Biomedical subjects

G A Farkas

Publications and source records attributed to G A Farkas.

At least 19 recordsLinked to original sources

PubMed2003

Exercise delays the hypoxic thermal response in rats.

Exercise exacerbates acute mountain sickness. In infants and small mammals, hypoxia elicits a decrease in body temperature (Tb) [hypoxic thermal response (HTR)], which may protect against hypoxic tissue damage. We postulated that exercise would counteract the HTR and promote hypoxic tissue damage. Tb was measured by telemetry in rats (n = 28) exercising or sedentary in either normoxia or hypoxia (10% O2, 24 h) at 25 degrees C ambient temperature (Ta). After 24 h of normoxia, rats walked at 10 m/min on a treadmill (30 min exercise, 30 min rest) for 6 h followed by 18 h of rest in either hypoxia or normoxia. Exercising normoxic rats increased Tb ( degrees C) vs. baseline (39.68 +/- 0.99 vs. 38.90 +/- 0.95, mean +/- SD, P < 0.05) and vs. sedentary normoxic rats (38.0 +/- 0.09, P < 0.05). Sedentary hypoxic rats decreased Tb (36.15 +/- 0.97 vs. 38.0 +/- 0.36, P < 0.05) whereas Tb was maintained in the exercising hypoxic rats during the initial 6 h of exercise (37.61 +/- 0.55 vs. 37.72 +/- 1.25, not significant). After exercise, Tb in hypoxic rats reached a nadir similar to that in sedentary hypoxic rats (35.05 +/- 1.69 vs. 35.03 +/- 1.32, respectively). Tb reached its nadir significantly later in exercising hypoxic vs. sedentary hypoxic rats (10.51 +/- 1.61 vs. 5.36 +/- 1.83 h, respectively; P = 0.002). Significantly greater histopathological damage and water contents were observed in brain and lungs in the exercising hypoxic vs. sedentary hypoxic and normoxic rats. Thus exercise early in hypoxia delays but does not prevent the HTR. Counteracting the HTR early in hypoxia by exercise exacerbates brain and lung damage and edema in the absence of ischemia.

Animals↗

PubMed2001

Role of nitric oxide in thermoregulation and hypoxic ventilatory response in obese Zucker rats.

To examine the role of nitric oxide (NO) on thermoregulation and control of breathing in obesity, awake obese and age-matched lean Zucker (Z) rats underwent a sustained hypoxic challenge. Body temperature (Tb), oxygen consumption (V O(2)) and ventilation (V E) were measured during room air and during 30-min of hypoxia (10% O(2)) after intraperitoneal administration of either 100 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME), a nonspecific NOS inhibitor, 25 mg/kg of 7-nitroindazole (7-NI), a selective neuronal NOS inhibitor, or equal volume of vehicle (dimethyl sulfoxide: DMSO) as control. Tb in obese rats during room air was significantly lower than that of lean rats. Hypoxia induced a more pronounced drop in Tb and V O(2) in lean rats than in obese rats. Tb in lean Z rats dropped significantly by approximately 0.2 degrees C after L-NAME and, more markedly, by approximately 1.1 degrees C after 7-NI compared with control during room air, whereas Tb in obese Z rats was unaffected. L-NAME and 7-NI attenuated hypoxia-induced hypothermia or hypometabolism in lean rats, but not in obese rats. Lean rats exhibited an abrupt increase in V E in response to hypoxia followed by a gradual decline in V E. In contrast, obese rats displayed an initial increase in V E that plateaued during sustained hypoxia. Both L-NAME and 7-NI induced marked decreases in V E during room air and hypoxia compared with control lean rats, whereas V E was virtually unaffected by either agent in obese rats. The present results suggest that the blunted thermoregulatory and ventilatory responses to hypoxia in obese Z rats may be attributed to reduced activity of NOS in the central nervous system.

Animals↗

PubMed2001

Opioidergic modulation of ventilatory response to sustained hypoxia in obese Zucker rats.

OBJECTIVE: To determine whether altered central and/or peripheral opioidergic mechanisms contribute to the altered ventilatory response to sustained hypoxia in obese Zucker rats. RESEARCH METHODS AND PROCEDURES: Eight lean (176 +/- 8 [SEM] g) and eight obese (225 +/- 12 g) Zucker rats were studied at 6 weeks of age. Pulmonary ventilation ((E)), tidal volume (V(T)), and breathing frequency (f) at rest and in response to sustained (30 minutes) hypoxic (10% O(2)) challenges were measured on three separate occasions by the barometric method after the randomized, blinded administration of equal volumes of saline (control), naloxone methiodide (N(M); 5 mg/kg, peripheral opioid antagonist), or naloxone hydrochloride (N(HCl); 5 mg/kg, peripheral and central opioid antagonist). RESULTS: Administration of N(M) and N(HCl) in lean animals had no effect on (E) either at rest or during 30 minutes of sustained exposure to hypoxia. Similarly, N(M) failed to alter (E) in obese rats. In contrast, N(HCl) significantly (p < 0.05) increased (E) and V(T) both at rest and during 2 to 10 minutes of hypoxic exposure in obese rats. After 20 to 30 minutes of hypoxic exposure, V(T) remained elevated with N(HCl), but the earlier elevation of (E) seemed to be attenuated due to a decrease in f at 20 minutes of exposure to hypoxia. DISCUSSION: Thus, endogenous opioids modulate both resting (E) and the ventilatory response to sustained hypoxia in obese, but not in lean, Zucker rats by acting specifically on opioid receptors located within the central nervous system.

Animals↗

PubMed2001

NMDA receptor-mediated modulation of ventilation in obese Zucker rats.

BACKGROUND: Ventilation in response to hypoxia is reduced in some obese humans and is believed to represent part of the pathogenesis of obesity hypoventilation syndrome (OHS). Ventilation in response to hypoxic exposure is closely related to the release of excitatory neurotransmitters, in particular glutamate, acting specifically on N-methyl-D-aspartate (NMDA) receptors. OBJECTIVES: The aim of the present study was to investigate whether NMDA receptor-mediated mechanisms are responsible for the altered ventilatory response to sustained hypoxia observed in obese Zucker (Z) rats. SUBJECTS: Seven lean and seven 15-week-old obese male Z rats were studied. MEASUREMENTS: Ventilation ([V](E)) at rest and during 30 min sustained hypoxic (10% O(2)) exposure was measured by the barometric method. [V](E) was assessed following the blinded-random administration of equal volumes of either saline (vehicle) or dextromethorphan (DM, 10 mg/kg), a non-competitive glutamate NMDA receptor antagonist. RESULTS: DM had no effects on resting [V(E) in both lean and obese rats during room air breathing. Lean rats treated with DM exhibited a significant (P<0.05) depression in [V](E), V(T), and V(T)/T(I) during either the early (5 min) or the late phase (30 min) of ventilatory response to sustained hypoxia. In contrast, DM administration in obese rats did not change [V(E), V(T), or V(T)/T(I) during the early phase of ventilatory response to hypoxia. During the late phase of ventilatory response to hypoxia. obese rats treated with DM exhibited a similar depression in [V](E) and V(T) as observed in lean rats, but had no significant change in V(T)/T(I) during the 30 min hypoxic exposure. CONCLUSION: Our findings indicate that altered glutamatergic mechanisms acting on NMDA receptors are partially responsible for a blunted early phase of ventilatory response to hypoxia noted in obese rats and also contribute to their reduced neural respiratory drive.

Animals↗

PubMed2001

GABAergic modulation of ventilation and peak oxygen consumption in obese Zucker rats.

Obesity is often associated with a reduced ventilatory response and a decreased maximal exercise capacity. GABA is a major inhibitory neurotransmitter in the mammalian central nervous system. Altered GABAergic mechanisms have been detected in obese Zucker rats and implicated in their hyperphagic response. Whether altered GABAergic mechanisms also contribute to regulate ventilation and influence exercise capacity in obese Zucker rats is unknown and formed the basis of the present study. Eight lean [317 +/- 18 (SD) g] and eight obese (450 +/- 27 g) Zucker rats were studied at 12 wk of age. Ventilation at rest and ventilation during hypoxic (10% O(2)) and hypercapnic (4% CO(2)) challenges were measured by the barometric method. Peak O(2) consumption (VO(2 peak)) in response to a progressive treadmill test to exhaustion was measured in a metabolic treadmill. Ventilation and VO(2 peak) were assessed after administration of equal volumes of DMSO (vehicle) and the GABA(A) receptor antagonist bicuculline (1 mg/kg). In lean animals, bicuculline administration had no effect on ventilation and VO(2 peak). In obese rats, bicuculline administration significantly (P < 0.05) increased resting ventilation (465 +/- 53 and 542 +/- 72 ml. kg(-1). min(-1) for control and bicuculline, respectively), ventilation during exposure to hypoxia (899 +/- 148 and 1,038 +/- 83 ml. kg(-1). min(-1) for control and bicuculline, respectively), and VO(2 peak) (62 +/- 3.7 and 67 +/- 3.5 ml. kg(-0.75). min(-1) for control and bicuculline, respectively). However, in obese Zucker rats, ventilation in response to hypercapnia did not change after bicuculline administration (608 +/- 96 vs. 580 +/- 69 ml. kg(-1). min(-1)). Our findings indicate that endogenous GABA depresses ventilation and limits exercise performance in obese Zucker rats.

Animals↗

PubMed2001

Serotonergic modulation of ventilation and upper airway stability in obese Zucker rats.

To elucidate the role of serotonin in the maintenance of normal breathing and upper airway (UA) patency in obesity, we studied the effects of systemic administration of ritanserin, a serotonin (5-HT) 2A and 2C receptor antagonist, on ventilation (V E) during room air breathing and during hypoxic (10% O2) and hypercapnic (4% CO2) ventilatory challenges in awake young (6-8 wk) and older (7-8 mo) obese and lean Zucker (Z) rats. Older obese Z rats adopted a more rapid shallow breathing pattern compared with older lean rats. The administration of ritanserin (1 mg/kg intraperitoneally) to older obese rats resulted in a reduction in V E (439 +/- 35 [SD] to 386 +/- 41 ml/kg/min, p < 0.01), a decrease in respiratory rate, a prolongation of inspiratory time, and an increase in V O2 (16.4 +/- 1.7 to 18.2 +/- 1.9 ml/kg(0.75)/min, p < 0.05) during room air breathing. By comparison, it had little effect on ventilation in young lean and obese Z or older lean Z rats. Ritanserin also had no effect on ventilatory responses to either hypoxia or hypercapnia in young or older lean and obese Z rats. The collapsibility of the isolated UA was examined in older Z rats. The pharyngeal critical pressure (Pcrit) of older obese rats was significantly greater than that of lean rats (p < 0.05), indicating that obese rats have more collapsible UA than lean rats. The administration of ritanserin significantly increased Pcrit in older obese rats (-1.6 +/- 0.3 to -0.8 +/- 0.2 cm H2O, p < 0.01) and in lean rats (-3.1 +/- 1.0 to -2.4 +/- 0.6 cm H2O, p < 0.05). We suggest that the 5-HT(2A/2C) receptor subtype plays an important role in the maintenance of UA stability and normal breathing in obesity, and we speculate that older obese Z rats may have augmented serotonergic control of UA dilator muscles as a mechanism to prevent pharyngeal collapse.

Age Factors↗

PubMed2000

Endogenous opioids modulate ventilation and peak oxygen consumption in obese Zucker rats.

Levels of endogenous opioids are increased in morbidly obese humans and obese rats. Endogenous opioids are important neuromodulators, and are involved in a wide range of functions including ventilatory control. We studied eight lean and eight obese Zucker (Z) rats at 6 and 16 wk of age. We assessed minute ventilation (V E) at rest and during hypercapnic challenges, as well as peak oxygen consumption (V O(2peak)) after the administration of saline (control), naloxone hydrochloride (N(HCl)), and naloxone methiodide (N(M)). Administration of N(HCl) and N(M) to lean animals had no effect on V E and V O(2peak). Similarly, N(M) failed to alter V E and V O(2peak) in obese rats studied at 6 or 16 wk of age. In young obese rats, N(HCl) significantly (p < 0.05) increased resting V E (721 +/- 154 [mean +/- SD] ml/kg/min versus 937 +/- 207 ml/kg/min, saline versus N(HCl), respectively); VE in response to 4% CO(2) (924 +/- 110 ml/kg/min versus 1,212 +/- 172 ml/ kg/min); V E in response to 8% CO(2) (1,233 +/- 172 ml/kg/min versus 1,565 +/- 327 ml/kg/min); and V O(2peak) (90.8 +/- 9.6 ml/kg(0.75)/min versus 98.3 +/- 5.9 ml/kg(0.75)/min). However, N(HCl) administration had no effect on V E or V O(2peak) in obese rats retested at 16 wk of age. Thus, endogenous opioids modulate resting ventilation, ventilatory responsiveness to CO(2), and V O(2peak) in young obese rats by acting specifically on receptors located within the central nervous system. This modulation disappears once the animals reach 16 wk of age.

Animals↗

PubMed1998

Effect of changing body temperature on the ventilatory and metabolic responses of lean and obese Zucker rats.

We measured body temperature (Tb) and ventilatory and metabolic variables in lean (n = 8) and obese (n = 8) Zucker rats. Measurements were made while rats breathed air, 4% CO2, and 10% O2. Under control conditions, Tb in obese rats was always less than that of their lean counterparts. Obese rats adopted a more rapid, shallow breathing pattern than lean rats in air and had a lower ventilation rate in 4% CO2. Respiration in 10% O2 was similar for the two groups. Metabolic variables did not differ between lean and obese rats whatever the gas breathed. When lean rats were cooled to match Tb in control obese rats with an implanted abdominal heat exchanger, they increased ventilation and metabolism in air; there was no effect of cooling on responses to 4% CO2; and ventilation increased while metabolism decreased in 10% O2. When obese rats were warmed to match Tb in control lean rats, trends in ventilation and metabolism resulted in a tendency toward hyperventilation in air and 4% CO2, but not in 10% O2. Taken overall, matching Tb in lean and obese rats accentuated differences in respiratory and metabolic variables between the two groups. We conclude that differences in respiration between lean and obese Zucker rats are not due to the difference in Tb.

Analysis of Variance↗

PubMed1998

Mechanism controlling sleep organization of the obese Zucker rats.

We tested the hypothesis that the obese (fa/fa) Zucker rat has a sleep organization that differs from that of lean Zucker rats. We used the polygraphic technique to identify and to quantify the distribution of the three main states of the rat: wakefulness (W), non-rapid-eye-movement (NREM), and rapid-eye movement (REM) sleep states. Assessment of states was made with light present (1000-1600), at the rats thermoneutral temperature of 29 degrees C. Obese rats, compared with lean ones, did not show significant differences in the total time spent in the three main states. Whereas the mean durations of W and REM states did not differ statistically, that of NREM did (P = 0.046). However, in the obese rats, the frequencies of switching from NREM sleep to W, which increased, and from NREM to REM sleep, which decreased, were statistically significantly different (P = 0.019). Frequency of switching from either REM or W state was not significantly different. We conclude that sleep organization differs between lean and obese Zucker rats and that it is due to a disparity in switching from NREM sleep to either W or REM sleep and the mean duration of NREM sleep.

Animals↗

PubMed1997

Diaphragm structure and function in health and disease.

The diaphragm is the primary muscle of inspiration, and as such uncompromised function is essential to support the ventilatory and gas exchange demands associated with physical activity. The normal healthy diaphragm may fatigue during intense exercise, and diaphragm function is compromised with aging and obesity. However, more insidiously, respiratory diseases such as emphysema mechanically disadvantage the diaphragm, sometimes leading to muscle failure and death. Based on metabolic considerations, recent evidence suggests that specific regions of the diaphragm may be or may become more susceptible to failure than others. This paper reviews the regional differences in mechanical and metabolic activity within the diaphragm and how such heterogeneities might influence diaphragm function in health and disease. Our objective is to address five principal areas: 1) Regional diaphragm structure and mechanics (GAF). 2) Regional differences in blood flow within the diaphragm (WLS). 3) Structural and functional interrelationships within the diaphragm microcirculation (DCP). 4) Nitric oxide and its vasoactive and contractile influences within the diaphragm (MBR). 5) Metabolic and contractile protein plasticity in the diaphragm (SKP). These topics have been incorporated into three discrete sections: Functional Anatomy and Morphology, Physiology, and Plasticity in Health and Disease. Where pertinent, limitations in our understanding of diaphragm function are addressed along with potential avenues for future research.

Aging↗

PubMed1997

Respiratory muscle reserve in rats during heavy exercise.

The extent to which the respiratory pump muscles limit maximal aerobic capacity in quadrupeds is not entirely clear. To examine the effect of reduced respiratory muscle reserve on aerobic capacity, whole body peak oxygen consumption (VO2 peak) was measured in healthy Sprague-Dawley rats before and after Sham, unilateral, or bilateral hemidiaphragm denervation (Dnv) surgery. VO2 peak was determined by using a graded treadmill running test. Hemidiaphragm paralysis was verified after testing by recording the absence of electromyographic activity during inspiration. Before surgery, VO2 peak averaged 86, 87, and 92 ml . kg-1 . min-1 for the Sham, unilateral, and bilateral Dnv groups, respectively. Two weeks after surgery, there was no significant change in VO2 peak for either the Sham or unilateral Dnv group. However, VO2 peak decreased approximately 19% in the bilateral Dnv group 2 wk after surgery. These findings strongly suggest that the pulmonary system in rats is designed such that during heavy exercise, the remaining respiratory pump muscles are able to compensate for the loss of one hemidiaphragm, but not of both.

Animals↗

PubMed1996

Contractility of the ventilatory pump muscles.

The ventilatory muscles are striated skeletal muscles, and their in situ function is governed by the same relationships that determine the contractile force of muscles in vitro. The ventilatory muscles, however, are functionally distinct from limb skeletal muscles in several aspects, the most notable being that the ventilatory muscles are the only skeletal muscles upon which life depends. Among the muscles that participate in ventilation, the diaphragm is closest to its optimal resting length at functional residual capacity (FRC) and has the greatest capacity for shortening and volume displacement, making it the primary muscle of inspiration. All inspiratory muscles shorten when the lung is inflated above FRC, but interactions among the various inspiratory muscles make for a wider range of high force output than could be achieved by any one muscle group acting in isolation. The velocity of inspiratory muscle shortening, especially diaphragmatic shortening, causes maximal dynamic inspiratory pressures to be substantially lower than maximal static pressures. This effect is especially pronounced during maximal voluntary ventilation, maximal exercise, and maximal inspiratory flow, volume maneuvers over the full vital capacity. During quiet breathing, the ventilatory muscles operate well below the limits of their neural activation and contractile performance. During intense activity, however, the diaphragmatic excursion approaches its limits over the entire vital capacity, and respiratory pressures may near their dynamic maximum. Because the system may operate near its available capacities during increased ventilatory demands, multiple strategies are available to compensate for deficits. For example, if the diaphragm is acutely shortened, it can still generate the required respiratory pressure if it receives more neural drive. Alternatively, other muscles can be recruited to take over for an impaired diaphragm. Thus, the whole system is highly versatile.

Animals↗

PubMed1996

Effects of aging and obesity on respiratory muscle phenotype in Zucker rats.

Because obesity results in an increased work of breathing, we tested the hypothesis that the oxidative properties and myosin heavy chain (MHC) isoform profiles in respiratory muscles would differ between lean and obese animals. Furthermore, we postulated that obesity-related changes in respiratory muscles would be independent of age. To test these hypothesis, samples of the costal diaphragm, crural diaphragm, and parasternal intercostal muscles were removed from three age groups (young, adult, and old) of obese and lean Zucker rats. Citrate synthase (CS) activity was measured as a marker of oxidative capacity, and MHC isoforms were identified with gel electrophoresis. Analysis revealed that CS activity was significantly higher in the crural and costal diaphragms and parasternal intercostal of obese animals compared with lean animals (P < 0.05); this obesity-related increased in CS activity was related independent of age. Furthermore, respiratory muscle percent type IIb MHC was lower and percent type I MHC isoforms were higher in obese animals compared with lean animals. These data support the notion that obesity results in a fast-to-slow shift in MHC phenotype and an increase in oxidative capacity in major inspiratory muscles. The shift in MHC isoforms in obese animals is also age related, whereas the obesity-mediated increase in oxidative capacity is relatively independent of age.

Aging↗

PubMed1995

Endogenous opioids modulate ventilation in the obese Zucker rat.

This study evaluated the modulatory role of endogenous opioids on ventilation in young and mature, lean and obese male Zucker rats. Naloxone, an opioid receptor antagonist, and saline (control) were administered subcutaneously to awake rats, and ventilation in air and in response to an hypoxic and an hypercapnic gas challenge measured. In response to naloxone young, obese but not lean rats exhibited a marked increase of ventilation in all three conditions. Older obese Zucker rats that were morbidly obese breathed at a frequency of over 200 breaths per minute and showed only a modest increase of ventilation in response to naloxone. Older lean rats increased ventilation with naloxone only when exposed to hypercapnia. Unlike the stimulatory effects hypoxia and hypercapnia had on ventilation in older, lean rats, the ventilatory responses of the obese, older rats to hypoxia and to hypercapnia were blunted. We conclude that the obese Zucker rat may be a good animal model to assess how chest wall loading and endogenous opioids interact in the development of ventilatory control abnormalities.

Animals↗

PubMed1995

Regional adaptations of rabbit diaphragm muscle fibers to unilateral denervation.

We hypothesized that adaptations of the rabbit diaphragm (Dia) after unilateral denervation (DNV) result from removal of a neural influence rather than from passive stress. Length changes of midcostal and sternal Dia regions were measured before and after DNV by using sonomicrometry. Midcostal fibers passively lengthened after DNV, whereas sternal fibers shortened. In both regions, these length changes were associated with minimal stress, as estimated from passive force-length relationships. Morphological and contractile adaptions of midcostal and sternal Dia regions were examined after 1 and 4 wk of DNV. In both Dia regions, type I fibers progressively hypertrophied, whereas type IIb fibers atrophied. After DNV, changes in isometric contraction were similar in both Dia regions. Twitch contraction and half-relaxation times increased, force-frequency relationships shifted leftward, and maximum tetanic force decreased. We conclude that passive length changes and mechanical stress are not the main determinants of the morphological and contractile adaptations of the Dia after unilateral DNV but that these adaptations result from DNV itself.

Adaptation, Physiological↗

PubMed1995

Experimental emphysema.

This animal model of emphysema exhibits the same abnormalities in respiratory mechanics as those seen in human emphysema. The histologic and radiographic findings also closely resemble changes of panacinar disease. Moreover, the progressive hypoxemia preceding hypercarbia also parallels the clinical course seen in human disease. Drawbacks of this model include the long time period required to develop significant changes and the cost of maintaining the animals for such a time period. Large cystic areas were not noted in our animals and one would have to turn to another model to address the problem of giant bullous emphysema. There is no ideal animal model of pulmonary emphysema, and the usefulness of an experimental model should be judged on how well it answers the specific questions. Significant information has been obtained using various animal models of emphysema in lung transplantation, diaphragmatic function, pulmonary hemodynamics, and in several other areas. The dog appears to be a suitable model for thoracic surgical research on emphysema.

Animals↗

PubMed1994

Contribution of the rib cage inspiratory muscles to breathing in baboons.

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.

Animals↗

PubMed1994

Finite-element analysis of stress in the canine diaphragm.

Stress in the diaphragm, transdiaphragmatic pressure, and diaphragm shape are interrelated by a balance of forces. Using precise in vivo measurements of diaphragm shape and transdiaphragmatic pressure distribution in combination with finite-element analysis (ANSYS), we determined the direction and magnitude of stress in the passive diaphragm at relaxation volume. Lead spheres sutured along muscle bundles identified muscle bundle location and orientation in vivo. The x, y, and z coordinates of the lead spheres and entire surface of the diaphragm, excluding the zone of apposition, were determined to within 1.4 mm. Thin shell elements were used to construct a finite-element model of the diaphragm with a 2.1- to 4.2-mm internodal spacing. The diaphragm was assumed to have a uniform thickness of 2.5 mm, and magnitude and direction of the principal stresses were computed. The results show that 1) diaphragm stress is nonuniform and anisotropic (i.e., varies both with location on diaphragm surface and direction examined), 2) largest stress (sigma 1) is aligned with muscle bundles and is two to four times larger than sigma 2 (perpendicular to sigma 1 in diaphragm plane), and 3) stress along the muscle bundles is larger in vivo under conditions of biaxial stress than at same length in vitro under uniaxial stress. Although diaphragm stress and tension have often been assumed to be uniform, our finding that stress is oriented primarily along the muscle fibers should be considered in future models of the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗