Current guidelines for the care of patients with acute spinal cord injuries (SCIs) recommend maintaining mean arterial pressure (MAP) values of 85-90 mm Hg for 7 days after an acute SCI however, little evidence supports this recommendation. We sought to better inform the relationship between MAP values and neurological recovery. A computer system automatically collected and stored q1 min physiological data from intensive care unit monitors on patients with SCI over a 6-year period. Data for 100 patients with acute SCI were collected. 74 of these patients had American Spinal Injury Association Impairment Scale (AIS) grades determined by physical examination on admission and at time of hospital discharge. Average MAP values as well as the proportion of MAP values below thresholds were explored for values from 120 mm Hg to 40 mm Hg in 1 mm Hg increments; the relationship between these measures and outcome was explored at various time points up to 30 days from the time of injury. A total of 994,875 q1 min arterial line blood pressure measurements were recorded for the included patients amid 1,688,194 min of recorded intensive care observations. A large proportion of measures were below 85 mm Hg despite generally acceptable average MAP values. Higher average MAP values correlated with improved recovery in the first 2-3 days after SCI while the proportion of MAP values below the accepted threshold of 85 mm Hg seemed a stronger correlate, decreasing in strength over the first 5-7 days after injury. This study provides strong evidence supporting a correlation between MAP values and neurological recovery. It does not, however, provide evidence of a causal relationship. Duration of hypotension may be more important than average MAP. It provides support for the notion of MAP thresholds in SCI recovery, and the highest MAP values correlated with the greatest degree of neurological recovery. The results are concordant with current guidelines in suggesting that MAP thresholds >85 mm Hg may be appropriate after acute SCI.

Electrical stimulation affects the deposition of extracellular matrices and cellular differentiation. Type I collagen is one of the most abundant extracellular matrix proteins; however, not much is known about the effects of electrical stimulation on collagen type I deposition in C2C12 cells. Thus, we studied the effects of electrical voltage and stimulation frequency in 3D cultured C2C12 muscle cells in terms of metabolic activity, type I collagen deposition and cell morphology. Electrically excitable C2C12 muscle cells were seeded in collagen scaffolds and stimulated with rectangular signals of voltage (2, 5, 7 V) and frequency (1, 2 Hz), using parallel carbon electrodes spaced 1 cm apart. Metabolic activity was quantified by the glucose: lactate concentration ratio in the medium. Apoptotic activity was assessed by TUNEL staining and changes in collagen deposition were identified by immunohistology. The ultrastructure of the tissue was examined by TEM. Glucose and lactate analysis indicated that all groups had similar metabolic activity. TUNEL stain showed no significant difference in apoptotic damage induced by electrical stimulation compared to the control. Samples stimulated at 2 Hz exhibited reduced collagen deposition compared to the control and 1 Hz stimulated samples. Muscle-protein marker desmin was highly expressed in constructs stimulated with 1 Hz/5 V sample. TEM revealed that the stimulated samples developed highly organized sarcomeres, which coincided with improved contractile properties in the 1 Hz/5 V-and 2 Hz/5 Vstimulated groups. Our data implicate that a specific electrical frequency may modulate type I collagen accumulation and a specific voltage may affect the differentiation of muscle sarcomeres in excitable cells.

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