Change in Contralateral Muscle Blood Volume During Passive Unilateral Muscle Stretching Before and After Surgery.

OBJECTIVE: Passive muscle stretching is a common physical therapy for critically ill patients in the intensive care units. This study aimed to evaluate the effects of unilateral passive stretching of the gastrocnemius muscle (GM) before and after surgery on blood volume (BV) in the contralateral (non-stretched) GM in patients who are sedated after surgery. METHODS: We enrolled eight patients with esophageal cancer. The patients completed two sessions of passive cyclical stretching (20-s hold, 10-s release, 10 cycles) of the right GM: one before surgery (awake) and one after (under sedation). We used near-infrared spectroscopy to measure the BV in the stretched and contralateral GM. BV kinetics were compared between the ipsilateral and contralateral GM. RESULTS: In seven of the eight patients, BV in the stretched GM decreased during stretching and increased during the stretch-relaxation phase, both before and after surgery. Both before and after surgery, the change in the BV in the contralateral GM was inversely synchronized to the stretching cycle. CONCLUSIONS: Unilateral passive stretching of the GM influenced the microcirculation of the contralateral GM. The mechanism underlying the synchronous change in the BV in the contralateral GM remains to be clarified.

Plasma branched-chain amino acid levels and muscle energy metabolism in patients with chronic obstructive pulmonary disease.

BACKGROUND & AIMS: Although several studies have shown that plasma concentrations of branched-chain amino acids (BCAAs) are reduced in patients with chronic obstructive pulmonary disease (COPD), little is understood about how low concentrations of BCAAs limit exercise in such patients. The present study investigated whether plasma BCAAs are related to energy metabolism in exercising muscle using (31)P-magnetic resonance spectroscopy (MRS). METHODS: We analyzed the plasma amino acid profiles of 23 male patients with COPD (aged 69.2+/-5.1 years) and of 7 healthy males (aged 64.1+/-6.0 years). We normalized the exercise intensity of repetitive lifting by adjusting the weight to 7% of the maximal grip power. The intracellular pH and the phosphocreatine (PCr) index (PCr/(PCr+Pi); Pi, inorganic phosphate) were calculated from MR spectra. We evaluated the relationship between intracellular pH and PCr index at the completion of exercise and the plasma BCAA concentration. RESULTS: Glutamine concentrations were elevated in patients with COPD compared with healthy individuals. Plasma concentrations of BCAAs correlated with intracellular pH and PCr index at the completion of exercise. CONCLUSIONS: The findings are consistent with the notion that BCAAs affect muscle energy metabolism during exercise in patients with COPD.

Deoxygenated hemoglobin/myoglobin kinetics of forearm muscles from rest to exercise in patients with chronic obstructive pulmonary disease.

Exercise capacity is frequently decreased in patients with chronic obstructive pulmonary disease (COPD), and muscle dysfunction is one factor in this reduction. Studies using (31)-phosphorus magnetic resonance spectroscopy ((31)P-MRS) have shown that phosphocreatine (PCr) and muscle pH (pHi) are significantly decreased in patients with COPD during mild exercise, suggesting the early activation of anaerobic glycolysis in their muscles. Thus, muscle oxygenation states during exercise might differ between patients with COPD and healthy individuals. We simultaneously measured oxygenation state and pHi in the muscles of patients with COPD during the transition from rest to exercise (on-transition) using near infrared spectroscopy (NIRS) and (31)P-MRS. Sixteen patients with COPD (aged 68.6 +/- 7.5 years) and 7 healthy males (controls; aged 63.3 +/- 7.5 years) performed dynamic handgrip exercise (lifting a weight by gripping at a rate of 20 grips per min for 3 min). Patients were classified based on pHi data at the completion of exercise as having a normal (>or= 6.9; n = 8) or a low (< 6.9; n = 8) pHi. The deoxygenated hemoglobin/myoglobin (deoxy-Hb/Mb) in NIRS recordings remained constant or slightly decreased initially (time delay), then increased to reach a plateau. We calculated the time delay and the time constant of deoxy-Hb/Mb kinetics during the on-transition. The time delay was shorter in the group with a low pHi than in the controls. These findings might reflect a slower increase in O(2) delivery in patients with a low pHi, which might partly account for altered muscle energy metabolism.

Liposome-encapsulated hemoglobin alleviates brain edema after permanent occlusion of the middle cerebral artery in rats.

Liposome-encapsulated hemoglobin (LEH) was proven to be protective in cerebral ischemia/reperfusion injury. The present study evaluated LEH in a rat model of permanent middle cerebral artery (MCA) occlusion to clarify its effect during ischemia and reperfusion. Five minutes after thread occlusion of the MCA, rats were infused with 10 mL/kg of LEH (LEH, n = 13), and compared with normal controls (n = 11). Additional animals received the same MCA occlusion with no treatment (CT, n = 11), saline (saline, n = 10), empty liposome solution (EL, n = 13), or washed red blood cells (RBC, n = 7). Severity of brain edema was determined 24 h later by signal strength in T2-weighted magnetic resonance imaging of the cortex, striatum, hippocampus, and pyriform lobe. The results showed that brain edema/infarction observed in any vehicle-infused control was significantly more severe than in LEH-treated rats. There was a tendency toward aggravated edema in rats receiving ELs. LEH infusion at a dose of 10 mL/kg significantly reduced edema formation as compared to other treatments in a wide area of the brain 24 h after permanent occlusion of the MCA. Low oncotic pressure of EL and LEH solution (vehicle solution) appeared to cause nonsignificant aggravation of edema and reduced protective effects of LEH.

Phosphate-related energy compounds are not exhausted in chronically hypoperfused rat brain cortex after cortical spreading depression.

Long-term bilateral common carotid occlusion (BCCAO) in rats induces brain hypoperfusion and structural injury, and could have relevance as a model of vascular dementia in which cortical metabolism is reduced. The present study was designed to assess whether phosphate-related energy compounds and blood supplies are markedly affected by KCI-induced cortical spreading depression (CSD), which leads to metabolic and cerebral blood flow changes in rats with chronic BCCAO, by means of near-infrared spectroscopy and phosphorus magnetic resonance spectroscopy. Male Wistar rats were divided into 4 groups: BCCAO for 1 week (n = 6) and 4 weeks (n = 15), and sham operation for 1 week (n = 7) and 4 weeks (n = 7). The phosphocreatine (Pcr) index (PCr/PCr+Pi) and intracellular pH (pHi) were measured pre-CSD, just after KCl application, and at 20 and 40 minutes after CSD. Brains were evaluated by histology with hematoxylin and eosin and immunohistochemical reaction for glial fibrillary acidic protein (GFAP). Rapid signal changes of oxy-, deoxy-, and total hemoglobin were observed in all KCl-applied brains. The PCr index and pHi values in BCCAO were not different than those in control rats. The percentage of vacuolated area in the optic tract and percentage values of GFAP-positive area in the frontoparietal cortex were significantly increased in BCCAO. The generation of CSD was seen in regions of cortical gliosis induced by BCCAO, and severe energy exhaustion did not occur during or after CSD. Our results may suggest that the functional interaction of neurons and glia is sustained even in brain tissue where the metabolic state of neurons is impaired and astrocytes are proliferated.

[Functional neural reorganization following ischemic stroke in the precentral knob: an fMRI study].

We evaluated a 63 year-old, right-handed woman by functional MRI (fMRI) in the early and the recovery stages following a cerebral infarction in the right precentral knob. An activated signal in the ipsilateral sensorimotor cortex and contralateral supplementary motor cortex during deteriorated hand grasping (left) was observed in the early stages, whereas being unable to detect in the functionally recovered period. When simultaneous bilateral hand grasping was performed, the activated signal around infarct region was enlarged in recovered period. The functionally neural reorganization processes relating recovered hand movement after localized cortical infarction (precentral knob) was suggested.