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Results for “Skeletal muscle dysfunction”

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PubMed1994

Postischemic extremities exhibit immediate release of tumor necrosis factor.

PURPOSE: Although reperfusion of acutely ischemic extremities can cause cardiopulmonary collapse and death, the humoral agent(s) released from limbs promoting this distant organ injury are not well characterized. We hypothesized that tumor necrosis factor-alpha (TNF-alpha), a cytokine that causes cardiopulmonary dysfunction in septic shock, may be released from postischemic extremities. METHODS: Isolated rat hindlimbs were perfused at constant pressure with a nonrecirculating crystalloid-based buffer. After 60 or 120 minutes of normothermic ischemia, TNF activity was measured in sequential samples of venous effluent by L929 bioassay. Associated limb injury was assessed by the extent of no-reflow after reperfusion, changes in endothelial permeability to iodine 125-labeled albumin and skeletal muscle injury by uptake of technetium 99 pyrophosphate. RESULTS: After 120 minutes of normothermic ischemia (n = 10), a 15-fold increase in TNF-alpha activity in venous effluent occurred, with peak activity at 1.5 minutes of reperfusion (30.6 +/- 8.7 U/ml) falling to near control levels by 5 minutes. This group had a 3.3-fold increase in vascular permeability, a 2.2-fold increase in the muscle injury index and a 71.2% decline in reperfusion flow (all p < 0.05 vs control). Pretreatment of extremities with an anti-TNF-alpha antibody in a second group of limbs undergoing 120 minutes of ischemia (n = 10) decreased TNF activity to levels not significantly different from the nonischemic control group (n = 12). The extent of no-reflow in limbs treated with antibodies was significantly attenuated (flow 44.9% of control vs 29.8% [untreated], p < 0.05). Antibody treatment affected neither muscle injury nor vascular permeability. CONCLUSIONS: Postischemic extremities exhibited a transient, early burst of TNF release on reperfusion, which likely represented washout of TNF produced during ischemia. Suppression of TNF activity with an antibody to TNF-alpha resulted in a salutary increase in postischemic flow rates, suggesting that TNF may play a role in the no-reflow phenomenon.

Animals↗

PubMed2004

Sequence analysis of the complete mitochondrial genome in patients with mitochondrial encephaloneuromyopathies lacking the common pathogenic DNA mutations.

The purpose of this study was to identify novel mitochondrial deoxyribonucleic acid (mtDNA) mutations in a series of patients with clinical and/or morphological features of mitochondrial dysfunction, but still no genetic diagnosis. A heterogeneous group of clinical disorders is caused by mutations in mtDNA that damage respiratory chain function of cell energy production. We developed a method to systematically screen the entire mitochondrial genome. The sequence-data were obtained with a rapid automated system. In the six mitochondrial genomes analysed we found 20 variants of the revised Cambridge reference sequence [Nat. Genet. 23 (1999) 147]. In skeletal muscle nineteen novel mtDNA variants were homoplasmic, suggesting secondary pathogenicity or co-responsibility in determination of the disease. In one patient we identified a novel heteroplasmic mtDNA mutation which presumably has a pathogenic role. This screening is therefore useful to extend the mtDNA polymorphism database and should facilitate definition of disease-related mutations in human mtDNA.

Adult↗

PubMed1994

[The effects of anterior cruciate ligament resection and subsequent running training on muscles around the knee joint in rat].

The purpose of this study was to evaluate the effects of running training on the muscles in rat after resection of the anterior cruciate ligament (ACL). The biochemical and histochemical changes were analyzed in the muscles around the knee joint from which the ACL was dissected, and the rats were subsequently forced to undergo endurance running. After ACL resection, the wet weights of all muscles around the knee joint decreased but an increase was found in the number of slow-twitch fibers, especially in the vastus lateralis and vastus medialis muscles. The activities of glycolytic and oxidative enzymes in all muscles tended to decrease following resection. Rats which had undergone ACL resection were put through training in the form of appropriate endurance running, causing significant increases in the wet weights of all muscles, except for the vastus medialis, and a decrease in the number of slow-twitch fibers in the vastus medialis. In addition, all the enzyme activities tended to decrease following training. Therefore, the influences of ACL resection and subsequent running training were clearly demonstrated in the vastus medialis muscle. These changes may have been caused by joint instability and sensory reflex dysfunction by deafferentation from the ACL mechanoreceptor (joint-ligament receptor). To maintain knee muscle function, stability of the joint and restoration of the skeletomotor system from the ACL and the muscles around the knee joint is necessary.

Animals↗

PubMed2005

A randomised, double-blind, dose-ranging study to evaluate efficacy and safety of three doses of botulinum toxin type A (Botox) for the treatment of spastic foot.

Botulinum toxin A (BTX) injections have been used successfully in the treatment of post-stroke foot spasticity, but the optimal dose-response relationship for selected muscles has yet to be established. The aim of this study was to outline beneficial and unwanted effects of three different doses of BTX in the treatment of spastic foot. In this randomised, double-blind, dose-ranging study, 45 spastic feet were randomly allocated to one of three groups, each of which was treated with a different dosage of BTX. The doses were decided on the basis of suggestions in the literature. Outcome measures (Modified Ashworth Scale, Medical Research Council Scale, gait assessment, presence of Achilles tendon clonus, Visual Analogue Scales for Gait Function and Pain, Adverse Effects scale) were applied at baseline, 4 weeks and 4 months after treatment. All the groups showed significant scales scores improvements after treatment with BTX. Group II (mean BTX total dose: 322 U) and Group III (mean BTX total dose: 540 U) showed a greater and more prolonged response than Group I (mean BTX total dose: 167 U). Group III showed the highest rate of adverse effects 4 weeks post-treatment. BTX injections constitute a useful and safe method of improving post-stroke foot spasticity, associated pain, gait speed and function. In particular, the medium BTX dosages (320 UI spread over 2-5 muscles) were found to be both safe and effective in producing long-lasting improvement of spastic foot dysfunction.

Aged↗

PubMed1998

Comparison of corticomotoneuronal EPSPs and macro-MUPs in amyotrophic lateral sclerosis.

We correlated the size of the corticomotoneuronal excitatory postsynaptic potential (CM-EPSP) arising in a single spinal motor neuron with the function of the target motor unit as measured by conventional and macro EMG in early amyotrophic lateral sclerosis (ALS). Macro motor unit potentials (macro-MUPs) were recorded from a surface electrode after spike-triggered averaging in the extensor digitorum communis muscle. The size of the CM-EPSP projecting to the same motor unit was measured from changes in the firing probability of single motor units induced by transcranial magnetic stimulation using peristimulus time histograms. In controls, the amplitudes of CM-EPSPs and macro-MUPs correlated inversely, probably reflecting a lower input resistance of larger spinal motoneurons. In ALS the amplitude of macro-MUPs did not correlate with that of CM-EPSPs and one third of normal ALS motor units had a reduced or temporally dispersed CM-EPSP. The findings indicate primary dysfunction of the corticomotoneuronal projection system in ALS that is independent of functional changes of spinal motoneurons.

Action Potentials↗

PubMed2007

Auditory startle reaction in primary blepharospasm.

Primary dystonia is associated with abnormal brainstem function, as shown by abnormalities of the blink reflex in blepharospasm (BSP) and of the auditory startle reaction in cervical dystonia. We examined the auditory startle reaction--a brainstem reflex elicited by an unexpected loud stimulus--in patients with primary BSP to expand knowledge on brainstem pathophysiology in primary focal dystonia. Thirteen patients with primary BSP were included and 13 age- and sex-matched healthy volunteers served as controls. Auditory startle responses (ASRs) were elicited by binaural high-intensity auditory stimuli, and reflex electromyographic activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. Patients with BSP showed higher ASR probabilities (masseter, sternocleidomastoid, biceps brachii), shorter ASR onset latencies (masseter, orbicularis oculi, sternocleidomastoid), and larger ASR area-under-the-curve (masseter, sternocleidomastoid) as compared with normal controls. Habituation of ASRs did not differ significantly between patients and controls. These results corroborate previous findings of increased brainstem excitability in primary BSP but point to a different pattern of brainstem dysfunction compared to cervical dystonia, indicating that different pathophysiological mechanisms are involved in the two types of focal dystonia.

Acoustic Stimulation↗

PubMed2006

The new Geriatric Nutritional Risk Index is a good predictor of muscle dysfunction in institutionalized older patients.

BACKGROUND & AIMS: The validity of Geriatric Nutritional Risk Index (GNRI), in predicting nutrition-related risk of complications in the elderly, has been recently underscored. Malnutrition may results also in muscle function impairment. Thus, the present study aims to investigate if GNRI might be a reliable detector of muscle dysfunction in institutionalized older people. METHODS: In total, 153 institutionalized elderly (71 males, 82 females; mean age+/-SD: 75.2+/-8.4; range: 65-96) were studied in anthropometric parameters, serum albumin concentration and total score on GNRI. Muscle function was assessed by handgrip strength (HG). RESULTS: Women were significantly older than men and presented lower values of HG and arm muscle area (AMA). In overall population, GNRI was significantly correlated with AMA, HG and strength for centimeter of muscle area (HG/AMA); however, in gender-separated analysis, men presented higher degrees of correlation. After dividing patients in four categories according to GNRI, a more significant difference was detected in HG and HG/AMA rather than the other clinical and anthropometric parameters. Moreover, ANOVA analysis between HG quartiles was highly significant for GNRI, AMA and HG/AMA. CONCLUSIONS: GNRI is a good predictor of muscle dysfunction, particularly in men, and useful in identifying patients suitable for nutritional support and physical activity.

Age Factors↗

PubMed2003

Electrodiagnostic evidence of phrenic nerve demyelination in Charcot-Marie-Tooth disease 1A.

OBJECTIVE: To determine whether neurophysiologic findings correlate to clinical respiratory signs or spirometric abnormalities in patients with hereditary motor and sensory neuropathy type 1 (Charcot-Marie-Tooth disease). DESIGN: A total of 11 patients with hereditary motor and sensory neuropathy type 1A, genetically identified, (age range, 10-58 yr) were included and studied by physical pulmonary examination, chest radiography, respiratory function tests, and bilateral transcutaneous phrenic nerve conduction. RESULTS: No patient complained of respiratory symptoms or revealed abnormal spirometric or maximal respiratory pressure data, despite a phrenic nerve conduction significantly slower (P < 0.0001; median conduction time, 18.6 msec; 95th percentile, 31.97 msec) than that recorded in the control group of healthy subjects (median, 6.05 msec; 95th percentile, 8.82 msec); the amplitudes of compound muscle action potentials were not statistically different from the controls. CONCLUSIONS: Our study confirms a dramatic phrenic nerve involvement in absence of clinical and laboratory evidence of diaphragmatic weakness; further studies and an adequate follow-up are necessary to discover whether the disease progress might encompass respiratory dysfunction at later stages.

Action Potentials↗

PubMedDate not supplied

The effect of exercise and nutrition on the mechanostat.

In this review, we discuss the effect of increased and decreased loading and nutrition deficiency on muscle and bone mass and strength (and bone length and architecture) independently and combined. Both exercise and nutrition are integral components of the mechanostat model but both have distinctly different roles. Mechanical strain imparted by muscle action is responsible for the development of the external size and shape of the bone and subsequently the bone strength. In contrast, immobilization during growth results in reduced growth in bone length and a loss of bone strength due to large losses in bone mass (a result of endosteal resorption in cortical bone and trabecular thinning) and changes in geometry (bone shafts do not develop their characteristic shape but rather develop a rounded default shape). The use of surrogate measures for peak muscle forces acting on bone (muscle strength, size, or mass) limits our ability to confirm a cause-and-effect relationship between peak muscle force acting on bone and changes in bone strength. However, the examples presented in this review support the notion that under adequate nutrition, exercise has the potential to increase peak muscle forces acting on bone and thus can lead to a proportional increase in bone strength. In contrast, nutrition alone does not influence muscle or bone in a dose-dependent manner. Muscle and bone are only influenced when there is nutritional deficiency--and in this case the effect is profound. Similar to immobilization, the immediate effect of malnutrition is a reduction in longitudinal growth. More specifically, protein and energy malnutrition results in massive bone loss due to endosteal resorption in cortical bone and trabecular thinning. Unlike loading however, there is indirect evidence that severe malnutrition when associated with menstrual dysfunction can shift the mechanostat set point upward, thus leading to less bone accrual for a given amount of bone strain.

Adolescent↗

PubMed2006

Novel threshold tracking techniques suggest that cortical hyperexcitability is an early feature of motor neuron disease.

The dying forward hypothesis of motor neuron disease (MND) suggests that corticomotoneurons induce excitotoxic anterior horn cell death, with involvement of the glutamatergic neurotransmitter system. The aim of the present study was to apply novel threshold tracking transcranial magnetic stimulation (TMS) techniques in conjunction with peripheral nerve excitability studies in MND patients to further investigate the dying forward hypothesis and possibly determine the site of disease onset. Studies were undertaken in 23 MND patients using a 90-mm circular coil connected to a BiStim magnetic stimulator for cortical studies and electrical stimulation for peripheral nerve excitability studies. Motor-evoked potentials and compound muscle action potentials (CMAPs) were recorded from the right abductor pollicis brevis in the same setting. Measures of cortical and peripheral nerve excitability were correlated with clinical and neurophysiological parameters of disease severity. Short-interval intracortical inhibition (SICI) was significantly reduced in MND patients compared with controls (MND group = 3.6 +/- 0.8%; controls = 8.5 +/- 1.0%, P < 0.001), most prominently in MND patients with limb-onset disease. Changes in intracortical inhibition were accompanied by alterations in the magnetic stimulus-response curve, cortical silent period duration and resting motor threshold, all indicative of cortical hyperexcitability. Although the reduction in SICI was more pronounced in MND patients with less severe disease, as assessed by the CMAP amplitude, it remained evident even in MND patients with advanced disease. Measures of peripheral disease burden, namely the CMAP amplitude (r = -0.6) and neurophysiological index (r = -0.6), correlated with cortical hyperexcitability changes, as did the strength-duration time constant (r = -0.6), a peripheral marker of axonal excitability. Simultaneous assessment of central and peripheral nerve excitability has established the presence of co-existent upper and lower motor neuron dysfunction, with cortical hyperexcitability an early feature in MND.

Action Potentials↗

PubMed2000

Mitochondrial myopathy and familial thiamine deficiency.

We studied two siblings with a mitochondrial myopathy, familial thiamine deficiency, and an A3243G mutation of the mitochondrial DNA (mtDNA). The elder brother (patient 1, now 36 years old) developed myopathy and beriberi heart at 20 years of age. Thiamine therapy resolved the cardiac symptoms and hyperpyruvicemia and improved the myopathy. The younger brother presented aged 19 years with a myopathy (patient 2, now 35 years old). Thiamine deficiency was present in the siblings and parents, and ragged-red fibers (RRFs) were noted in muscle biopsies from the siblings. Analysis 17 years later demonstrated thiamine malabsorption and an A3243G mutation of the mtDNA in both siblings and their mother, progressive myopathy, and an increased number of RRFs and elevated serum CKMB activity in patient 1. Thiamine treatment decreased the serum concentrations of lactate and pyruvate in patient 2, but not patient 1. The role of thiamine in mitochondrial dysfunction caused by an electron transfer disorder in the setting of A3243G mtDNA mutation is discussed.

Adult↗

PubMed2005

An 18-month follow-up study on vibrotactile sense, muscle strength and symptoms in computer users with and without symptoms.

OBJECTIVES: The aim was to explore whether symptoms, sensory perception and muscle strength among computer users with and without symptoms in forearm or hand had changed after 18 months. METHODS: Twenty-six out of 30 females, experienced computer users, from a baseline study participated in the follow-up. In addition, five control subjects participated. The subjects completed a questionnaire regarding exposure to computer work, prevalence and severity of symptoms, health status and physical activity. Perceived thresholds for vibration were measured twice with 3 h in between on the right hand on four different sites innervated by the radial, median or ulnar nerve. Furthermore, sensory perception was measured on the left hand on two sites innervated by the median and ulnar nerve, respectively. Skin temperature was measured at each site prior to sensory perception measurements. Maximal handgrip strength and maximal pinch-grip strength were measured for both hands. RESULTS: Eighty-three percent of the subjects who had symptoms at baseline still had symptoms and 21% of the subjects who did not have symptoms at baseline experienced symptoms at follow-up. The first and the second sensory perception measurement were highly correlated. Vibrotactile sensory threshold representing the radial nerve was increased since baseline among the subjects who originally had symptoms. At follow-up, the vibrotactile sense for the computer users who reported symptoms in forearm or hand at baseline was deteriorated for the sites representing the median, ulnar and radial nerves compared to the control group. Among the original symptom free subjects with intensive computer work increases in vibrotactile perception thresholds were found for the sites representing the median and ulnar nerves. Handgrip muscle strength remained unchanged for all groups. CONCLUSIONS: The study indicates that sensory dysfunctions as well as symptoms in forearm and hand among computer users to a high degree are persistent. Muscle strength seems to be well maintained.

Adult↗

PubMed2005

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise.

OBJECTIVES: Because the muscle response to incremental exercise is not well documented in patients suffering from chronic fatigue syndrome (CFS), we combined electrophysiological (compound-evoked muscle action potential, M wave), and biochemical (lactic acid production, oxidative stress) measurements to assess any muscle dysfunction in response to a routine cycling exercise. DESIGN: This case-control study compared 15 CFS patients to a gender-, age- and weight-matched control group (n=11) of healthy subjects. INTERVENTIONS: All subjects performed an incremental cycling exercise continued until exhaustion. MAIN OUTCOME MEASURES: We measured the oxygen uptake (VO2), heart rate (HR), systemic blood pressure, percutaneous O2 saturation (SpO2), M-wave recording from vastus lateralis, and venous blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid (LA), and three markers of the oxidative stress (thiobarbituric acid-reactive substances, TBARS, reduced glutathione, GSH, and ascorbic acid, RAA). RESULTS: Compared with control, in CFS patients (i) the slope of VO2 versus work load relationship did not differ from control subjects and there was a tendency for an accentuated PvO2 fall at the same exercise intensity, indicating an increased oxygen uptake by the exercising muscles; (ii) the HR and blood pressure responses to exercise did not vary; (iii) the anaerobic pathways were not accentuated; (iv) the exercise-induced oxidative stress was enhanced with early changes in TBARS and RAA and enhanced maximal RAA consumption; and (v) the M-wave duration markedly increased during the recovery period. CONCLUSIONS: The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients.

Analysis of Variance↗

PubMed2002

Mitochondrial dysfunction in Friedreich's ataxia: from pathogenesis to treatment perspectives.

Friedreich's ataxia (FRDA), the most common inherited ataxia, is an autosomal recessive degenerative disorder caused by a GAA triplet expansion or point mutations in the FRDA gene on chromosome 9q13. The FRDA gene product, frataxin, is a widely expressed mitochondrial protein, which is severely reduced in FRDA patients. The demonstration that deficit of frataxin in FRDA is associated with mitochondrial iron accumulation, increased sensitivity to oxidative stress, deficit of respiratory chain complex activities and in vivo impairment of cardiac and skeletal muscle tissue energy metabolism, has established FRDA as a "new" nuclear encoded mitochondrial disease. Pilot studies have shown the potential effect of antioxidant therapy based on idebenone or coenzyme Q10 plus Vitamin E administration in this condition and provide a strong rationale for designing larger randomized clinical trials.

Antioxidants↗

PubMed2003

Insulin and myocardial blood flow.

The renaissance of glucose-insulin-potassium infusion (GIK) as a treatment of acute myocardial infarction both in diabetic and nondiabetic subjects has raised new interests to clarify the effects and mechanisms of insulin on myocardium. Although the action of insulin on substrate metabolism is quite well studied in heart, the cardiovascular effects were until recent years poorly known. Insulin induces skeletal muscle vasodilation mainly via the endothelium-dependent mechanism and appears to have an important role in normal vascular function. There is increasing amount of evidence that insulin acts as a vasodilatory hormone also in coronary arteries. Insulin enhances myocardial blood flow and decreases coronary vascular resistance in a dose-dependent manner in healthy subjects. Moreover, insulin is able to increase myocardial blood flow also in subjects who are characterized by coronary dysfunction such as subjects with obesity, type 1 diabetes and coronary artery disease. However, vasodilatory effect of insulin may be blunted in these patients. Since already very small increase in myocardial blood flow can reduce significantly myocardial ischemia, these vasodilatory actions of insulin in coronary arteries might partly contribute to beneficial effects of GIK therapy. On the other hand, in contrast to these acute beneficial effect of insulin, epidemiological studies have indentified chronic hyperinsulinemia, a common feature in subjects with insulin resistance to glucose uptake, as an independent risk factor for coronary artery disease. The present article review the physiological and pathophysiological role of insulin in cardiac vasculature and its clinical importance during myocardial ischemia and development of coronary artery disease.

Coronary Circulation↗

PubMed2006

Genetic neurological channelopathies.

Ion channels are crucial for the normal function of excitable tissues such as neurons and skeletal muscle. Since the discovery that the paroxysmal muscle disorder periodic paralysis is caused by mutations in genes that encode voltage-gated ion channels, many genetic neurological channelopathies have been defined. These channelopathies include epilepsy syndromes that show a mendelian pattern of inheritance, certain forms of migraine and disorders of cerebellar function, as well as periodic paralysis. The clinical diversity of these disorders relates in part to the tissue-specific expression of the dysfunctional channel, but is probably influenced by other, as yet unidentified, genetic and non-genetic factors. The complementary disciplines of molecular genetics and cellular and in vitro electrophysiology have resulted in significant advances in understanding of the basic molecular pathophysiology of some of these disorders. The single-gene neurological channelopathies are generally regarded as a paradigm for understanding common human paroxysmal disorders, such as epilepsy and migraine. This article reviews the clinical and molecular features of some of the single-gene channelopathies that affect muscle and brain. The possible role of ion-channel functional and genetic variation in predisposing individuals to common forms of human epilepsy and migraine are also considered. The implications for accurate genetic diagnosis and therapeutic intervention are highlighted.

Humans↗

PubMed2003

Post-traumatic TMJ internal derangement: impact on facial growth (findings in a pediatric age group).

Many clinical studies have shown how jaw injuries sustained during impact trauma to the face or mandible are the single most important cause of TMJ subsequent internal derangement. Proper function of the masticatory system is certainly the most influential variable in the TMJ remodelling; once a TMJ is internally deranged, adaptative or degenerative osteocartilagineous processes take place in the mandible, temporal bones and muscles. To evaluate relationships between consequences of post-traumatic TMJ internal derangement and disturbed facial skeleton growth in children, 25 patients (16 boys 9 girls), 14 year of age or younger, were selected out of a group of 74 and analysed. They all had been treated by physiotherapy and had undergone combined clinical and radiographic examination for five years. Symptoms included either individually or in various combination, pain, mechanical TMJ dysfunction and facial skeletal abnormalities, such as mandibular retrognathia and lower facial asymmetry manifested by chin deviation from the midline. Seventeen patients were found to have at least one abnormal and internally deranged TMJ on imaging studies; in twelve of them a mandibular asymmetry with chin deviation from the midline to the smaller or more degenerated TMJ was evident. Of the eight retrognathic patients, five were found to have bilateral TMJ derangement. In three patients both TMJ(s) were normal with normal facial structure. These data suggest that TMJ derangement in children may potentially have an impact on facial growth and lead to the development of retrognathia, with or without asymmetry, in many cases.

Adolescent↗

PubMed1981

Pulmonary clearance of blood-borne bacteria.

Clearance of blood-borne bacteria has been attributed primarily to a fixed macrophages in the liver and spleen. Although many important nonrespiratory functions of the lung have been reported, a major role for this organ in the clearance of circulating bacteria has not been described. To investigate mechanisms of sepsis induced lung dysfunction and pneumonia, we measured lung clearance, tissue accumulation and morphologic effect of blood-borne. Pseudomonas aeruginosa in pigs. Single pass pulmonary clearance of 60 to 80 per cent occurred over a wide range of infusion concentrations. Tissue concentrations of viable, hematogenously delivered bacteria were greatest in the lungs and exceeded inflowing blood concentrations in the lungs, liver and spleen but were less than inflowing blood concentrations in the heart, kidney and skeletal muscle. Electron microscopy showed phagocytosis of bacteria predominantly by mononuclear cells located within small pulmonary vessels. Viable test organisms were recovered from the upper airways of pigs receiving high dose bacterial infusions but not from pigs in the control group. In this experimental model, an important nonrespiratory function of the lungs is clearance of blood-borne bacteria. If lungs in humans have a similar capacity, retention of circulating organisms may be one mechanism of sepsis induced pulmonary failure.

Animals↗