Alteration in diaphragmatic function induced by acute necrotizing pancreatitis in a rodent model.

Some of the common complications of acute necrotizing pancreatitis also involve pulmonary complications. These manifestations are often associated with a cephalad diaphragmatic shift. We hypothized that diaphragmatic function might be directly compromised by the acute abdominal process. This hypothesis was tested on an acute necrotizing pancreatitis (ANP) rat model. We assessed the diaphragm and peripheral (Extensor Digitorum Longus and Soleus) muscle properties in vitro using strips in control (C) and ANP animals. Contractile parameters included single twitch and a force-frequency curve (10 to 100 Hz), and an endurance capacity index (T50%) was calculated after a repetitive stimulation (30 Hz). Breathing pattern was not different between control and ANP animals, and muscular histologic examination was normal. However, ANP was associated with a marked decrease in diaphragmatic strength for all frequencies of stimulation when compared with C. Endurance capacity was also reduced in ANP animals as assessed by a lower T50% (ANP: 31 +/- 10.5 s; C: 49 +/- 10.3 s; p < 0.05). By contrast, no significant change in peripheral muscle function was observed in both groups. We conclude that ANP causes impairment in diaphragmatic strength and endurance capacity, whereas peripheral muscles are spared. These findings suggest that alterations in the respiratory pump may be involved in the genesis of acute respiratory failure in ANP.

Diaphragmatic function is markedly altered in cerulein-induced pancreatitis.

OBJECTIVE: To assess diaphragmatic function in vitro during experimental cerulein-induced acute pancreatitis. DESIGN: Prospective, randomized, controlled animal trial. SETTING: Research laboratory at a large university medical center. SUBJECTS: Twenty male Sprague-Dawley rats, weighing 180 to 200 g. INTERVENTIONS: Sodium chloride 0.9% or cerulein (5 microg/kg/hr) was infused for 6 hrs. MEASUREMENTS AND MAIN RESULTS: Isometric force generated during electrical stimulation of costal diaphragmatic strips was measured 6 hrs after the end of infusion. Diaphragmatic strength was assessed at different frequencies (10, 20, 30, 50, and 100 Hz). Endurance index was the time until the force generated during the 30 Hz repetitive stimulation decreased to 50% of the initial value (T50%). Histologic examination of the diaphragm was performed. A decrease averaging 40% in diaphragmatic strength generation was observed for all frequencies of stimulation in the pancreatitis group. Compared with the control group, this decrease was associated with a reduction in T50% (30.9 +/- 12.5 [SD] and 46.4 +/- 10.8 secs in pancreatitis and control, respectively; p< .05). No histologic alteration of the diaphragm was observed. CONCLUSIONS: Acute pancreatitis induced marked diaphragmatic dysfunction. Although the precise mechanisms responsible for this alteration are not precisely determined, diaphragmatic dysfunction may play a role in pancreatitis-associated respiratory failure.

Alteration in nutritional status and diaphragm muscle function.

Diet-induced undernutrition causes deleterious changes in the structure and function of the diaphragm muscle. Diseases associated with somatic washing cause atrophy of the respiratory muscles. In cachectic subjects, the diaphragm muscle mass and thickness are reduced in proportion to the reduction in body weight. In addition, respiratory muscle strength and endurance are reduced more dramatically than the weight loss. This finding suggests that malnutrition induces a reduction in muscular mass which is associated with a decrease in contractility. Diaphragmatic weakness may increase the risk of respiratory failure in patients with chronic obstructive pulmonary disease (COPD). The primary goal of a successful nutritional programme is to improve the diaphragm strength by correcting the mineral, electrolyte and energetic disturbances at the muscular level, the latter being responsible for the decreased contractability associated with malnutrition.