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Biomedical subjects

M D Altose

Publications and source records attributed to M D Altose.

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

Effect of norepinephrine on diaphragm contractility and blood flow.

Recent studies have shown that diaphragm fatigue can be reversed by mechanical augmentation of phrenic arterial flow. The purpose of the present experiment was to determine whether it was possible to pharmacologically augment diaphragm blood flow and reverse fatigue by the administration of norepinephrine. Four groups of studies were performed, all employing our previously described in situ isometric canine diaphragm strip preparation (Supinski et al., J. Appl. Physiol. 60: 1789-1796, 1986). Group I studies examined the effects of norepinephrine on the contractility of the nonfatigued diaphragm in normotensive dogs, group II studies examined the effects of this drug on the contractility of the fatigued diaphragm in normotensive animals, and group III studies examined the effect of this drug on the contractility of the fatigued diaphragm in hypotensive animals. Group IV studies examined the effect of norepinephrine in normotensive animals in which the phrenic artery was cannulated and pump perfused at constant flow. Fatigue was induced in group II, III, and IV studies by rhythmically stimulating the diaphragm via intramuscular electrodes. Norepinephrine had no effect on the contractility of the nonfatigued diaphragm (group I). In normotensive (group II) and hypotensive animals (group III), norepinephrine elicited dramatic increases in arterial blood pressure and phrenic arterial flow and produced a significant upshift in the force-frequency curve of the fatigued diaphragm. However, when phrenic flow was held constant (group IV experiments), norepinephrine failed to augment the contractility of the fatigued diaphragm. These results indicate that 1) norepinephrine can increase phrenic blood flow and augment the contractility of the fatigued diaphragm in both normotensive and hypotensive conditions and 2) this effect of norepinephrine to partially reverse fatigue is secondary to its action to augment diaphragmatic blood flow.

Animals↗
PubMed1989

Alterations in respiratory muscle activation in the ischemic fatigued canine diaphragm.

The purpose of the present study was to examine the respiratory motor response to diaphragm fatigue. Studies were performed using in situ diaphragm muscle strips dissected from the left costal diaphragm in anesthetized dogs. The left inferior phrenic artery was isolated, and diaphragmatic strip fatigue was elicited by occluding this vessel. Strip tension, strip electromyographic activity, parasternal electromyographic activity, and the electromyogram of the right hemidiaphragm were recorded during spontaneous breathing efforts before, during, and after periods of phrenic arterial occlusion. In separate trials, we examined the neuromuscular responses to phrenic arterial occlusion at arterial PCO2 (PaCO2) of 40, 55, and 75 Torr. No fatigue and no alteration in electromyographic activities were observed in trials at PaCO2 of 40 Torr. During trials at PaCO2 of 55 and 75 Torr, however, diaphragm tension fell, the peak height of the diaphragm strip electromyogram decreased, and the peak heights of the parasternal and right hemidiaphragm electromyograms increased. Relief of phrenic arterial occlusion resulted in a return of strip tension and all electromyograms toward base-line values. In additional experiments, the left phrenic nerve was sectioned in the chest after producing fatigue. Phrenic section was followed by an increase in the peak height of the left phrenic neurogram (recorded above the site of section). This latter finding suggests that diaphragm strip motor drive may be reflexly inhibited during the development of fatigue by neural traffic carried along phrenic afferents.

Animals↗
PubMed1987

Physician's guide to spirometers.

Three pulmonary specialists compare the manual volume spirometer with the latest high-tech models and answer key questions on choosing the one that's right for your office. Also included: a buyer's guide to available models.

Catalogs, Commercial as Topic↗
PubMed1987

Effects of voluntary constraining of thoracic displacement during hypercapnia.

The study evaluated the interrelationships between the extent of thoracic movements and respiratory chemical drive in shaping the intensity of the sensation of dyspnea. Normal subjects rated their sensations of dyspnea as PCO2 increased during free rebreathing and during rebreathing while ventilation was voluntarily maintained at a constant base-line level. Another trial evaluated the effects on the intensity of dyspnea, of voluntary reduction in the level of ventilation while PCO2 was held constant. During rebreathing, there was a power function relationship between changes in PCO2 and the intensity of dyspnea. At a given PCO2, constraining tidal volume and breathing frequency to the prerebreathing base-line level resulted in an increase in dyspnea. The fractional differences in the intensity of dyspnea between free and constrained rebreathing were independent of PCO2. However, the absolute difference in the intensity of dyspnea between free and constrained rebreathing enlarged with increasing hypercapnia. At PCO2 of 50 Torr, this difference correlated significantly with the increase in both minute ventilation (r = 0.675) and tidal volume (r = 0.757) above the base line during free rebreathing. Similarly, during steady-state hypercapnia at 50 Torr PCO2, the intensity of dyspnea increased progressively as ventilation was voluntarily reduced from the spontaneously adopted free-breathing level. These results indicate that dyspnea increases with the level of respiratory chemical drive but that the intensity of the sensation is further accentuated when ventilation is constrained below that demanded by the level of chemical drive. This may be explained by a loss of inhibitory feedback from lung or chest wall mechanoreceptors acting on brain stem and/or cortical centers.

Adult↗
PubMed1987

Activation of the inspiratory intercostal muscles by electrical stimulation of the spinal cord.

Electrical stimulation of the spinal cord was evaluated as a method of activating the inspiratory intercostal muscles. Studies were performed in anesthetized dogs after hyperventilation-induced apnea. A stainless steel electrode, rubberized along its entire length except for 2 to 3 mm at the distal tip, was introduced epidurally onto the dorsal surface of the thoracic spinal cord. Stimulating electrodes were also placed in each hemidiaphragm. Intercostal electromyograms, inspired volume, and thoracoabdominal movements were monitored. The inspiratory capacity was determined in each animal as the volume required to achieve an airway pressure of +25 cm H2O during passive lung inflation. Spinal cord stimulation at the T2-T3 spinal level resulted in maximal inspired volume generation and electrical activation of the parasternal, external, and internal intercostal muscles of the upper and midrib cage regions as determined by electromyograms. Intrathoracic pressure swings increased progressively with increasing stimulus amplitude and frequency until plateaus were reached at 6 mA and 40 Hz, respectively. Postphrenicotomy spinal cord stimulation resulted in expansion of the rib cage and reduction in circumference of the abdominal compartment. Inspired volumes during spinal cord stimulation were 537 +/- 49 ml (prephrenicotomy, prone), 347 +/- 19.6 ml (postphrenicotomy, prone), and 303 +/- 30.6 ml (postphrenicotomy, supine). Bilateral diaphragm activation alone resulted in inspired volumes of 404 +/- 39 ml. Combined diaphragm and postphrenicotomy spinal cord stimulation (supine) resulted in an inspired volume of 712 +/- 72 ml, which approximated the inspiratory capacity (803 +/- 35 ml). Our results suggest that spinal cord stimulation may be a useful physiologic and clinical tool to produce coordinated contraction of the inspiratory intercostal muscles.

Animals↗
PubMed1987

Management of chronic alveolar hypoventilation with nasal positive pressure breathing.

Negative pressure ventilation is the most common method of providing assisted ventilation without a tracheostomy. Unfortunately, negative pressure devices have several disadvantages and are not well tolerated by all patients. We present a patient in whom intermittent assisted ventilation was applied successfully by using a nasal mask to provide positive pressure ventilatory support.

Adult↗
PubMed1987

Mechanisms of dyspnea.

An unpleasant sensation of difficulty in breathing is a common complaint in a variety of disease states. The psychophysical approach to the study of respiratory sensations has contributed greatly to the understanding of the mechanisms of dyspnea. Although dyspnea, in large part, is an expression of the sense of the effort of breathing, the intensity and quality of the subjective experiences during breathing are also dependent on afferent feedback primarily from receptors in the respiratory muscles. These inputs may act either by changing the level and pattern of respiratory motor activity or by a direct effect on higher brain centers. Finally, the expression of the symptoms of dyspnea in patients with cardiopulmonary disease is shaped by individual behavioral styles, personality, and emotional state. All of these factors must be taken into consideration in the management of the dyspneic patient.

Diaphragm↗
PubMed1986

Effects of volume and frequency of mechanical ventilation on respiratory activity in humans.

This study evaluated the interaction between respiratory chemical drive and non-chemical factors related to the frequency and level of thoracic displacement during mechanical ventilation in shaping respiratory activity. Ten normal subjects were artificially hyperventilated with a positive-pressure mechanical respirator to a baseline end-tidal PCO2 of approximately 30 Torr. Thereafter, in separate trials, the end-tidal PCO2 was increased by (a) progressively raising the concentration of CO2 in the inspired gas (FICO2) while holding tidal volume (VT) and breathing frequency (f) constant, (b) lowering f while holding VT and FICO2 constant, and (c) lowering VT while maintaining a constant f and FICO2. Initially, as the PCO2 rose above baseline levels with increases in FICO2, there was no change in inspiratory muscle activity, as measured by the peak inspiratory airway pressure, until the PCO2 reached 40 Torr. This PCO2 threshold for a change in respiratory activity was significantly reduced when the tidal volume or frequency of mechanical ventilation was lowered. These results suggest that non-chemical drives related to the frequency and level of thoracic displacement interact with chemical stimuli in shaping respiratory activity.

Adult↗
PubMed1985

The effects of inspiratory resistive training on respiratory muscle function in patients with muscular dystrophy.

The effects of inspiratory resistive training on respiratory muscle function was evaluated in 11 patients with Duchenne, limb-girdle, and facio-scapulo-humeral (FSH) type muscular dystrophy. Muscle training consisted of breathing against an inspiratory resistance for two 15-minute sessions each day while at home. Following 6 weeks of training, there were significant increases in the maximum resistance that could be tolerated for at least 5 minutes (P < 0.01) and also in the maximum duration that ventilations equal to 30%, 50%, 70%, and 90% of the maximum voluntary ventilation could be sustained (P < 0.05). In six patients who trained for an additional 6-week period, respiratory muscle endurance increased even further. The degree of improvement in respiratory muscle endurance was positively correlated with baseline vital capacity (r = 0.84, P < 0.05) and maximal inspiratory pressure (r = 0.76, P < 0.05). Spirometry, functional residual capacity, and maximal inspiratory and expiratory pressures were not affected by training. We conclude that inspiratory resistive training improves respiratory muscle endurance in muscular dystrophy patients. Improvement in respiratory muscle function may serve to delay the onset of respiratory complications in patients with muscular dystrophy.

Adolescent↗
PubMed1985

Effects of age and respiratory efforts on the perception of resistive ventilatory loads.

The present study examined the effects of age on the ability to quantitate changes in inspiratory resistive loads using signals related to the size of the load, per se. Magnitude scaling of inspiratory resistive loads was performed in different trials during breathing at small, large, and varied size tidal volumes. Subjects were specifically instructed to scale the magnitude of the airflow resistance. In both young and older adults, the perceived magnitude of a given resistance was the same in the small-, large-, and varied-sized breath trials despite substantial differences in inspiratory duration and peak inspiratory airway pressure. The change in sensation for a given change in resistance, however, was less in the older than in the younger adults. These results indicate that airflow resistance can be scaled independently of the effort used in breathing. The perception of airflow resistance is blunted in elderly adults probably as a result of an impairment in the central nervous system processing of separate signals of pressure and flow.

Adolescent↗
PubMed1985

Cavitating lung infarction after bland pulmonary thromboembolism in patients with the adult respiratory distress syndrome.

During one year five patients were observed with the adult respiratory distress syndrome who were found at necropsy to have cavitated lung infarcts following bland (non-infected) pulmonary thromboembolism. There were three instances of bronchopleural fistula and in one person a tension pneumothorax was the immediate cause of death. Four of the five patients had severe lung infections. In all patients airway pressure was raised as a result of positive pressure mechanical ventilation. It is postulated that diffuse microvascular injury, bacterial pneumonia, and high airway pressures may be important factors predisposing patients with adult respiratory distress syndrome to develop lung necrosis, cavitation, and bronchopleural fistula after bland pulmonary thromboembolism. This complication may occur more frequently than has been previously recognised.

Adult↗
PubMed1985

Effects of changes in CO2 partial pressure on the sensation of respiratory drive.

The purpose of this study was to determine whether a change in respiratory sensation accompanies an increase in CO2 partial pressure (PCO2) in the absence of any changes in the level and pattern of thoracic displacement and respiratory muscle force. Eleven normal subjects were artificially hyperventilated with a positive-pressure mechanical respirator. In separate trials the tidal volume (VT) was set at 10 and 18 ml/kg and the frequency of ventilation (f) was adjusted to maintain the base-line end-tidal PCO2 at approximately 30 Torr. Thereafter, at a constant controlled VT and f, the PCO2 was progressively increased by raising the inspired CO2 concentration. There were no changes in respiratory motor activity as determined from the peak inspiratory airway pressure (Paw) until the PCO2 reached 40.8 +/- 1.0 and 40.1 +/- 1.0 (SE) Torr in the large and small VT trials, respectively. Initially there was no conscious awareness of the change in respiratory activity. Subjects first signaled that ventilatory needs were not being satisfied only after a further increase in PCO2 to 44.7 +/- 1.3 and 42.3 +/- 1.0 (SE) Torr in the large and small VT trials and after the Paw had fallen to 55-60% of the base-line value. The results suggest that changes in respiratory sensation produced by increasing chemical drive are a consequence of increases in respiratory efferent activity, but a direct effect of changes in PCO2 on respiratory sensation cannot be excluded.

Adult↗
PubMed1985

Respiratory responses to ventilatory loading following low cervical spinal cord injury.

This study compared the respiratory responses to ventilatory loading in 8 normal subjects and 11 quadriplegic patients with low cervical spinal cord transection. Progressive hypercapnia was produced by rebreathing. Rebreathing trials were carried out with no added load and with inspiratory resistive loads of 5 and 16 cmH2O. l-1 X s. Measurements were made of ventilation and of diaphragmatic electromyographic activity. Base-line hypercapnic ventilatory responses were significantly lower than normal in the quadriplegic patients, but the effects of resistive loading on the ventilatory responses were comparable in the two groups. The change in peak moving-average diaphragmatic electrical activity (DI peak) for a given change in CO2 partial pressure (PCO2) and DI peak at PCO2 55 Torr increased significantly with resistive loading both in the normal subjects and the quadriplegic patients. In the normal subjects, but not in the quadriplegic patients, inspiratory duration increased progressively with increasing resistance. The increase in DI peak during ventilatory loading in the normal subjects was a consequence of inspiratory prolongation. In contrast, in the quadriplegic patients during breathing against the larger resistive load, there was a significant increase in the average rate of rise (DI peak divided by the time from onset to peak) of diaphragmatic activity. The change in DI rate of rise for a given change in PCO2 increased to 137 +/- 13% (SE), and the DI rate of rise at PCO2 55 Torr increased to 128 +/- 8% (SE) of control values. These results indicate that compensatory increases in diaphragmatic activation during ventilatory loading occur in quadriplegic patients in whom afferent feedback from rib cage receptors is disrupted.

Adolescent↗
PubMed1985

Comparative effects of aminophylline on diaphragm and cardiac contractility.

The mechanisms by which aminophylline increases inspiratory muscle contractility are unclear. The present study compared the effects of aminophylline on cardiac as well as on diaphragm contractility and examined the interaction of aminophylline with verapamil, a calcium channel-blocking agent, on both types of muscle. Experiments were performed in mongrel dogs anesthetized with pentobarbitone. Diaphragm contractility was assessed from transdiaphragmatic pressure (Pdi) developed during supramaximal electrical stimulation of the cervical phrenic rootlets, and cardiac contractility was assessed from peak left ventricular (LV) pressure and its rate of rise (dPv/dt). Measurements were made before and after each of 3 sequential IV infusions of aminophylline (6 mg/kg) and subsequent IV infusions of verapamil (0.1 mg/kg bolus and 0.02 mg/kg/min for 5 to 7 min.). Transient decreases in Pdi were frequently observed immediately after aminophylline infusion in association with decreases in mean arterial blood pressure. With recovery of mean blood pressure, Pdi increased above baseline values. Aminophylline increased Pdi in a dose-dependent fashion over the entire frequency range studied (1 to 40 Hz). Aminophylline increased the rate of rise of Pdi (dPd/dt) without affecting the period over which pressure was developed or dissipated during single twitches. Aminophylline increased both peak LV pressure and dPv/dt. The magnitude of the cardiac response was greater than the diaphragmatic response. Subsequent verapamil infusion completely reversed the effects of aminophylline on LV contractility but had only a small effect on diaphragm contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminophylline↗
PubMed1985

Respiratory sensation in chronic obstructive pulmonary disease.

Previous work has demonstrated that the perception of added resistive loads is blunted in patients with chronic obstructive pulmonary disease (COPD). It is not clear, however, whether this is due to reduced levels of respiratory muscle force during loaded breathing or to a specific abnormality in respiratory sensation. In the present study, the psychophysical technique of magnitude scaling was used to evaluate the sensation of external resistive and elastic ventilatory loads as well as the perception of inspired volume and inspiratory muscle force in 14 patients with COPD and in 12 normal subjects of similar age. The exponents of the power function relationships between load magnitude and sensation intensity for both resistive and elastic loads were significantly reduced in the patients with COPD compared with those in the normal subjects. While breathing against any given ventilatory load, the peak inspiratory mouth pressure and inspiratory duration were comparable in the 2 groups. Thus, the exponents of the power function relationships between peak inspiratory mouth pressure and sensation intensity were significantly lower in the patients with COPD (0.92 +/- SE 0.17 and 0.96 +/- SE 0.17 for resistive and elastic loads, respectively) compared with those obtained in the normal subjects (1.47 +/- SE 0.12 for resistive loads and 1.52 +/- SE 0.17 for elastic loads) (p less than 0.05). In contrast, the perception of inspired volume and of respiratory muscle force during static inspiratory maneuvers as determined by magnitude estimation and production were no different in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗