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Biomedical subjects

C Roussos

Publications and source records attributed to C Roussos.

At least 163 records · Page 9Linked to original sources
PubMed1983

Respiratory factors limiting exercise.

The question of respiratory factors limiting exercise has been examined in terms of possible limitations arising from the function of gas exchange, the respiratory mechanics, the energetics of the respiratory muscles, or the development of respiratory muscle fatigue. Exercise capacity is curtailed in the presence of marked hypoxia, and this is readily observed in patients with chronic airflow limitation and interstitial lung disease and in some athletes at high intensities of exercise. In patients with interstitial lung disease, gas exchange abnormality--partly the result of diffusion disequilibrium for oxygen transfer--occurs during exercise despite abnormally high ventilations. In contrast, in certain athletes arterial hypoxemia has been documented during heavy exercise, apparently as a result of relative hypoventilation. During strenuous exercise the maximum expiratory flow volume curves are attained both by patients with chronic airflow limitation and by normal subjects, in particular when they breathe dense gas, so that a mechanical constraint is imposed on further increases in ventilation. Similarly, the force velocity characteristics of the inspiratory muscles may also impose a constraint to further increases in inspiratory flows that affects the ability to increase ventilation. In addition, the oxygen cost of maintaining high ventilations is large. Analysis of results from blood flow experiments reveal a substantial increase in blood flow to the respiratory muscles during exercise, with the result that oxygen supply to the rest of the body may be lessened. Alternatively, high exercise ventilations may not be sustained indefinitely owing to the development of respiratory muscle fatigue that results in hypoventilation and reduced arterial oxygen tension.

Animals↗
PubMed1983

Changes in relaxation rate with diaphragmatic fatigue in humans.

Maximum relaxation rate (MRR) and the time constant of relaxation (tau) of transdiaphragmatic pressure (Pdi) was measured in four male subjects and compared with the high-to-low frequency ratio (H/L) of the diaphragmatic electromyogram (EMG) as a predictor of diaphragmatic fatigue. Pdi and inspiratory time-to-total breath duration ratios (TI/TT) were varied, and TT and tidal volume were held constant; inspiratory resistances were used to increase Pdi. Studies were performed at various tension-time indices (TTdi = Pdi/Pdimax X TI/TT). Base-line MRR/Pdi was 0.0100 +/- 0.0004 (SE) ms-1, and baseline tau was 53.2 +/- 3.2 ms. At TTdi greater than 0.20, MRR and H/L decreased and tau increased, with maximum changes at the highest TTdi. At TTdi less than 0.20, there was no change in H/L, MRR, or tau. The time course of changes in H/L correlated with those of MRR and tau under fatiguing conditions. In this experimental setting, change in relaxation rate was as useful a predictor of diaphragmatic fatigue as fall in H/L of the diaphragmatic EMG.

Adult↗
PubMed1983

Diaphragm in emphysematous hamsters: sarcomere adaptability.

We investigated whether the shift in the diaphragmatic length-tension curve of emphysematous animals was due to changes in either sarcomere number or sarcomere length. In vitro length-tension characteristics of the diaphragm were evaluated in control and emphysematous hamsters. Emphysema was induced by a single endotracheal instillation of elastase. Functional residual capacity, measured by means of a plethysmograph, was about twice that measured in emphysematous animals compared with control animals. Small diaphragmatic bundles were isolated and evaluated for their length-tension characteristics. The length-tension curve of diaphragms from emphysematous animals was displaced toward the left. Maximal tetanic tensions were similar in both groups, whereas optimal bundle length was significantly decreased in the emphysematous animals. Sarcomere number and sarcomere length at optimal length were then calculated for the diaphragmatic bundles. The bundles from emphysematous animals were found to have a significantly reduced number of sarcomeres, as well as a significantly decreased sarcomere length at optimal compared with control values. The total number of sarcomeres were also found to be significantly negatively correlated with the animal's functional residual capacity. From these results, we conclude that the decrease in diaphragmatic length, seen with hyperinflation, is due mainly to a loss of sarcomeres and possibly to a small decrease in sarcomere length measured at optimal bundle length.

Adaptation, Physiological↗
PubMed1983

Expiratory threshold load under extracorporeal circulation: effects of vagal afferents.

Nine anesthetized dogs breathed against an expiratory threshold load (ETL) applied by switching the expiratory circuit into a column of H2O to a depth of 20-30 cm. Arterial blood gas tensions were maintained in the normal range by placing the dogs under arteriovenous bypass to avoid any uncontrolled chemostimulation. There was an increase in integrated electromyogram activity of the diaphragm with the ETL. This was rarely observed after cold block of the vagus nerves which also reduced the evoked expiratory activity. The ventilatory response to hypercapnia was greatly depressed under loaded breathing whether vagal afferents were intact or blocked by cold. Both inspiratory drive and ventilatory timing were affected, suggesting that the central integration of chemosensitive afferents was altered. Proof of supraspinal projections of proprioceptive inputs from abdominal muscles was provided by the demonstration of changes in ventilatory timing during selective activation of muscle spindles in abdominal muscles by high-frequency mechanical vibration applied to the linea alba. Thus these observations suggest that during ETL breathing, a possible interaction exists between chemoreflex drive and proprioceptive afferents.

Afferent Pathways↗
PubMed1983

Vagal feedback with expiratory threshold load under extracorporeal circulation.

In 11 anesthetized dogs placed under extracorporeal circulation, the vagal feedback was tested by electrical stimulation of the vagus nerves with cold block of their caudal part and by passive lung hyperinflation. The apneic response to such vagal stimulation progressively disappeared during expiratory threshold load breathing but then returned to control values some minutes after the load was removed. This suppression of the inhibitory response to stimulation of the vagus nerves was usually observed when vagal afferents were intact or blocked by cold. However, it was not observed whether no evoked activity continued in expiratory muscles after the cold block, or after suppression of all proprioceptive muscular afferents after transection of the spinal cord at C6 level. These results strongly suggest that enhancement of proprioceptive inputs to the respiratory centers counteracts the vagally mediated inspiratory "off-switch" mechanisms.

Abdominal Muscles↗
PubMed1983

Regional blood flow distribution in dog during induced hypotension and low cardiac output. Spontaneous breathing versus artificial ventilation.

Respiratory muscle blood flow and organ blood flow was studied in two groups of dogs with radioactively labeled microspheres to assess the influence of the working respiratory muscles on the regional distribution of blood flow when arterial pressure and cardiac output were lowered by pericardial tamponade. In one group (n = 6), the dogs were paralyzed and mechanically ventilated (Mv), while in the other (n = 6), they were left to breathe spontaneously (Sb). Cardiac output fell to 30% of control values during tamponade in both groups and was maintained constant. None of the dogs was hypoxic. Ventilation in the Sb group peaked after 50 min of hypotension, but remained unchanged in the Mv group. Duplicate measurements of blood flow were made during a control period and after 50 min of tamponade (corresponding to the peak ventilation in Sb). Blood flow to the respiratory muscles increased significantly (P less than 0.001) during tamponade in Sb (diaphragmatic flow increased to 361% of control values), while it decreased in Mv. Although the arterial blood pressure and cardiac output were comparable in the two groups, blood flow distribution during tamponade was different. In Sb, the respiratory muscles received 21% of the cardiac output, compared with only 3% in the Mv group. Thus, by muscle paralysis and Mv, a large fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during low cardiac output state: blood flows to the liver, brain, and quadriceps muscles were significantly higher during tamponade in the Mv group compared with the Sb group. Similarly, blood lactate at all times after the induction of low cardiac output and hypotension was significantly lower in the Mv animals (P less than 0.005).

Animals↗
PubMed1983

Endurance of hyperventilation in chronic airflow limitation.

The capacity to sustain an increase in ventilation (VE) sufficient to decrease the end-tidal partial pressure of carbon dioxide (PETCO2) by about 10 mm Hg was studied in six hypercapnic patients with moderate to severe chronic airflow limitation (CAL). Patients could continue such an increased VE for a finite time (range 5 to 54 minutes). During hyperventilation (H), ventilation was approximately doubled and represented 77.1 +/- 8.4 (mean +/- SE) percent of maximum voluntary ventilation, mean oxygen consumption (VO2) increased 44 percent (p less than 0.005) and mean inspiratory pleural pressure (Ppl) swings were 43.8 +/- 10.5 percent of maximum Ppl. Four patients achieved reductions of PETCO2 less than 10 mm Hg, and two patients achieved or exceeded the target decrease in PETCO2. The decrease in PaCO2 was correlated with the wasted ventilation ratios (VD/VT) during H, the greatest decrease in PaCO2 being related to the lowest VD/VT (p less than 0.05). Electromyographic (EMG) evidence of inspiratory muscle fatigue developed in four of the six patients during H. Five normal subjects achieved an equal or greater decrease in PETCO2, and none showed EMG evidence of inspiratory muscle fatigue. We conclude that, although impaired gas exchange limits the capacity to voluntarily reduce the PaCO2, the development of respiratory muscle fatigue in some patients with CAL may also contribute by limiting the capacity to sustain the substantial increase in respiratory muscle work done in the attempt.

Adult↗
PubMed1983

Thoracicoabdominal mechanics during resuscitation maneuvers.

The importance of intrathoracic pressure in generating blood flow during cardiopulmonary resuscitation has recently been emphasized. The purpose of this study was to investigate the factors involved in generating intrathoracic pressure. Studies were performed in anesthetized paralyzed dogs with the circulation intact. Balloon-tipped catheters were placed in the abdomen and esophagus for measurement of intra-abdominal and intrathoracic pressures and cannula placed in the airway for airway pressure. The following four maneuvers were studied: (1) chest compression with open airway; (2) chest compression with closed airway; (3) pulmonary inflation to transpulmonary pressure (TP) of 30 cm H2O (TP = 30); and (4) chest compression plus pulmonary inflation (TP = 30). We found that under static conditions, chest compression alone produced small positive intrathoracic pressures (9 +/- 8 cm H2O), but these could be increased by closing the airway pressure (18 +/- 6 cm H2O) or inflating the lungs (15 +/- 7 cm H2O). The combination of inflating the lung and compressing the chest produced the highest intrathoracic pressure (48 +/- 18 cm H2O; p less than 0.001). The pressure developed was highly variable and the distribution of pressures within the thorax was not uniform. As the intrathoracic pressure became large, a pressure gradient developed from thorax to abdomen, and the diaphragm everted; this pressure gradient could divert blood from the brain.

Abdomen↗
PubMed1982

Low-frequency fatigue in isolated skeletal muscles and the effects of methylxanthines.

1. A form of skeletal muscle fatigue was examined with isolated animal and human muscle preparations. The possibility that methylxanthines could overcome this was investigated. 2. Prolonged contractile activity resulted in a long-lasting impairment of force generation at low frequencies of stimulation at times when the force at higher frequencies had substantially recovered. This was seen with both fast-twitch and slow-twitch animal muscles and with samples of isolated human muscle. 3. The decrease in low-frequency force was due to a decrease in twitch amplitude, suggesting damage to the processes involved in excitation--contraction coupling. 4. Caffeine and theophylline at concentrations of 1 mmol/l rapidly and completely reversed the effects of this form of fatigue in both animal and human muscle preparations. 5. Agents that potentiate muscle force production could be an effective means of counteracting the effects of an important form of skeletal muscle fatigue, but a clinically useful compound would need to be more potent than the methylxanthines currently in use.

Animals↗
PubMed1982

Changes in EMG power spectrum (high-to-low ratio) with force fatigue in humans.

During and following high-load fatiguing voluntary contractions, the force response of skeletal muscle to electrical stimulation is altered so that the frequency-force curve is moved to the right. Fatiguing contractions also result in a shift to the left of the electromyographic (EMG) power spectrum. In the quadriceps muscle and the diaphragm of normal subjects the change in the force response to electrical stimulation has been correlated with the EMG changes. After repeated submaximal contractions in the quadriceps and diaphragm, the forces produced by electrical stimulation at low frequencies were reduced, indicating low-frequency fatigue. This type of fatigue persisted for several hours but did not result in any change in the EMG high-to-low ratio. Low-frequency fatigue is probably an important aspect of the failure of skeletal muscle to generate adequate force, and the EMG high-to-low ratio may not recognize this type of fatigue.

Diaphragm↗
PubMed1982

Adaptability of the hamster diaphragm to exercise and/or emphysema.

In vitro contractile properties of the diaphragm were measured in four groups of inbred adult hamsters (greater than 40wk), randomly divided into sedentary control (SC), exercise control (EC), sedentary emphysematous (SE), and exercise emphysematous (EE) groups. Emphysema was induced by a single endotracheal instillation of elastase. Exercise consisted of running 1 h/day, 7 days/wk for 20 wk. Functional residual capacity (FRC), measured by means of a pressure box, was approximately 2.5 times greater in both emphysematous groups compared with control groups. Small diaphragmatic bundles were then isolated and subjected to in vitro analysis of isometric contractile properties. No differences were observed among the four groups in time to peak tension, half-relaxation time, and shape of the force-frequency curve. The diaphragmatic length-tension curve of emphysematous animals was displaced toward the left; maximal tetanic tension was similar in all groups, while optimal length (Lo), defined as the length at which maximal twitch tension occurred, was significantly shorter in both emphysematous groups. The Lo was negatively correlated with the FRC. Exercise tended to increase the in vitro endurance of the diaphragm bundles in control animals only. Diaphragms from both emphysematous groups, however, did show the greatest resistance to fatigue. It is concluded that 1) daily running for 1 h does not influence the diaphragmatic contractile properties in the hamster, but fatigue was reduced; 2) the load of chronic emphysema decreased the hamster's diaphragm fatiguability; and 3) the diaphragms of emphysematous hamsters chronically adapt by decreasing diaphragmatic length in proportion to the degree of hyperinflation and thus probably continue to operate at an Lo.

Adaptation, Physiological↗
PubMed1982

The effect of aminophylline on inspiratory muscle contractility.

The effects of aminophylline on diaphragmatic muscle contractility were studied in 8 dogs. The relationships of the electromyographic signal from the diaphragm and the pressures developed by this muscle were compared before and after the administration of aminophylline in doses of 6, 20, 40, 80, and 120 mg/kg. Measurements were made during occluded inspiratory efforts at functional residual capacity. In a second group of 4 dogs the relationships were compared while the rib cage expansion was limited by a plaster cast. Finally, in a third group of 4 dogs after the diaphragm had been paralyzed by phrenicotomy, the relationship of pleural pressure to the electromyographic signal of the intercostal muscles was assessed before and after administration of aminophylline. In all cases, aminophylline progressively shifted the electromyographic pressure relationship up and to the left. This effect became significant (p less than 0.01) at a dose of 20 mg/kg, reached a peak at 80 mg/kg, and then declined at a dose of 120 mg/kg. The amount producing blood concentrations closest to the human therapeutic blood concentration was 20 mg/kg. The peak increase in pressure compared with the control values were 58% in the first group, 27% in the second group, and 52% in the third group (p less than 0.01). We conclude that aminophylline increases respiratory muscle contractility in a dose-related manner. This may have important therapeutic and pathophysiologic implications.

Aminophylline↗
PubMed1982

Respiratory muscle contribution to lactic acidosis in low cardiac output.

The role of the respiratory muscles in the evolution of experimental low cardiac output and lactic acidosis was studied in 2 groups of dogs. One group (6 dogs) was paralyzed and artificially ventilated, and the other (6 dogs) was breathing spontaneously. Shock was induced by cardiac tamponade; cardiac output during shock amounted to 25 to 35% of control values in both groups. All the spontaneously breathing dogs died from ventilatory failure (mean time, 2 h), whereas the artificially ventilated dogs were still alive 3 h after the onset of cardiogenic shock. At any given time after the onset of shock, arterial pH was significantly lower in the spontaneously breathing dogs than in the artificially ventilated ones. This was due to a greater increase in arterial blood lactate in the spontaneously breathing dogs than in the artificially ventilated ones (9.47 +/- 2.7 versus 4.74 +/- 56 mmoles/L at 2 h, respectively). Greater glycogen depletion associated with higher muscle lactate concentrations were found in the respiratory muscles of the spontaneously breathing dogs when compared with that in the artificially ventilated ones. It is concluded that artificial ventilation in cardiogenic shock decreases substantially the severity of lactic acidosis and prolongs survival.

Abdominal Muscles↗
PubMed1982

Clinical manifestations of inspiratory muscle fatigue.

Twelve patients exhibiting difficulties during discontinuation of artificial ventilation permitted us to investigate physical examination techniques used in diagnosing inspiratory muscle fatigue. Diaphragmatic and intercostal electromyographic tracings, arterial blood gases, rate and depth of ventilation, and thoracoabdominal motion were monitored during spontaneous breathing. Six patients showed electromyographic evidence of inspiratory muscle fatigue. A sequence of events leading to respiratory acidemia emerged--namely electromyographic evidence of fatigue, accompanied or followed by an increased respiratory rate, in turn followed by alternation between abdominal and rib cage breathing (respiratory alternans), paradoxical inward abdominal motion during inspiration (abdominal paradox), and finally an increase in PaCO2 associated with a fall in minute ventilation and respiratory rate, and worsening of respiratory acidemia. The abnormalities of respiratory movements may be reliable clinical signs of inspiratory muscle fatigue, particularly when accompanied by tachypnea and hypercapnia.

Adult↗
PubMed1981

Aminophylline improves diaphragmatic contractility.

In an attempt to explain the clinical efficacy of aminophylline, we studied its effect on diaphragmatic function in eight normal subjects. The relation between the electrical activity of the diaphragm and the pressure generated by the diaphragm was assessed during voluntary contractions before and after aminophylline infusion. Aminophylline shifted the electrical activity/pressure curve to the left; the pressure at a given electrical activity increased an average of 15 per cent (P less than 0.001). In four subjects, pressure was also measured during stimulation of the phrenic nerve at various frequencies before and after diaphragmatic fatigue was produced by resistive breathing, with and without aminophylline infusion. Pressure increased after fatigue at all stimulation frequencies with aminophylline, as compared with the pressure after identical fatigue runs at the same stimulation frequencies without aminophylline. The mean plasma aminophylline concentration associated with these responses was 13 +/- 0.9 mg per liter. We conclude that aminophylline improves the diaphragm's contractility and renders it less susceptible to fatigue.

Adult↗
PubMed1981

Neural drive and electromechanical alterations in the fatiguing diaphragm.

It is suggested that respiratory failure in the compromised circulation might occur as a result of respiratory muscle fatigue in the presence of adequate neural drive and muscle excitation. As the cardiac output decreases acidosis develops and ventilation increases, resulting in an increase in the work of breathing, which requires the delivery of large supplies of energy. As these demands cannot be met by the energy supply, because of low cardiac output, the diaphragm fails as a force generator and respiratory failure ensues. Diaphragmatic fatigue may occur in normal subjects if the pressure developed with each breath is greater than 40% of the maximum transdiaphragmatic pressure and hypoxia predisposes the diaphragm to fatigue. Diaphragmatic fatigue, as in other skeletal muscles, might be located either at the neuromuscular junction or distal to it and can be detected either by phrenic stimulation or by frequency analysis of the myoelectric signal. Phrenic stimulation shows that after fatigue the diaphragm develops less force at any frequency of stimulation, but the loss of force at low frequencies persists for a longer period than at high frequencies. Frequency analysis of the electromyogram reveals that the power spectrum shifts to lower frequencies. This shift occurs long before the diaphragm fails as a force generator.

Animals↗