[ADVANCES IN THE TREATMENT OF RESPIRATORY INSUFFICIENCY].
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We have measured the electromyograms of the rib cage inspiratory muscles, including the neck muscles, in five lightly anesthetized baboons breathing at rest in the supine and head-up postures. When supine, the animals did not have any activity in the scalene (three heads) or sternomastoid muscles. In contrast, a phasic inspiratory electrical activity was invariably recorded from the parasternal intercostals, external intercostals, and levator costae. Measurements of the changes in length of the parasternal intercostals indicated that these muscles also shortened during inspiration, and they further showed that this inspiratory shortening was eliminated after selective muscle denervation. Similar observations were made in the head-up posture, although the inspiratory shortening of the parasternal intercostals was smaller in this posture. These observations thus indicate that: (1) the inspiratory expansion of the rib cage in baboons results entirely from the actions of the inspiratory intercostal muscles and mostly from the action of the parasternal intercostals; and (2) the load imposed on these muscles is greater in the head-up posture, presumably because of the action of gravity on the chest wall.
There is a mediolateral gradient in activation of the parasternal intercostal (PI) muscle during inspiration. In the present study, we tested the hypotheses that serotonergic [5-hydroxytryptamine (5-HT)] input from descending central drive and/or intrinsic size-related properties of PI motoneurons leads to the differential activation of PI muscles. In dogs, PI motoneurons innervating the medial and lateral regions of the PI muscles at the T(3)-T(5) interspaces were retrogradely labeled by intramuscular injection of cholera toxin B subunit. After a 10-day survival period, PI motoneurons and 5-HT terminals were visualized by using immunohistochemistry and confocal imaging. There were no differences in motoneuron morphology among motoneurons innervating the medial and lateral regions of the PI muscle. However, the number of 5-HT terminals and the 5-HT terminal density (normalized for surface area) were greater in motoneurons innervating the medial region of the PI muscle compared with the lateral region. These results suggest that differences in distribution of 5-HT input may contribute to regional differences in PI muscle activation during inspiration and that differences in PI motoneuron recruitment do not relate to size.
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The time (tlim) required to produce inspiratory muscle fatigue was measured in five normal subjects breathing at functional residual capacity (FRC) against a variety of high inspiratory resistive loads. In every breathing test the subjects generated with each inspiration a mouth pressure (Pm) that was a predetermined fraction of maximum Pm (Pmmax). They continued breathing until they were unable to generate this Pm. The Pm/Pmmax that could be generated indefinitely (Pmcrit) was around 60%. The inspiratory power output at that level of breathing was 6.6 kg.m/min (Wcrit). In three of those subjects the same experiment was conducted at an end-expiratory volume of FRC + one-half inspiratory capacity (1/2IC). The higher lung volume was actively maintained by the subjects watching end-expiratory transpulmonary pressure on an oscilloscope. For any fraction of the maximum mouth pressure at FRC + 1/2IC (Pm'max), tlim was shorter than FRC. Pmcrit decreased to 30% Pm'max and Wcrit to 2.6 kg.m/min. Monitoring the abdominal pressure revealed that the contribution of the diaphragm and intercostal accessory muscles alternated in time, possibly postponing the onset of fatigue.
The technique of an axillary vertical incision thoracotomy sparing pectoralis major muscle and latissimus dorsi muscle for a closure of patent ductus arteriosus is presented. After an mid-axillary vertical incision, serratus anterior muscle is incised on the third intercostal space between pectoralis major muscle and latissimus dorsi muscle. The space between serratus anterior muscle and rib cage (Spatium intermusc. thoracale) is dissected with a finger, through this space the 3rd intercostal thoracotomy is performed in the axillary and dorsal portion. The ventral part of intercostal muscle is incised from inside of the thoracic cavity for sparing the pectoralis major muscle. We performed this technique in two patients aged 1 year, and secured equally good operative fields as could be secured by the original axillary vertical incision thoracotomy described by Browne.
Single motor unit potentials from the eighth internal intercostal (IIC) muscle were recorded along with tracheal pressure and end-tidal CO2 (PETCO2) in spontaneously breathing, Dial-urethane anesthetized cats during hypercapnia (3, 5, or 7% CO2) and during lung inflation (LI, 100 ml above functional residual capacity) before and after vagotomy. Hypercapnia depressed IIC activity in 5 of 7 cats; the higher the PETCO2, the lower was the firing rate and the fewer the number of spikes per breath. LI evoked an initial silent phase (ISP) in 6 of 10 cats followed by a prolonged IIC burst. Hypercapnia combined with LI abolished or diminished the ISP and shortened the prolonged burst with an increase in firing rate and a recruitment of new units. Vagotomy silenced IIC activity in 7 of 10 cats, but LI after vagotomy activated IIC activity in 10 of 10 cats, though neither an ISP nor prolonged activity occurred. Our data suggest that major factors in controlling IIC activity are reciprocal inhibition from bulbospinal inspiratory neurons, excitatory and inhibitory inputs mediated by vagal afferents, and a modulation of IIC activity via gamma-loop. Hypercapnia affects the former two factors.
Bacterial beta-galactosidase cDNA was injected without lipofectin into 41 sites in dog muscle and expression was seen in 22 of them. The cDNA and lipofectin was injected into 35 similar sites and expression was seen in 21. Expression was seen in a maximum of 2.5% of muscle fibers and 23.21% of nonmuscle cells. A total of 106 muscle sites were injected with the minigene with and without lipofectin. In 4 of the 45 sites injected with the minigene without lipofectin human dystrophin was expressed around the periphery of 0.3% of the fibers. Bacterial beta-galactosidase cDNA was injected into the peritoneal cavity of 4 pups, 2 of which also received lipofectin. In all 4, expression was seen in liver, spleen, and mesenteric lymph node. In the 2 pups that received lipofectin, expression was also seen in the diaphragm, intercostal, and abdominal muscles of 1 and in the diagphragm and intercostal muscles of the other. These experiments show that human dystrophin transgene expression can be obtained in dog muscle. However, other methods will be required to increase the degree of expression before gene therapy trials can be undertaken.
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Using a respiratory inductive plethysmograph (Respitrace) we studied thoracoabdominal movements in eight normal subjects during inspiratory resistive (Res) and elastic (El) loading. The magnitude of loads was chosen so as to produce a fall in inspiratory mouth pressure of 20 cmH2O. The contribution of rib cage (RC) to tidal volume (VT) increased significantly from 68% during quiet breathing (QB) to 74% during El and 78% during Res. VT and breathing frequency did not change significantly. During loading a phase lag was present on inspiration so that the abdomen led the rib cage. However, outward movement of the abdomen ceased in the latter part of inspiration, and the RC became the sole contributor to VT. These observations suggest greater recruitment of the inspiratory musculature of the RC than the diaphragm during loading, although changes in the mechanical properties of the chest wall may also have contributed. Indeed, an increase in abdominal end-expiratory and end-inspiratory pressures was observed in five out of six subjects, indicating abdominal muscle recruitment which may account for part of the reduction in abdominal excursion. Both Res and El increased the rate of emptying of the respiratory system during the ensuing unloaded expiration as a result of a reduction in rib cage expiratory-braking mechanisms. The time course of abdominal displacements during expiration was unaffected by loading.
We examined chest wall and rib cage configuration in seven normal subjects during a variety of breathing maneuvers. Magnetometers were used to measure lower rib cage anteroposterior, lower rib cage transverse, upper rib cage anteroposterior, and abdomen anteroposterior diameters. Changes of these diameters were recorded during voluntary maneuvers, rebreathing, reading, and "natural" breathing. Relative motion of the rib cage and abdomen was displayed with the rib cage represented by the product of its lower anteroposterior and transverse diameters. During spontaneous breathing the rib cage and chest wall are near their relaxation configuration. During chemically driven ventilation the chest wall and rib cage progressively depart from this configuration. Much greater distortions of the chest wall and rib cage occurred during some voluntary maneuvers. Additionally, esophageal pressure and gastric pressure were measured during voluntary distortion of the rib cage. Substantial changes in lower rib cage shape occurred during voluntary maneuvers when compared with spontaneous breaths at the same transmural pressure. We conclude that the unitary behavior of the rib cage in normal subjects requires muscle coordination.
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