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T K Aldrich

Publications and source records attributed to T K Aldrich.

At least 37 records · Page 2Linked to original sources
PubMed1990

Temperature dependence of rat diaphragm muscle contractility and fatigue.

The diaphragm is a skeletal muscle of mixed fiber type that is unique in its requirement to maintain contractile function and fatigue resistance across a wide range of temperatures to sustain alveolar ventilation under conditions of hypo- or hyperthermia. The direct effect of temperature (15-41 degrees C) on rat diaphragm isometric contractility and fatigue was determined in vitro. As temperature decreased from 37 to 15 degrees C, contraction and relaxation times increased, and there was a left shift of the diaphragm's force-frequency curve, with decreased contractility at 41 and 15 degrees C. Fatigue was induced by 10 min of stimulation with 30 trains/min of 5 Hz at a train duration of 900 ms. Compared with 37 degrees C, fatigue resistance was enhanced at 25 degrees C, but no difference in fatigue indexes was evident at extreme hypothermia (15 degrees C) or hyperthermia (41 degrees C). Only when the fatigue program was adjusted to account for hypothermia-induced increases in tension-time indexes was fatigue resistance evident at 15 degrees C. These findings indicate that despite the diaphragm's unique location as a core structure, necessitating exposure to in vivo temperatures higher than found in limb muscle, the temperature dependence of rat diaphragm muscle contractility and fatigue is similar to that reported for limb muscle of mixed fiber type.

Animals↗
PubMed1990

Adaptations in the diaphragm's in vitro force-length relationship in patients on continuous ambulatory peritoneal dialysis.

In patients on continuous ambulatory peritoneal dialysis (CAPD) for more than 6 wk, we measured functional residual capacity (FRC), maximum inspiratory and transdiaphragmatic pressure, diaphragm length, and radius of curvature (roentgenographic methods) as functions of the volume of peritoneal dialysate (PD) instilled within the abdominal cavity. This allowed in vivo characterization of the human diaphragm's force-length relationship. As PD volume increased from zero to 3 L, FRC decreased from 2.41 +/- 0.29 L to 1.93 +/- 0.072 L; mean total diaphragm length index (TDLI) increased from 0.22 +/- 0.01 to 0.28 +/- 0.01, and diaphragm radius of curvature remained unchanged. Respiratory muscle strength increased as a function of dialysate volume, reaching its maximum after the infusion of 3 L PD. In contrast, normal subjects achieved maximal inspiratory muscle force at their normal FRC, with a mean TDLI of 0.26 +/- 0.01 and showed no further increase as the diaphragm lengthened. We conclude that the human diaphragm may be capable of an adaptive rightward shift in its force-length relationship when it is chronically lengthened by CAPD.

Adaptation, Physiological↗
PubMed1990

Maximal inspiratory pressure is not a reliable test of inspiratory muscle strength in mechanically ventilated patients.

Maximal Inspiratory pressure (MIP) is an important clinical method used to assess respiratory muscle strength. The reliability and reproducibility of this measurement in mechanically ventilated patients is not certain. In 14 stable, mechanically ventilated patients, capable of spontaneous inspiratory efforts, we assessed maximal inspiratory efforts using the technique originally described by Marini and associates. MIP was measured in triplicate, by one to five experienced investigators, on one to seven successive days, for a total of 396 determinations on 54 patient days. The coefficients of variation among the triplicate efforts averaged 12 +/- 1%, indicating the test to be highly reproducible. There was significant variation among the MIP reported by different investigators studying the same patient on the same day (32 +/- 4%). The differences between best MIP by different investigators averaged 12.6 +/- 1.3cm H2O (40 +/- 4%). In 17 of 44 cases, one investigator placed MIP above -30cm H2O, whereas another placed it below. ANOVA showed that MIP was significantly affected by investigator (p less than 0.0001) as well as by patient (p less than 0.0001). Because "true" MIP must be equal to or greater than the best measured MIP, these data indicate that the MIP is commonly underestimated in patients receiving mechanical ventilation, even when standardized technique is used. Furthermore, our data show that reproducibility of triplicate MIP determination by a single observer does not indicate that the test is reliable.

Aged↗
PubMed1990

Inspiratory flow dynamics during mechanical ventilation in patients with respiratory failure.

We studied the effect of inspiratory flow rate on respiratory resistance during mechanical ventilation in 15 patients with acute respiratory failure (ARF). Resistance was measured by both constant flow inflation and occlusion methods as inspiratory flow rates were increased from 0.66 to 2.0 L/s. Endotracheal tube resistance was subtracted from total resistance to obtain respiratory resistance. In contrast to the flow-dependent increase in endotracheal tube resistance, respiratory resistance decreased continuously as flow rate and airway pressure increased, except in four of six patients with asthma in whom respiratory resistance increased as flow increased. Mechanical airway dilatation, tissue resistance, stress relaxation, and time-constant inequalities may contribute to the decrease in respiratory resistance. In status asthmaticus, however, the effects of turbulence, noncompliant airways, and/or "reflex" bronchoconstriction may be sufficient to cause a flow-dependent increase in resistance.

Airway Resistance↗
PubMed1990

Adverse effects of drugs on the respiratory muscles.

Over 100 drugs can impair muscle function, either by inhibiting neural drive, causing peripheral neuropathy, blocking neuromuscular junctions, precipitating myasthenia gravis, or producing myopathy. Many of these drugs affect respiratory muscles, particularly the diaphragm. Although a great deal is known about the drug effects on central respiratory drive and neuromuscular blockade, little is known about the depressant effects of drugs specifically on phrenic nerve function or diaphragm contractility. This article has reviewed what is known about the effects of drugs on respiratory myoneural function and what can be inferred from studies on other striated muscles. We hope that this review serves to stimulate further investigation; meanwhile, until more is known, continued clinical caution is justified.

Diaphragm↗
PubMed1989

Lung lymphocytes in bleomycin-induced pulmonary disease.

Previous studies have not clearly defined the role of cell-mediated immunity in bleomycin-induced lung injury. In this report the functional activity of T lymphocytes obtained from minced lung preparations, bronchoalveolar lavage, and blood of rabbits treated with bleomycin was examined in cell proliferation and cell-mediated cytotoxicity assays. Four days after instillation of bleomycin (10 units/kg) into the right lung, histologic examination revealed mononuclear cell interstitial infiltrates and alveolar exudates. Right lung bronchoalveolar lavage (BAL) cell counts were similar in both groups, but the percentage of lymphocytes and neutrophils was elevated in bleomycin-treated groups (25% vs. 7% and 35% vs. 0% respectively; p less than 0.05). Spontaneous proliferation of cultured BAL and blood lymphocytes was similar in bleomycin-treated rabbits and controls. After 24 h of incubation with interleukin-2 (IL-2), BAL lymphocytes from bleomycin-treated rabbits had nearly a 4-fold greater proliferative response than lymphocytes from untreated rabbits. Concanavalin-A-dependent cell-mediated cytotoxicity (CDCMC) assays were performed to evaluate cytolytic lymphocyte activity. Spontaneous CDCMC activity was not detected in BAL fluid or in blood lymphocytes from either treated or control animals. After 24 h of incubation with IL-2, significant CDCMC activity was detected in lung lymphocytes from bleomycin-treated animals, but not in lung lymphocytes from control animals. These results indicate that stimulated lymphocytes are present in the lungs of rabbits 4 days after exposure to bleomycin.

Animals↗
PubMed1989

Raja pleural biopsy needle. A comparison with the Abrams needle in experimental pleural effusion.

The Raja pleural biopsy needle, 3 mm in external diameter and fitted with a titanium alloy biopsy flap, was compared with the Abrams needle in six dogs with experimentally induced pleural effusion. One hundred twenty-four pleural biopsies were performed using either the Raja needle or the Abrams needle (62 with each needle). No complication occurred with either needle. The Raja pleural biopsy needle yielded a statistically significant larger pleural tissue specimen with a statistically significant lower frequency of crush artifacts. The size of the pleura obtained by the Abrams needle averaged 4,401 +/- 559 microns2 (mean +/- SE) compared with 8,652 +/- 1,099 microns2 with the Raja needle (p less than 0.01; Student two-tailed t test). Biopsies by the Abrams needle showed crush artifacts in 25.8% of the specimens, whereas 8.06% of biopsies with the Raja needle showed crush artifacts (p less than 0.02; Fisher's two-tailed exact test). In conclusion, the Raja pleural biopsy needle is safe to use and, despite its smaller diameter (3mm versus 4mm external diameter of the Abrams needle), yields significantly larger and less frequently distorted pleural specimens.

Animals↗
PubMed1989

Alveolar pressure and airway resistance during maximal and submaximal respiratory efforts.

A digital computing technique was used to extract continuous calculations of average alveolar pressure and airway resistance from body plethysmographic measurements during forced inspiratory and expiratory vital capacity maneuvers and tidal breathing in human subjects. Derived alveolar pressures were similar to those obtained using an interrupter technique (linear regression slope, 0.99 +/- 0.02; r = 0.98) and by comparison with esophageal pressure measurements. Studies in normal subjects revealed a characteristic pattern of increasing airway resistance throughout the expiratory phases of maximal and submaximal respiratory maneuvers, with maximal resistance of 33 to 110 cm H2O/L/s at low lung volumes during forced vital capacities. In contrast, inspiratory resistance remained low and constant throughout maximal and submaximal inspiratory maneuvers. Patients with COPD showed substantially higher inspiratory and expiratory resistances. In three patients with flow-volume loops suggestive of variable extrathoracic upper airway obstruction, measurements of alveolar pressure and airway resistance made it clear that two of the patients had upper airway obstruction, whereas the other was exerting an inadequate effort. We conclude that this noninvasive technique provides valid estimates of alveolar pressure and airway resistance continuously throughout both phases of the respiratory cycle over a wide range of volumes and flow rates. It may prove to be useful in the assessment of effort and airway obstruction in patients with a variety of pulmonary conditions.

Adult↗
PubMed1989

The patient at risk of ventilator dependency.

Respiratory failure may result from inadequate central respiratory drive, excessive respiratory workload, or inadequate respiratory muscle endurance. With the exception of drug overdoses, central causes of respiratory failure are uncommon in the adult, and respiratory failure can be considered an imbalance between workload and endurance. Excessive workload can result from airway obstruction or chest wall or lung restriction. Anything that increases the required minute ventilation will increase the workload proportionately. Inadequate endurance results from neuromuscular disease, malnutrition, and a variety of metabolic factors. In most cases, treatment of the precipitating cause allows weaning from mechanical ventilation. However, when respiratory failure persists, often because the precipitating cause cannot be treated, all possible contributing conditions must be identified and corrected to the greatest possible extent. In that way, many patients with apparently intractable respiratory failure can be weaned. Four new approaches are showing some promise in the treatment of persistent respiratory failure: pharmacologic therapy to strengthen respiratory muscles, periodic respiratory muscle rest, sedation, and inspiratory muscle training.

Humans↗
PubMed1989

Weaning from mechanical ventilation: adjunctive use of inspiratory muscle resistive training.

We used inspiratory resistive training (IRT) in an effort to improve the respiratory muscle endurance of 27 patients with respiratory failure who had failed repeated weaning attempts using standard techniques. Seven patients had primary neuromuscular diseases; the other 20 had primary lung diseases. All patients had stable respiratory failure, without gross malnutrition or electrolyte disorders. Their best initial T-piece duration averaged 6.4 +/- 8.4 (SD) h, with pHa 7.33 +/- 0.09 and PCO2 63 +/- 4 torr at the end of the T-piece trial. We provided a mean of five weekly training sessions of spontaneous breathing through an adjustable nonlinear resistor, with gradually increasing duration and resistance. When initial T-piece tolerance was less than 2 h, two to ten breaths of mechanical ventilation were provided during IRT sessions. No training session exceeded 30 min, and mechanical ventilation was provided between IRT sessions. Under this regimen, maximal inspiratory pressure improved from -37 +/- 15 to -46 +/- 15 cm H2O (p less than .001) and vital capacity improved from 561 +/- 325 to 901 +/- 480 ml (p less than .001). Twelve of the 27 patients were successfully weaned after 10 to 46 days; five more were weaned to nocturnal ventilation, for a total of 63%. We conclude that IRT can improve respiratory muscle strength and endurance in patients with respiratory failure, and can allow many of them to be weaned from mechanical ventilation.

Aged↗
PubMed1988

Central fatigue of the rabbit diaphragm.

This study evaluates the importance of central fatigue of the diaphragm in rabbits subjected to inspiratory muscle resistive loading (IRL). Ten rabbits were subjected to constant IRL while unanesthetized and breathing supplemental oxygen. During 10-20 minutes of spontaneous breathing against IRL, there were no significant changes in arterial oxygen saturation or in diaphragm contractility, measured by the quasi-static transdiaphragmatic pressure response to a 0.3-sec train of 100 Hz supramaximal phrenic nerve stimuli. After an initial decrease due to application of the load, the minute ventilation decreased further, by an average of 15%, while arterial pCO2 increased to an average of 59 mmHg (p less than 0.05). The normalized diaphragm pressure-time index initially increased from 0.02 to 0.18 during IRL, then decreased an average of 29% (p less than 0.05). These results show that severe IRL causes a decrease in the level of diaphragmatic effort over time despite increased chemical drive and despite a preserved ability of the muscle to respond to phrenic nerve stimuli. This adaptation may help to prevent peripheral diaphragm fatigue.

Acidosis, Respiratory↗
PubMed1988

The effect of digoxin on contractility and fatigue of isolated guinea pig and rat hemidiaphragms.

Digoxin could improve diaphragm contractility and fatigability if inhibition of sodium-potassium adenosine triphosphatase enhances calcium influx from extracellular sources, or it could impair contractility and worsen fatigue if it impairs maintenance of the membrane potential. We studied the effects of digoxin on isometric force production, fatigue, and recovery in isolated, directly stimulated, guinea pig and rat diaphragms. Digoxin had no effect on maximal twitch or tetanic tensions compared with control diaphragms in either rat (2 ng/ml to 20 micrograms/ml) or guinea pig (2 ng/ml to 2 micrograms/ml) hemidiaphragms. Digoxin worsened high frequency fatigue and impaired recovery from fatigue in guinea pigs (200 ng/ml to 2 micrograms/ml) but not in rat (2 micrograms/ml) hemidiaphragms. We conclude that digoxin has no effect on diaphragm contractility. Hypopolarization of the membrane potential is the likely cause for the increased fatigability. The difference in responsiveness between species is likely due to insensitivity of rat sodium-potassium adenosine triphosphatase to digoxin.

Aminophylline↗
PubMed1988

Respiratory muscle fatigue.

Respiratory muscle fatigue is caused by excessive effort relative to the strength and endurance of the respiratory muscles. It can be manifested by reductions in respiratory drive (central fatigue), by impaired neuromuscular transmission (transmission fatigue), by decreased contractility (contractile fatigue), or by a combination of these factors. Respiratory muscle fatigue probably contributes to the difficulties some patients have with weaning from mechanical ventilation, the symptoms of exercise intolerance and dyspnea in chronic lung disease, and CO2 retention. Therapy depends on a reduction in the required level of respiratory effort and/or an improvement in respiratory muscle strength and endurance.

Dyspnea↗
PubMed1987

Transmission fatigue of the rabbit diaphragm.

This study evaluates the role of transmission fatigue of the diaphragm in rabbits subjected to inspiratory resistive loading (IRL) sufficiently severe to increase peak tidal airway pressure to about 50% of that elicited by 100 Hz phrenic nerve stimulation. After 58 +/- 14 min of IRL, the transdiaphragmatic pressure (Pdi) responses to phrenic nerve stimulation at 20, 60, and 100 Hz were reduced by approximately one third. In contrast, IRL induced no significant change in the response to direct diaphragm stimulation (in the presence of transient neuromuscular blockade). Although respiratory acidosis occurred during IRL (pH 7.04 +/- 0.04, PCO2 90 +/- 10, PO2 131 +/- 38), it was not sufficient to explain the reduced contractility. In a separate series of experiments, the diaphragm compound action potential elicited by unilateral phrenic nerve stimuli was recorded by implanted diaphragm electrodes and the Pdi elicited by contralateral phrenic nerve stimulation at 100 Hz was measured. Both action potential amplitude and Pdi declined during IRL and both improved after 10 min of recovery. These findings demonstrate that transmission fatigue plays a major role in rabbit diaphragm fatigue induced by spontaneous breathing against inspiratory resistance.

Acidosis, Respiratory↗
PubMed1987

The maintenance of total ventilatory requirements through a chronic bronchopleural cutaneous fistula.

In patient with a chronic post-tuberculous bronchopleural cutaneous fistula (BPCF), minute ventilation, dead space, flow rates, arterial blood gas tensions, and oxygen consumption were measured during mouth breathing and after 30 min of steady-state breathing solely through the BPCF. Despite a 390-ml (18%) decrease in dead space when breathing took place through the BPCF, there were no significant changes in minute ventilation or respiratory rate. BPCF breathing was also associated with an increase in airways resistance as reflected by a 300-ml (35%) decrease in the FEV1 and a 16% decrease in the FEV1/FVC ratio. The increased resistance resulted in a 20 ml/min (18%) increase in oxygen consumption. Arterial blood gas tensions remained constant. We conclude that although ventilatory efficiency was not improved, this patient was able to satisfy his total minute ventilatory requirements, for the 30-min period, solely through BPCF breathing.

Bronchial Fistula↗