months and 2 years after surgery. Two years after surgery, lung volumes deteriorated to preoperative values, but patients showed persistent improvements in 6-min walking distance (p < 0.05). Three months after surgery, maximal transdiaphragmatic pressure (p < 0.05), twitch transdiaphragmatic pressure (p < 0.01), and diaphragmatic neuromechanical coupling (p < 0.01) had increased over preoperative values. The improvements in neuromechanical coupling resulted from improvements in diaphragmatic strength and, to a lesser extent, from a decrease in transdiaphragmatic pressure required to maintain tidal breathing. The change in respiratory muscle function at 2 years varied among patients: diaphragmatic contractility was > 10% of preoperative value in half of the patients who concluded our study, and neuromechanical coupling was > 10% of preoperative value in three fourths of the patients who concluded our study. Patients who maintained their gains in neuromechanical coupling also maintained their gains in 6-min walking distance. Patients undergoing lung volume reduction surgery can maintain early gains in neuromechanical coupling and exercise capacity 2 years later.

Effect of hypercapnia on maximal voluntary ventilation and diaphragm fatigue in normal humans.

Relatively little is known about the combined effects of hypercapnia and fatigue on the human diaphragm. We examined the effects of acute hypercapnia and fatigue in seven subjects by measuring changes in transdiaphragmatic pressure (Pdi) elicited by cervical magnetic stimulation after 2 min maximal voluntary ventilation (MVV) while breathing air and also with the inspired PCO(2) increased to 8% for 12 min before and during the MVV. Diaphragm strength was assessed before and at 0, 20, 40, 60, and 90 min after the MVV in both studies with the subjects breathing air. There was no difference in the level of ventilation for each run. Mean (+/- SD) twitch Pdi (TwPdi) fell significantly (p < 0.01) at 20 min after the control and hypercapnic MVV; (30.4 [7.8] to 27.0 [8.1] cm H(2)O control and 30.3 [4.1] to 27.3 [5.0] cm H(2)O CO(2)) and remained significantly (p < 0.01) below baseline. The changes in TwPdi at 20 to 90 min were not significantly different between the control and CO(2) runs. The decrease in TwPdi at 0 min after MVV, however, was greater (15%) in the hypercapnic run than in the control run (8.1%) (p < 0.05) when compared with baseline valves. Hypercapnia does not intensify long lasting fatigue but may reduce diaphragm contractility immediately after MVV.

RETRACTED ARTICLE: Nicardipine inhibits amrinone-enhanced contractility in fatigued diaphragm

The purpose of this study was to examine the effect of amrinone, a bipyridine derivative, with and without nicardipine, a calcium channel blocker, on the contractility of fatigued diaphragm in dogs. Twenty dogs were divided into two groups of ten each: amrinone group (group A) and combined amrinone and nicardipine group (group AN). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (Pdi). In group A, after producing fatigue, amrinone (0.75 mg·kg(-1) loading dose plus 10 μg·kg(-1)·min(-1) maintenance dose) was administered iv. In group AN, nicardipine 5 μg·kg(-1)·min(-1) was infused iv simultaneously with amrinone during this period. After diaphragmatic fatigue, Pdi at low-frequency (10-30 Hz) stimulation decreased compared with the prefatigue values (P<0.05), whereas no change in Pdi was observed at high-frequency (50-100 Hz), stimulation. The Pdi at each stimulus were increased compared with the fatigued values (P<0.05) by administering amrinone, and returned to these values after this agent was discontinued. The Pdi values at any frequency of stimulation did not change when amrinone was administered with nicardipine. Our results suggest that amirinone may enhance contractility in fatigued diaphragm via its effect on transmembrane calcium movement.

Nicardipine inhibits amrinone-enhanced contractility in fatigued diaphragm

The purpose of this study was to examine the effect of amrinone, a bipyridine derivative, with and without nicardipine, a calcium channel blocker, on the contractility of fatigued diaphragm in dogs. Twenty dogs were divided into two groups of ten each: amrinone group (group A) and combined amrinone and nicardipine group (group AN). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (Pdi). In group A, after producing fatigue, amrinone (0.75 mg·kg−1 loading dose plus 10 μg·kg−1·min−1 maintenance dose) was administered iv. In group AN, nicardipine 5 μg·kg−1·min−1 was infused iv simultaneously with amrinone during this period. After diaphragmatic fatigue, Pdi at low-frequency (10–30 Hz) stimulation decreased compared with the prefatigue values (P<0.05), whereas no change in Pdi was observed at high-frequency (50–100 Hz), stimulation. The Pdi at each stimulus were increased compared with the fatigued values (P<0.05) by administering amrinone, and returned to these values after this agent was discontinued. The Pdi values at any frequency of stimulation did not change when amrinone was administered with nicardipine. Our results suggest that amirinone may enhance contractility in fatigued diaphragm via its effect on transmembrane calcium movement.

RETRACTED ARTICLE: Dobutamine increases contractility of fatigued diaphragm in dogs: The relationship between dose and diaphragmatic contractility

The dose-related effects of dobutamine (DOB) on the contractility of fatigued diaphragm were studied in 16 anesthetized, mechanically ventilated dogs. The animals were divided into two groups of eight: the control (group C) and the DOB (group D). Diaphragmatic fatigue was induced by intermittent supramaximal electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (Pdi). After the induction of diaphragmatic fatigue, Pdi at low-frequency (20-Hz) stimulation decreased significantly compared with the prefatigue values (P<0.05), whereas no change in Pdi was observed at high-frequency (100-Hz) stimulation. In group D, after producing fatigue, Pdi at 20-Hz stimulation increased significantly with a continuous infusion of DOB (5 and 10 μg·kg(-1)·min(-1)) i.v. (P<0.05). The Pdi at 100-Hz stimulation increased significantly with administration of DOB 10 μg·kg(-1)·min(-1) i.v. (P<0.05). There was a significant correlation between dose of DOB and Pdi at both stimuli (P<0.05). In group C, the speed of Pdi recovery at 20-Hz stimulation was relatively slower. The integrated diaphragmatic electric activity (Edi) in each group did not change at any frequency of stimulation throughout the study. It is concluded that DOB increases the contractility of fatigued diaphragm in a dose-dependent manner.

Dobutamine increases contractility of fatigued diaphragm in dogs: the relationship between dose and diaphragmatic contractility

The dose-related effects of dobutamine (DOB) on the contractility of fatigued diaphragm were studied in 16 anesthetized, mechanically ventilated dogs. The animals were divided into two groups of eight: the control (group C) and the DOB (group D). Diaphragmatic fatigue was induced by intermittent supramaximal electrophrenic stimulation at a frequency of 20Hz applied for 30min. Diaphragmatic con- tractility was assessed from changes in transdiaphragmatic pressure (Pdi). After the induction of diaphragmatic fatigue, Pd~ at low-frequency (20-Hz) stimulation decreased signifi- cantly compared with the prefatigue values (P < 0.05), whereas no change in Pdi was observed at high-frequency (100-Hz) stimulation. In group D, after producing fatigue, Pd~ at 20-Hz stimulation increased significantly with a continuous infusion of DOB (5 and 10 ~tg.kg z-rain-l) i.v. (P < 0.05). The P~ at 100-Hz stimulation increased significantly with adminis- tration of DOB 10~tg.kg-l.min -1 i.v. (P < 0.05). There was a significant correlation between dose of DOB and Pd~ at both stimuli (P < 0.05). In group C, the speed of Pa~ recovery at 20- Hz stimulation was relatively slower. The integrated diaphrag- matic electric activity (Edi) in each group did not change at any frequency of stimulation throughout the study. It is concluded that DOB increases the contractility of fatigued diaphragm in a dose-dependent manner.

RETRACTED ARTICLE: The dose-response relationship of amrinone in increasing the contractility of fatigued diaphragm in dogs

We studied the dose-related effects of amrinone on the contractility of a fatigued diaphragm in 16 anesthetized, mechanically ventilated dogs. The animals were divided into two groups: the control group (Group C,n=8) and the amrinone group (Group A,n=8). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. The contractility of the diaphragm was assessed from changes in transdiaphragmatic pressure (P di). After inducing fatigue,P di at low-frequency (20 Hz) stimulation decreased significantly compared with the pre-fatigue values (P<0.05), whereas no change was observed at high-frequency (100 Hz) stimulation. In Group A, after producing fatigue,P di at 20 Hz stimulation increased significantly with a bolus injection (0.75 mg·kg(-1)) followed by continuous infusion of amrinone (2.5, 5 and then 10μg·kg(-1)min(-1)) IV (P<0.05).P di at 100 Hz stimulation increased significantly with an administration of amrinone (10μg·kg(-1)min(-1) IV (P<0.05). There was a significant positive correlation betweenP di at both stimuli and amrinone dose (P<0.01). In Group, C, the speed of recovery ofP di at 20 Hz stimulation was relatively slower. The integrated electric activity of the diaphragam (E di) in each group did not change at any frequency of stimulation throughout the experiment. We conclude that amrinone exerts a dose-dependent enhancement of the contractility of a fatigued diaphragm in dogs.

The dose?response relationship of amrinone in increasing the contractility of fatigued diaphragm in dogs

We studied the dose-related effects of amrinone on the contractility of a fatigued diaphragm in 16 anesthetized, mechanically ventilated dogs. The animals were divided into two groups: the control group (Group C, n = 8) and the amrinone group (Group A, n = 8). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral elec- trophrenic stimulation at a frequency of 20 Hz applied for 30min. The contractility of the diaphragm was assessed from changes in transdiaphragmatic pressure (Pai). After inducing fatigue, Pd~ at low-frequency (20Hz) stimulation decreased significantly compared with the pre-fatigue values (P < 0.05), whereas no change was observed at high-frequency (100Hz) stimulation. In Group A, after producing fatigue, P< at 20Hz stimulation increased significantly with a bolus injection (0.75 mg.kg 1) followed by continuous infusion of amrinone (2.5, 5 and then 10vg.kg-l.min ~) IV (P < 0.05). Pdi at 100Hz stimulation increased significantly with an administration of amrinone (10~g.kg-a.min a) IV (P < 0.05). There was a sig- nificant positive correlation between Pd~ at both stimuli and amrinone dose (P < 0.01). In Group C, the speed of recovery of P~i at 20Hz stimulation was relatively slower. The inte- grated electric activity of the diaphragam (Edi) in each group did not change at any frequency of stimulation throughout the experiment. We conclude that amrinone exerts a dose- dependent enhancement of the contractility of a fatigued diaphragm in dogs.

RETRACTED ARTICLE: Effects of nicardipine on diaphragmatic fatigue in the dog: The relationship between dosage and fatigability

We examined the dose-related effects of nicardipine on the diaphragmatic fatigability in 24 anesthetized, mechanically ventilated dogs. Animals were divided into three groups of eight each: the control group (group C), the nicardipine 3 μg·kg(-1) I.V. group (group N1) and the nicardipine 5 μg·kg(-1)·min(-1) I.V. group (group N2). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. In groups N1 and N2, nicardipine was continuoulsy infused intravenously during this fatigueproducing period. Diaphragmatic contractility was assessed by changes in transdiaphragmatic pressure (Pdi). After induction of diaphragmatic stimulation at low-frequency (20 Hz), Pdi decreased significantly in all groups compared with the prefatigue value (P<0.05), whereas no change was observed in Pdi at high-frequency (100 Hz) stimulation. The Pdi at 20 Hz stimulation was significantly lower in groups N1 and N2 compared with that in group C (P<0.05). The decrease in Pdi at 20 Hz stimulation was significantly larger in group N2 than in group N1 (P<0.05). The speed of recovery of Pdi at 20 Hz stimulation was dose dependent. The integrated diaphragmatic electric activity (Edi) in each group did not change at any frequency of stimulation throughout the study. Our results demonstrate that nicardipine causes a dose-dependent reduction of the contractility of the fatigued diaphragm.

Effects of nicardipine on diaphragmatic fatigue in the dog: the relationship between dosage and fatigability

We examined the dose-related effects of nicardi- pine on the diaphragmatic fatigability in 24 anesthetized, mechanically ventilated dogs. Animals were divided into three groups of eight each: the control group (group C), the nicardipine 3~tg.kg -1 I.V. group (group Nt) and the nicardipine 5 ,ug-kg-Umin ~ I.V. group (group N2). Diaphrag- matic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 rain. In groups N1 and N2, nicardipine was continuoulsy infused intravenously during this fatigue- producing period. Diaphragmatic contractility was assessed by changes in transdiaphragmatic pressure (Pdi)" After induc- tion of diaphragmatic stimulation at low-frequency (20 Hz), Pal decreased significantly in all groups compared with the pre- fatigue value (P < 0.05), whereas no change was observed in Pal at high-frequency (100 Hz) stimulation. The Pd~ at 20 Hz stimulation was significantly lower in groups N1 and N2 com- pared with that in group C (P < 0.05). The decrease in Pd~ at 20 Hz stimulation was significantly larger in group N2 than in group N1 (P < 0.05). The speed of recovery of Pd~ at 20 Hz stimulation was dose dependent. The integrated diaphrag- matic electric activity (Ed~) in each group did not change at any frequency of stimulation throughout the study. Our results demonstrate that nicardipine causes a dose-dependent reduc- tion of the contractility of the fatigued diaphragm.

RETRACTED ARTICLE: Effects of dobutamine on the fatigued diaphragm: A comparison with dopamine

We examined the effects of dopamine (DOA) 10 μg·kg(-1)·min(-1) I.V. and dobutamine (DOB) 10 μg·kg(-1). min(-1) I.V. on the contractility of the fatigued diaphragm in 26 anesthetized, mechanically ventilated dogs. Animals were divided into two groups of 13 each: the DOA and DOB groups. Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (Pdi). After diaphragmatic fatigue, Pdi at low-frequency (20 Hz) stimulation decreased significantly compared with the prefatigue value (P<0.05), whereas no change in Pdi was observed at high-frequency (100 Hz) stimulation. In the fatigued diaphragm, Pdi at both stimuli increased with an infusion of either DOA (P<0.05) or DOB (P<0.05). The increase of Pdi at 20 Hz stimulation was significantly larger in the DOB group compared with that of the DOA group (P<0.05). In each group, Pdi at both stimuli decreased after the cessation of administration. The integrated diaphragmatic electric activity (Edi) in the two groups did not change at any frequency of stimulation throughout the study. We conclude that DOB in comparison with DOA is more effective in improving the contractility of the fatigued diaphragm.

Pleural pressure measured in the zone of apposition of diaphragm to rib cage in rabbits.

In 10 anesthetized adult rabbits, we studied the effect of spontaneous breathing and positive pressure ventilation on pleural pressure on the costal lung surface (Ppl) and in the zone of apposition of the rib cage to the diaphragm (Papp). Ppl and Papp were measured by rib capsules installed in the 5th or 6th rib and 11th or 12th rib, respectively. Esophageal (Pes) and gastric (Pga) pressures were measured with air-filled balloons. At end expiration (functional residual capacity), Ppl was subatmospheric (-2.5 +/- 1.4 cm H2O), decreased during spontaneous inspiration, and was in phase with Pes. In contrast, Papp was above atmospheric pressure (2.1 +/- 1.8 cm H2O), increased during inspiration, and was in phase with Pga. Papp lagged Ppl by 180 degrees during spontaneous inspiration but was in phase with Ppl during mechanical ventilation. Changes in Ppl (delta Ppl) during inspiration were greater in magnitude than either delta Papp or delta Pga. Changes in transdiaphragmatic pressure in the zone of apposition (delta Pga-delta Papp) were near zero (-0.4 +/- 0.3 cm H2O), much smaller in magnitude than those (delta Pga-delta Ppl) associated with the lung (3.0 +/- 1.5 cm H2O). These results are consistent with the concept that during breathing, abdominal pressure is transmitted to the zone of apposition of the rib cage to the abdomen. During spontaneous breathing at rest, the pleural space in the zone of apposition is mechanically independent of the pleural space associated with the lung.

Effects of β2-agonists on the contractility of fatigued canine diaphragm in vivo

We examined the effects of four β 2-agonists, clenbuterol, metaproterenol, procaterol, and albuterol, on the contractility of fatigued canine diaphragm. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (Pdi) generated by supramaximal electrical stimulation of the phrenic nerve. Diaphragmatic fatigue was developed by applying an inspiratory resistive load to spontaneously breathing dogs for 30–50 min. Four doses of each β 2-agonist were intravenously administered to dogs when the decreased Pdi became stable. Clenbuterol increased Pdi at doses of 10 and 20 μ/kg ( P<0.05). Metaproterenol improved Pdi of the fatigued diaphragm at low stimulation frequencies in a dose-dependent manner ( P<0.05). Procaterol increased Pdi at a low dose but decreased Pdi at higher doses, possibly due to a marked decrease in systemic blood pressure. Albuterol did not change Pdi at any dose. These results suggest that both clenbuterol and metaproterenol have a positive inotropic effect on fatigued canine diaphragm, while procaterol has a negative effect at high doses. Albuterol showed no inotropic effect.

The Effect of Respiratory and Lactic Acidosis on Diaphragm Function

The relative effects of respiratory and metabolic acidosis on diaphragm function are not known. To determine these effects, we compared the effects of respiratory and lactic acidosis on the contractile properties of the diaphragm. We estimated diaphragmatic performance from the change in transdiaphragmatic pressure after supramaximal stimulation of the phrenic nerves in an open-chested, casted-abdomen dog. Similarly, we stimulated the gastrocnemius motor nerve and examined force production and relaxation rate to determine if there was a difference in the response of this skeletal muscle. There was a fall in diaphragm performance with respiratory acidosis (77.1 +/- 16.9 cm H2O versus 93.8 +/- 15.0 cm H2O baseline), but not with lactic acidosis (96.7 +/- 15.7 cm H2O versus 93.8 +/- 15.0 cm H2O baseline); and the gastrocnemius was unaffected by either acidosis. The changes with respiratory acidosis were similar to those seen with diaphragmatic fatigue and had similar relaxation rate changes, suggesting that intracellular pH may play a mechanistic role in respiratory muscle fatigue. In addition, the absence of a respiratory acidosis effect on a non-diaphragmatic skeletal muscle's function represents another physiologic difference between the diaphragm and other skeletal muscles.

Effects of aminophylline on regional diaphragmatic shortening after thoracotomy in the awake lamb.

Aminophylline has been reported to augment diaphragmatic contraction, although this remains a controversial finding. We studied the effect of aminophylline on regional diaphragmatic shortening, changes in transdiaphragmatic pressure (delta Pdi), and integrated regional electromyographic (EMG) activity of the diaphragm (Edi) after a right thoracotomy in nine lambs using sonomicrometry, esophageal and gastric balloons, and EMG. Sonomicrometer crystals and EMG leads were implanted into the costal and crural regions of the diaphragm through a right thoracotomy, and a tracheostomy was performed. The animals were studied while awake within 4 days after surgery. Fractional costal and crural diaphragmatic shortening was measured using the sonomicrometer; delta Pdi was calculated from esophageal and gastric pressures. Respiratory variables were measured through the tracheostomy. Data were collected during quiet breathing and during CO2 rebreathing. After control measurements, aminophylline (10 mg/kg) was administered intravenously, producing a serum concentration of 17.7 +/- 1.5 micrograms/ml. Aminophylline did not augment shortening, increase delta Pdi, or overcome postoperative diaphragmatic inhibition acutely in the awake sheep after a right lateral thoracotomy. A small decrease of end-tidal CO2, from 5.2% to 4.9%, was measured at rest during aminophylline infusion, but Edi was unchanged. Although during CO2 rebreathing diaphragmatic shortening increased, the addition of aminophylline did not further augment shortening. Our data in awake lambs suggest that aminophylline does not improve diaphragmatic contraction in the acute postoperative period.

Effects of PGF 2α on the EMG of costal and crural parts of the diaphragm of the newborn pig

We investigated the effects of PGF 2α on the breathing patterns and electric activity of costal and crural parts of the diaphragm in 9 anesthetized newborn pigs. The change in diaphragmatic tension was evaluated as the change in transdiaphragmatic pressure. Because PGF 2α induces bronchoconstriction and an increase in respiratory resistances, the changes induced by prostaglandin were evaluated as differences between bronchoconstriction after PGF 2α and resistive load obtained by applying gradual occlusion to the inspiratory line of the breathing circuit. Our results show that PGF 2α decreased respiratory frequency with lengthening of expiratory time, while the resistive load increased both respiratory phases. The changes in breathing pattern were associated with different electrical activities of the diaphragm. While resistive load did not significantly change the EMG power spectrum, PGF 2α recruited new motor units. Furthermore, resistive load induced synchronization of the inspiratory time discharge of the costal and crural parts of the diaphragm, while after PGF 2α infusion there was an early inspiratory discharge of the crural part.