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Harlequin syndrome: the sudden onset of unilateral flushing and sweating.

Facial flushing and sweating were investigated in five patients who complained of the sudden onset of unilateral facial flushing in hot weather or when exercising vigorously. One patient probably suffered a brainstem infarct at the time that the unilateral flush was first noticed, and was left with a subtle Horner's syndrome on the side opposite to the flush. The other four had no other neurological symptoms and no ocular signs of Horner's syndrome. Thermal and emotional flushing and sweating were found to be impaired on the non-flushing side of the forehead in all five patients whereas gustatory sweating and flushing were increased on that side in four of the five patients, a combination of signs indicating a deficit of the second sympathetic neuron at the level of the third thoracic segment. CT and MRI of this area failed to disclose a structural lesion but latency from stimulation of the motor cortex and thoracic spinal cord to the third intercostal muscle was delayed on the non-flushing side in one patient. The complaint of unilateral flushing and sweating was abolished in one patient by ipsilateral stellate ganglionectomy. The unilateral facial flushing and sweating induced by heat in all five patients was thus a normal or excessive response by an intact sympathetic pathway, the other side failing to respond because of a sympathetic deficit. The onset in the four cases of peripheral origin followed strenuous exertion, which suggested that an anterior radicular artery may have become occluded at the third thoracic segment during torsion of the thoracic spine.

Adult↗

Electrophysiological study of diaphragmatic myoclonus.

This is the first reported detailed electrophysiological study of diaphragmatic myoclonus. An 86 year old woman had rapid, intermittent epigastric pulsations. Neurological examination and imaging studies of the brain and spinal cord were normal. Needle EMG showed rhythmic contractions of the diaphragm and external intercostal muscles at 4 to 5 Hz. These contractions were often associated with suppression of normal breathing and were capable of maintaining adequate ventilation. Both diaphragms were involved but showed considerable variability in their relative latencies. Automated interference pattern analysis suggested a change in recruitment order, with selective activation of large phrenic motoneurons. The supraspinal mechanisms mediating diaphragmatic myoclonus are different from that of voluntary and involuntary rhythmic breathing, and seem to be unrelated to palatal myoclonus. The generator source is likely related to respiratory centres in the rostral medulla.

Aged↗

Effect of cold exposure on energy metabolism in the young pig.

Twenty-four piglets were weaned at 3 weeks of age and received 615 kJ metabolizable energy/(kg body weight X day). The temperature was reduced from 29 to 25 degrees C by 4 weeks of age. Six pigs were exposed to cold by reducing the temperature to 10 degrees C by 5 weeks of age while the other six were exposed to 23 degrees C. These two temperatures were maintained for 3 weeks. Each week the three pigs closest to the mean weight of each group were used for measurements of heat production for 23 h by open-circuit calorimetry and glucose turnover by continuous infusion of [6-3H]- and [U-14C]-glucose. The animals were sacrificed at 8 weeks of age, a sample of their intercostal muscle was used for in vitro measurement of muscle respiration, and the carcass was analyzed. There was no change in heat production, glucose turnover, and rectal temperature during the 3 weeks of cold exposure, so the data were pooled. Cold exposure increased heat production by 50%, forced mobilization of fat reserves (1000 g over the 3 weeks), and increased glucose replacement rate by 20%. The decline in rectal temperature to 37.6 from 38.8 degrees C could be regarded as a strategy to reduce energy needed to regulate body temperature. In the cold, heat production equalled metabolizable energy intake, but protein deposition was maintained at the same level as that in the pigs at the thermoneutral temperature, using the energy derived from the mobilization of body fat. The increase in Na+-K+ ATPase dependent respiration accounted for 70% of the increase in O2 consumption of muscle from cold-exposed pigs and thus is potentially an important component of cold-induced thermogenesis in the pig.

Animals↗

Superior marginal rib defects in traumatic quadriplegia.

The interpretation of the chest films of hospitalized quadriplegic and paraplegic patients over a one-year period revealed three quadriplegic patients with superior marginal rib defects. The resorptive defect involved the posterior portion of the third through seventh ribs. The etiology is probably intercostal muscle atrophy with resulting loss of muscle stress causing bone resorption.

Adult↗

Myotonic dystrophy (Steinert's disease) in the neonate.

Radiological abnormalities of the ribs are reported in 5 newborn infants with myotonic dystrophy. In all 5, the ribs appeared very thin, in contrast to the normal appearance of the rest of the skeleton. This slenderness, which is important for diagnosis and prognosis, seems to be caused by hypotonia of the intercostal muscles. However, it is not pathognomonic of myotonic dystropy, for it can be observed in other myopathies.

Female↗

Surgical flaps in the chest: anatomic considerations, applications, and radiologic appearance.

PURPOSE: To determine the frequency of use of surgical flaps--tissue that is transposed from its normal location to promote healing and prevent complications--in noncardiac thoracic surgery and to demonstrate the typical radiologic appearances of such flaps. MATERIALS AND METHODS: The surgical records of 200 patients who underwent thoracotomy or median sternotomy for noncardiac thoracic surgery were reviewed. Postoperative radiologic studies of randomly selected cases were also reviewed. RESULTS: A total of 213 surgical flaps were used in these patients, including 80 pericardial fat pad flaps (37.6%), 78 greater omental flaps (36.6%), 21 intercostal muscle flaps (9.9%), 16 anterior serratus muscle flaps (7.5%), and 18 greater pectoral muscle, latissimus dorsi muscle, pleural, thymic, or mediastinal fat flaps (8.5%). The flaps produced unusual opacity or attenuation and/or contour of the mediastinum, hilum, or chest wall. CONCLUSION: Knowledge of common thoracic surgical flaps is helpful in interpretation of postoperative radiologic studies.

Adipose Tissue↗

Rattlesnake venom shock in the rat: development of a method.

A model in Wistar rats (n = 30, 279-345 g) was developed to study circulatory, respiratory, metabolic, and lethal effects of an intravenous infusion (30 min; 1.25, 1.5, 1.75, and 2.0 mg/kg) of rattlesnake (Crotalus viridis helleri) venom. Venom produced perfusion failure with lactacidemia, hemoconcentration, hypoproteinemia, and death. The severity of poisoning was proportional to the quantity of venom given and to the elevation in lactic acid and hematocrit. Hemorrhages in the diaphragm, intercostal muscles, and intestine were observed at necropsy. In a separate test, rats (n = 12, 311-355 g) received an infusion of 1.5 mg/kg of venom or physiological salt solution. Blood volume was measured 30 min after the end of infusion in both groups with radioiodinated (125I) human serum albumin (RIHSA) and 51Cr-labeled rat red cells. Venom produced a significant reduction in total blood volume index (35%, P less than 0.001), plasma volume index (46%, P less than 0.001), and red cell mass indec (22% P less than 0.005). The slope of the RIHSA-disappearance curve of animals that received venom was more than twice that of the control group. We conclude that perfusion failure following rattlesnake envenomation is associated with hypovolemia due to increases in vascular permeabiltiy and hemorrhage.

Animals↗

Regional circulatory responses to head-out water immersion in conscious dogs.

We determined the regional blood flow responses to head-out water immersion (WI) in intact (INT) and cardiac-denervated (CD) conscious dogs. Immersing dogs in thermoneutral water (37 degrees C) in the quadruped position for 100 min resulted in significant increases in cardiac output (Qco) above control values by 38.7% in the INT dogs and 39.2% in the CD dogs (P less than 0.01). Arterial pressure increased by 32 and 34.7% in the INT and CD groups, respectively, during WI, with no significant changes occurring in the calculated total peripheral resistance. Regional blood flow responses were measured with 15-microns radiolabeled microspheres. Flows in the INT and CD groups increased significantly to the heart (40, 38%), skin (93, 96%), fat (79, 83%), diaphragm (44, 48%), and intercostal muscles (58, 55%), whereas there were no changes in renal cortical blood flows during WI. Total brain blood flows did not change significantly on immersion; however, blood flows in both INT and CD animals were increased to the cerebellum (19, 22%), but a significant decrease in pituitary flow (52%) was observed only in the CD group during WI. Gastrointestinal tissue flows increased only during early WI in both INT (45%) and CD (47%) animals. However, blood flows to the skeletal muscles increased only during late WI in the INT (53%) and CD (47%) groups. There were no significant differences between the INT and CD groups. Rectal temperatures and systemic O2 consumption (VO2) were unchanged during WI in both groups of animals. These observations indicate that WI leads to a sustained elevation of Qco accompanied by selective increases in regional tissue perfusion that may be accounted for in some tissues by an increase in metabolic demand or by local heating responses and produces a time-dependent redistribution of blood flow away from the gastrointestinal tissues toward skeletal muscle tissues, which may be due to a partial uncoupling of the normal Q/VO2 relationship. This may be caused by thermal or central neurohumoral mechanisms. These regional circulatory responses are not dependent on the presence of the cardiac nerves.

Animals↗

Sex differences in blood flow distribution of normothermic and heat-stressed rabbits.

Sex differences in blood flow (BF) distribution of male and female mature laboratory rabbits were determined in normothermic and heat-stressed states. Animals were anesthetized with alpha-chloralose, and BF distribution was determined by radioactive microspheres in the thermoneutral state and then again during hyperthermia after 2 h of heat exposure. Cardiac output did not change in either sex during heat stress. BF to the toe and ear skin and to nasal turbinates was lower in females than in males, whereas that to the diaphragm, sternum, intercostal muscles, spleen, and skeletal muscles was higher in females. A thermal state-by-sex interaction was detected in several organs, indicating that during heat stress in males, BF is significantly higher than in the controls, whereas in females a decline, no change, or only a slight increase was recorded. Males did not exhibit any decrease in inner organ BF during heat stress, whereas females did. Results show sex differences in BF distributions under normothermia and hyperthermia, suggesting that males and females differ in their BF regulation in both peripheral organs, which are active in heat dissipation, and inner body organs.

Animals↗

Mechanics of the rib cage and diaphragm during sleep.

The pattern of motion of the rib cage and abdomen/diaphragm was studied in three normal subjects during sleep. Sleep state was monitored by electroencephalograph and electrocculograph. Intercostal electromyographs (EMG's) were recorded from the second interspace parasternally. Abdominothoracic motion was monitored with magnetometers and these signals calibrated by isovolume lines either immediately before going to sleep, or if there was movement, on awakening. Respiration was recorded using a jerkin plethysmograph. In the awake subject in the supine position, the rib cage contributed 44% to the tidal volume and had essentially the same contribution in quiet sleep. However, in active or rapid eye movement sleep the rib cage contribution fell to 19% of the tidal volume. This was accompanied by a marked reduction in the intercostal EMG. With the subject in the upright position the rib cage appears to be passively driven by the diaphragm. However, the present data suggest that active contraction of the intercostal muscles is required for normal rib cage expansion in the supine position.

Abdomen↗

Effect of chest wall vibration on ventilation in patients with spinal cord lesion.

Changes of respiration caused by chest wall vibration were studied in 13 patients with cervical cord lesions. Vibrators applied on the chest wall were intermittently triggered by the patient's respiratory movements. The vibrators were triggered to be applied in three ways. 1) Upper vibrations were bilaterally applied during inspiration on the 2nd or 3rd parasternal intercostal spaces (insp "in-phase" vibration). 2) Lower vibrations were bilaterally applied during expiration on the 7th-to 10th intercostal spaces anterior to midaxillary lines (exp "in-phase" vibration). 3) Inspiratory and expiratory vibrations were combined to produce alternating in phase vibration. Both inspiratory and expiratory vibrations increased tidal volume (VT), but the alternating in-phase vibration increased it to significantly higher values (P less than 0.05). Minute volume of ventilation (VE l/min) also increased with insp or exp in-phase vibration. The alternating in-phase vibration increased VE l/min to even higher values (P less than 0.05). The responses described probably depend on segmental vibration reflexes arising in the inspiratory and expiratory intercostal muscles underlying the vibrators. The alternating in-phase vibration may well be useful to improve the breathing in patients with respiratory insufficiency.

Adolescent↗

Configuration of the chest wall and occlusion pressures in awake humans.

During CO2 rebreathing in sitting position seven of nine conscious men showed a progressive fall in expiratory reserve volume, most of it due to a decrease in abdominal volume. Diaphragm length at end expiration was thus increased, and some elastic recoil pressure became available to drive inspiration. In four out of six subjects, when CO2 tension was greater than 55 Torr, there was a dip in abdominal pressure at the beginning of inspiration, and the change in transdiaphragmatic pressure during the first 100 ms of an occluded inspiration was smaller than the simultaneous change in mouth pressure (P0.1). In the subjects who showed the smallest diaphragmatic pressure in this 100 ms, electromyogram recordings showed that abdominal activity ceased before the onset of inspiration, and diaphragm activity did not appear until later than 100 ms into inspiration. We conclude that, in four our of our six subjects in the sitting posture, P0.1 can be generated in whole or in part by release of chest wall elastic recoil or in intercostal muscle contraction. In the supine posture, there was no change by end-expiratory chest wall configuration, and onset of diaphragm contraction coincided with beginning of inspiration in the two subjects in whom diaphragm electromyogram was recorded.

Abdomen↗

Function of canine diaphragm with hypovolemic shock and beta-adrenergic blockade.

In anesthetized mongrel dogs we investigated the effects of hypovolemia and beta-adrenergic stimulation on the decrease in force generation by the diaphragm [transdiaphragmatic pressure (Pdi)] during electrical stimulation of the phrenic nerves for 1 h. In seven normovolemic dogs with arterial pressure (Pa) of approximately 125 Torr, Pdi fell approximately 48% from an initial value of 35 +/- 4.8 Torr. In dogs made moderately hypovolemic, Pdi was actually higher than with normovolemia (P less than 0.01). In dogs made severely hypovolemic, Pa approximately 50 Torr, Pdi at the start of pacing was less than with normovolemia (25 +/- 1.5 Torr) and remained so during phrenic nerve stimulation. When beta-adrenergic blockade with propranolol was added to moderate hypovolemia, the values of Pdi became similar to those of severe hypovolemia. Analysis of the relative contributions of gastric pressure and pleural pressure revealed that the factor responsible for maintaining Pdi with moderate hypovolemia was pleural pressure. Changes in thoracic gas volume and chest wall configuration did not explain the changes we saw in diaphragm function. Analysis of the relationship between rib cage motion and pleural pressure confirmed our finding of the greater pleural pressure generation with sympathetic stimulation that accompanies hypovolemia. These studies demonstrated that 1) severe hypovolemia impaired diaphragm function, 2) diaphragm function was maintained with moderate hypovolemia by beta-adrenergic stimulation, and 3) with hypovolemia-associated sympathetic stimulation there was an increase in force generation by the intercostal muscles.

Adrenergic beta-Antagonists↗

Pleural liquid pressure measured by micropipettes in rabbits.

Pleural liquid pressure (Ppl) was measured by the micropipette servo-nulling method. In anesthetized, paralyzed, and mechanically ventilated rabbits, windows were made by dissecting away the intercostal muscle layers, exposing the parietal pleura over the right caudal lung lobe. Repeated measurements of Ppl were made at the windows by puncturing the parietal pleura with micropipettes during apnea at functional residual capacity. In five supine rabbits, Ppl relative to atmospheric pressure averaged -3.32 +/- 1.22 (SD) cmH2O at a distance of 5.64 +/- 0.34 (SD) cm above the lung base and -1.64 +/- 0.79 cmH2O at a distance of 2.35 +/- 0.64 cm above the lung base; the vertical Ppl gradient was 0.51 cmH2O/cm height. Ppl interpolated to midlung height was equal in absolute magnitude to mean lung static recoil (Pst) of 2.00 cmH2O. In prone rabbits, Ppl measured near the dorsal surface, 3.9 cm above the lung base, averaged -1.32 +/- 0.46 cmH2O on the costal surface, not statistically different in magnitude from mean Pst of 1.59 +/- 0.09. In contrast, Ppl measured at the same vertical height off the edge of the caudal lung in the costo-diaphragmatic recess was -4.64 +/- 0.65 cmH2O. We concluded from these data that Ppl was equal to pleural surface pressure over the costal surface and that the vertical gradient in Ppl was not hydrostatic, except in large fluid spaces off the sharp edges of the lung.

Animals↗

Pleural liquid pressure in dogs measured using a rib capsule.

We have developed a minimally invasive method for measuring the hydrostatic pressure in the pleural space liquid. A liquid-filled capsule is bonded into a rib and a small hole is cut in the parietal pleura to allow direct communication between the liquid in the capsule and the pleural space. The pressure can be measured continuously by a strain gauge transducer connected to the capsule. The rib capsule does not distort the pleural space or require removal of intercostal muscle. Pneumothoraces are easily detected when they occur inadvertently on puncturing the parietal pleura. We examined the effect of height on pleural pressure in 15 anesthetized spontaneously breathing dogs. The vertical gradients in pleural pressure were 0.53, 0.42, 0.46, and 0.23 cmH2O/cm height for the head-up, head-down, supine, and prone body positions, respectively. These vertical gradients were much less than the hydrostatic value (1 cmH2O/cm), indicating that the pleural liquid is not in hydrostatic equilibrium. In most body positions the magnitudes of pleural liquid pressure interpolated to midchest level were similar to the mean transpulmonary (surface) pressure determined postmortem. This suggests that pleural liquid pressure is closely related to the lung static recoil.

Animals↗

Pleural space thickness in situ by light microscopy in five mammalian species.

The thickness of the pleural space was measured by a focusing method using a light microscope (X157, 2.5-micron depth of focus). In anesthetized animals, thin transparent parietal pleural windows were made by dissection of intercostal muscle. Multiple postmortem measurements were made of the combined thickness of the pleural space and the window by focusing in sequence on the lung surface and on 1- to 2-micron tantulum particles sprayed on the window. The window thickness was measured after creating a pneumothorax and retracting the lungs. In supine rabbits the pleural space measured at various heights on the costal surface was of uniform thickness (16 micron) except for a thicker region (62 micron) located within 3 mm of the most dependent part of the lung. The thicker region reverted to the uniform thickness after it was placed in a nondependent position by inverting the animal from the supine to prone position, indicating fluid drainage by gravity. In the prone position near midchest, pleural space thickness (t) averaged 6.9 micron in the mouse, 10.2 in the rat, 17.2 in the rabbit, 18.3 in the cat, and 23.6 in the dog. Animals of larger body mass (M, kg) had a wider pleural space: t = 13.1 X M0.20. There was no contact between the two pleurae, indicating that fluid lubrication facilitates sliding between the lung and chest wall. Based on the t vs. M relationship and estimates of the viscous flow of pleural liquid, pleural fluid exchange rate would be proportional to body mass and the work of sliding as a fraction of the work of breathing would be smaller in larger animals.

Animals↗

Obesity alters regional ventilation in lateral decubitus position.

Alterations of regional ventilation were determined as a function of body position in five morbidly obese subjects using 81mKr to assess ventilation (V) and 127Xe at equilibrium to determine lung volume (V). With subjects in seated and supine positions, the left lung contributed an average of 43% of the total V/V. When the apical-basal gradient within each lung was examined in subjects in the seated position, V/V was greatest in the dependent (basal) regions in half of the subjects, whereas the others showed greater V/V near the upper lung regions. All obese subjects preferentially ventilated the nondependent lung in both the left and right lateral decubitus positions. In a control group of three nonobese subjects, V/V was found to be equally distributed between left and right lungs in both the seated and supine positions. In contrast with the results in the obese group, V/V was slightly greater in the dependent lung in both lateral decubitus positions. Although the combination of 127Xe images and He-dilution measurement of functional residual capacity in the lateral decubitus positions indicated a reduction in the volume of the dependent lung of the obese when compared with values in the seated position, other factors affecting the mechanical function of either the diaphragm or the intercostal muscles could also have produced these positional alterations of ventilation.

Adult↗

A method for microinjection into subpleural alveoli of rat lung in situ.

A new technique is described for the micropuncture of rat lung in the intact thorax. Under pentobarbital sodium anesthesia a glass micropipette is passed through a small area of the parietal pleura, which has been cleared of overlying intercostal muscle. The micropipette is passed into the lung parenchyma and withdrawn again without collapsing the lung. The current application of this technique is in the microinjection of fluid into subpleural alveoli, which is illustrated using a suspension of colloidal gold. The gold particles are immediately dispersed over the surface of many alveoli, a small proportion spreading laterally as far as 4-6 mm. There is no evidence of alveolar flooding.

Animals↗