Role of hemodynamics and vagus nerves in development of fibrin-induced pulmonary edema

1990 ◽  
Vol 69 (6) ◽  
pp. 2227-2232 ◽  
Author(s):  
F. J. Bosso ◽  
S. A. Lang ◽  
M. B. Maron

The interosseous external intercostal (EI) muscles of the upper rib cage are electrically active during inspiration, but the mechanical consequence of their activation is unclear. In 16 anesthetized dogs, we simultaneously measured EI (3rd and 4th interspaces) and parasternal intercostal (PA) (3rd interspace) electromyogram and length. Muscle length was measured by sonomicrometry and expressed as a percentage of resting length (%LR). During resting breathing, each muscle was electrically active and shortened to a similar extent. Sequential EI muscle denervation (3rd and 4th interspaces) followed by PA denervation (3rd interspace) demonstrated significant reductions in the degree of inspiratory shortening for each muscle. Mean EI muscle shortening of the third and fourth interspaces decreased from -3.4 +/- 0.5 and -3.0 +/- 0.4% LR (SE) under control conditions to -0.2 +/- 0.2 and -0.8 +/- 0.3% LR, respectively, after selective denervation of each of these muscles (P less than 0.001 for each). After selective denervation of the PA muscle, its shortening decreased from -3.5 +/- 0.3 to +0.6% LR (SE) (P less than 0.001). PA muscle denervation also caused the EI muscle in the third interspace to change from inspiratory shortening of -0.2% to inspiratory lengthening of +0.2% +/- 0.2 (P less than 0.05). We conclude that during eupneic breathing 1) the EI muscles of the upper rib cage, like the PA muscles, are inspiratory agonists and actively contribute to rib cage expansion and 2) PA muscle contraction contributes to EI muscle shortening.

1990 ◽  
Vol 69 (6) ◽  
pp. 2222-2226 ◽  
Author(s):  
A. F. DiMarco ◽  
J. R. Romaniuk ◽  
G. S. Supinski

The interosseous external intercostal (EI) muscles of the upper rib cage are electrically active during inspiration, but the mechanical consequence of their activation is unclear. In 16 anesthetized dogs, we simultaneously measured EI (3rd and 4th interspaces) and parasternal intercostal (PA) (3rd interspace) electromyogram and length. Muscle length was measured by sonomicrometry and expressed as a percentage of resting length (%LR). During resting breathing, each muscle was electrically active and shortened to a similar extent. Sequential EI muscle denervation (3rd and 4th interspaces) followed by PA denervation (3rd interspace) demonstrated significant reductions in the degree of inspiratory shortening for each muscle. Mean EI muscle shortening of the third and fourth interspaces decreased from -3.4 +/- 0.5 and -3.0 +/- 0.4% LR (SE) under control conditions to -0.2 +/- 0.2 and -0.8 +/- 0.3% LR, respectively, after selective denervation of each of these muscles (P less than 0.001 for each). After selective denervation of the PA muscle, its shortening decreased from -3.5 +/- 0.3 to +0.6% LR (SE) (P less than 0.001). PA muscle denervation also caused the EI muscle in the third interspace to change from inspiratory shortening of -0.2% to inspiratory lengthening of +0.2% +/- 0.2 (P less than 0.05). We conclude that during eupneic breathing 1) the EI muscles of the upper rib cage, like the PA muscles, are inspiratory agonists and actively contribute to rib cage expansion and 2) PA muscle contraction contributes to EI muscle shortening.


1992 ◽  
Vol 73 (3) ◽  
pp. 979-986 ◽  
Author(s):  
A. F. DiMarco ◽  
J. R. Romaniuk ◽  
G. S. Supinski

Recent studies suggest that the external intercostal (EI) muscles of the upper rib cage, like the parasternals (PA), play an important ventilatory role, even during eupneic breathing. The purpose of the present study was to further assess the ventilatory role of the EI muscles by determining their response to various static and dynamic respiratory maneuvers and comparing them with the better-studied PA muscles. Applied interventions included 1) passive inflation and deflation, 2) abdominal compression, 3) progressive hypercapnia, and 4) response to bilateral cervical phrenicotomy. Studies were performed in 11 mongrel dogs. Electromyographic (EMG) activities were monitored via bipolar stainless steel electrodes. Muscle length (percentage of resting length) was monitored with piezoelectric crystals. With passive rib cage inflation produced either with a volume syringe or abdominal compression, each muscle shortened; with passive deflation, each muscle lengthened. During eupneic breathing, each muscle was electrically active and shortened to a similar degree. In response to progressive hypercapnia, peak EMG of each intercostal muscle increased linearly and to a similar extent. Inspiratory shortening also increased progressively with increasing PCO2, but in a curvilinear fashion with no significant differences in response among intercostal muscles. In response to phrenicotomy, the EMG and degree of inspiratory shortening of each intercostal muscle increased significantly. Again, the response among intercostal muscles was not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 75 (6) ◽  
pp. 2360-2367 ◽  
Author(s):  
A. F. DiMarco ◽  
G. S. Supinski ◽  
B. Simhai ◽  
J. R. Romaniuk

The pattern of electrical activation and muscle length changes of the internal intercostal (II) muscles (9th or 10th interspace) of the lower rib cage were evaluated in supine anesthetized dogs. Studies were performed during resting breathing and expiratory threshold loading. Results were compared with simultaneous measurements of the better-studied triangularis sterni muscle (4th interspace). In general, both muscles lengthened with passive inflation and shortened with passive deflation. During resting breathing, both the II and TS muscles were electrically active and shortened below resting length, 7.7 +/- 1.6% (SE) and 5.3 +/- 1.7%, respectively. With the addition of positive end-expiratory pressure, the degree of electrical activation and muscle shortening increased progressively for both muscles, although to a somewhat greater extent for II muscles. Isolated denervation of the II muscles eliminated their shortening during resting breathing and often resulted in muscle lengthening, indicating that II muscle shortening was secondary to its own activation. Expiration was associated with lateral inward movement of the lower rib cage below its relaxation position. This motion was not significantly affected by abdominal muscle section but was markedly reduced by bilateral II denervation (7th-11th spaces). Our results indicate that the II muscles of the lower rib cage 1) are electrically active and shorten below resting length during resting breathing, 2) respond to positive end-expiratory pressure by increasing their level of activation and degree of shortening, and 3) are primarily responsible for inward lateral motion of the lower rib cage below its relaxation position during expiration.


1988 ◽  
Vol 65 (6) ◽  
pp. 2440-2445 ◽  
Author(s):  
E. van Lunteren ◽  
M. A. Haxhiu ◽  
N. S. Cherniack ◽  
J. S. Arnold

Studies in mammals have found that during breathing the triangularis sterni (TS) muscle regulates expiratory airflow and the end-expiratory position of the rib cage and furthermore that the respiratory activity of this muscle is influenced by a variety of chemical and mechanical stimuli. To assess the role of the TS during coughing and sneezing, electromyograms (EMGs) recorded from the TS were compared with EMGs of the transversus abdominis (TA) in eight pentobarbital-anesthetized dogs. During coughing induced by mechanically stimulating the trachea or larynx (n = 7 dogs), peak EMGs increased from 23 +/- 2 to 74 +/- 5 U (P less than 0.00002) for the TS and from 21 +/- 6 to 66 +/- 4 U (P less than 0.0002) for the TA. During sneezing induced by mechanically stimulating the nasal mucosa (n = 3 dogs), peak EMG of the TS increased from 10 +/- 3 to 66 +/- 7 U (P less than 0.005) and peak EMG of the TA increased from 10 +/- 2 to 73 +/- 7 U (P less than 0.02). For both muscles the shape of the EMG changed to an early peaking form during coughs and sneezes. Peak expiratory airflow during coughs of different intensity correlated more closely with peak TS EMG in three dogs and with peak TA EMG in four dogs; peak expiratory airflow during sneezes of different intensity correlated more closely with peak TS than TA EMG in all three animals. These results suggest that the TS is actively recruited during coughing and sneezing and that different neuromuscular strategies may be utilized to augment expiratory airflow.


1999 ◽  
Vol 86 (4) ◽  
pp. 1231-1235 ◽  
Author(s):  
S.-I. Sekizawa ◽  
T. Ishikawa ◽  
F. B. Sant’Ambrogio ◽  
G. Sant’Ambrogio

This study was performed to evaluate the characteristics of esophageal receptors in anesthetized and artificially ventilated dogs. The electrical activity of the esophageal afferents was recorded from the peripheral cut end of the cervical vagus nerve. A cuffed catheter was inserted into the esophagus at the level of the third tracheal ring and was used to establish the esophageal location of the endings. Most of the receptors were localized in the intrathoracic portion of the esophagus. The majority of the receptors studied (36 of 43) showed a slow adaptation to a maintained stretch of the esophageal wall. Vagal cooling blocked receptor activity at temperatures ranging from 3.5 to 25°C. Twenty-eight of 43 receptors, including 4 rapidly adapting endings (RAR), were challenged with saline, HCl + pepsin (HCl-P; pH 1) and distilled water (8 ml, 37°C). HCl-P solutions specifically stimulated only three receptors; saline or water did not. Five slowly adapting receptors and two RARs were also challenged with topically applied capsaicin; only one RAR was stimulated. To ascertain a possible effect of smooth muscle contraction, 17 receptors were tested with intravenous injections of ACh and/or asphyxia; only 4 were stimulated. These characteristics do not support an important reflexogenic role of the esophagus in response to chemical stimuli.


1995 ◽  
Vol 269 (4) ◽  
pp. H1467-H1472 ◽  
Author(s):  
M. R. Hill ◽  
D. W. Wallick ◽  
L. R. Mongeon ◽  
P. J. Martin ◽  
M. N. Levy

We used three vasoactive intestinal polypeptide (VIP) antagonists, VIP-(10-28), [p-Cl-D-Phe6,Leu17]VIP, and NT-VIP, to evaluate the role of VIP as a mediator of vagally induced tachycardia in chloralose-anesthetized dogs. After we administered muscarinic and beta-adrenergic receptor antagonists, we evoked vagally induced tachycardia either directly, by stimulating the vagus nerves for 2 min, or reflexly, by injecting phenylephrine to increase blood pressure. Furthermore, each of the antagonists attenuated the tachycardias induced by vagal stimulation by approximately 50% and the reflexly induced tachycardias by approximately 70%. Each VIP antagonist attenuated the chronotropic responses that we evoked by injecting VIP (5.2 ng/kg) into the sinus node artery. We tested the specificity of these VIP antagonists by determining whether they attenuated the increases in heart rate evoked by two other neuropeptides [peptide histidine isoleucine (PHI) and glucagon]. VIP-(10-28) attenuated the response to PHI, but not to glucagon. The other two VIP antagonists did not alter the chronotropic responses to PHI or glucagon. Our results support the hypothesis that neurally released VIP is the principal mediator of vagally induced tachycardia in the dog.


1984 ◽  
Vol 57 (4) ◽  
pp. 1254-1260 ◽  
Author(s):  
M. Decramer ◽  
A. De Troyer

In an attempt to understand the role of the parasternal intercostals in respiration, we measured the changes in length of these muscles during a variety of static and dynamic respiratory maneuvers. Studies were performed on 39 intercostal spaces from 10 anesthetized dogs, and changes in parasternal intercostal length were assessed with pairs of piezoelectric crystals (sonomicrometry). During static maneuvers (passive inflation-deflation, isovolume maneuvers, changes in body position), the parasternal intercostals shortened whenever the rib cage inflated, and they lengthened whenever the rib cage contracted. The changes in parasternal intercostal length, however, were much smaller than the changes in diaphragmatic length, averaging 9.2% of the resting length during inflation from residual volume to total lung capacity and 1.3% during tilting from supine to upright. During quiet breathing the parasternal intercostals always shortened during inspiration and lengthened during expiration. In the intact animals the inspiratory parasternal shortening was close to that seen for the same increase in lung volume during passive inflation and averaged 3.5%. After bilateral phrenicotomy, however, the parasternal intercostal shortening during inspiration markedly increased, whereas tidal volume diminished. These results indicate that 1) the parasternal intercostals in the dog are real agonists (as opposed to fixators) and actively contribute to expand the rib cage and the lung during quiet inspiration, 2) the relationship between lung volume and parasternal length is not unique but depends on the relative contribution of the various inspiratory muscles to tidal volume, and 3) the physiological range of operating length of the parasternal intercostals is considerably smaller than that of the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 61 (2) ◽  
pp. 539-544 ◽  
Author(s):  
V. Ninane ◽  
M. Decramer ◽  
A. De Troyer

The purpose of the present studies was to assess the functional coupling between the parasternal intercostals and the triangularis sterni (transversus thoracis) muscles during resting breathing, and we measured the electrical activity and the respiratory changes in length of these two muscles in 13 supine anesthetized dogs. The changes in muscle length were defined relative to their respective in situ relaxation length (Lr). During inspiration, the parasternal intercostals were active and shortened below Lr, causing the triangularis sterni to be passively stretched above Lr. Shortly after the cessation of parasternal contraction, the triangularis sterni became active and shortened below Lr, and in nine animals this active shortening was associated with a forcible distension of the parasternal intercostals above Lr. Deactivation of the triangularis sterni at end expiration caused both muscles to return to their respective Lr. This pattern was essentially unchanged after supplemental anesthesia and bilateral phrenicotomy. We conclude that in dogs breathing quietly the length of the rib cage muscles during the expiratory pause is not passively determined as conventionally thought.


1989 ◽  
Vol 66 (3) ◽  
pp. 1414-1420 ◽  
Author(s):  
A. De Troyer ◽  
G. A. Farkas

We have previously demonstrated that the shortening of the canine parasternal intercostals during inspiration results primarily from the muscles' own activation (J. Appl. Physiol. 64: 1546–1553, 1988). In the present studies, we have tested the hypothesis that other inspiratory rib cage muscles may contribute to the parasternal inspiratory shortening. Eight supine, spontaneously breathing dogs were studied. Changes in length of the third or fourth right parasternal intercostal were measured during quiet breathing and during single-breath airway occlusion first with the animal intact, then after selective denervation of the muscle, and finally after bilateral phrenicotomy. Denervating the parasternal virtually eliminated the muscle shortening during quiet inspiration and caused the muscle to lengthen during occluded breaths. After phrenicotomy, however, the parasternal, while being denervated, shortened again a significant amount during both quiet inspiration and occluded breaths. These data thus confirm that a component of the parasternal inspiratory shortening is not active and results from the action of other inspiratory rib cage muscles. Additional studies in four animals demonstrated that the scalene and serratus muscles do not play any role in this phenomenon; it must therefore result from the action of intrinsic rib cage muscles.


1990 ◽  
Vol 69 (6) ◽  
pp. 2175-2182 ◽  
Author(s):  
W. M. Petroll ◽  
H. Knight ◽  
D. F. Rochester

Diaphragmatic volume displacement (Vdi) is calculated from two models using measurements obtained from anteroposterior fluoroscopic images of supine anesthetized dogs. In model 1, diaphragmatic descent was treated as if it were a "piston in a cylinder." In contrast, model 2 incorporated thoracic configuration as well as inspiratory changes in rib cage diameter and diaphragm shape. In one dog, a computerized tomography reconstruction of Vdi was compared with Vdi calculated using the models. Vdi calculated from model 2 lay within 11% of the computerized tomographic value, whereas Vdi based on model 1 was 30% larger. In seven animals, radiopaque markers were sewn to the right costal diaphragm. Digitized fluoroscopic images were used to measure intermarker distance, an index of muscle shortening. For four tidal breaths per dog, in model 2 Vdi averaged 49 +/- 18% of tidal volume and was weakly correlated with costal diaphragm muscle shortening (R = 0.74). It is concluded that Vdi can be estimated from linear dimensions in the coronal plane, provided that inspiratory changes in rib cage diameter and diaphragmatic shape change are taken into account.


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