Methylprednisolone in Spinal Cord Compression

Acute Changes in Systemic Hemodynamics and Serum Vasopressin After Complete Cervical Spinal Cord Injury in Piglets

“…Our main findings were that complete cervical SCI caused an immediate tachycardia which lasted for approximately 1 h, immediate hypotension which was sustained for the 4-h duration of the study, decreases in both systemic and pulmonary vascular resistance, and a compensatory increase in cardiac output, which resulted initially from an increase in HR but was later sustained after resolution of tachycardia by an increase in cardiac stroke volume. These data are consistent with previously published findings in adult small and large animal models as well as in humans, which consistently demonstrate reductions in HR, MAP, and systemic vascular resistance over the first few hours and in clinical studies for up to 2 weeks after SCI [3][4][5][6][7][8][9][17][18][19][20][21][22][23]. Levi et al invasively measured hemodynamics beginning 11 ± 6 h after complete and incomplete cervical SCI in adults and found that 82% required vasopressors for an average of 5.7 days after injury to maintain MAP >90 mmHg [8].…”

“…This injury mechanism differs from classical traumatic SCI in that blood flow falls to near zero during compression and is followed by hyperemia, suggestive more of an ischemic mechanism, whereas after traumatic contusional SCI hyperemia does not occur. In addition, balloon compression SCI does not cause acute physical disruption of longitudinal tracts in the spinal cord, although electrophysiological function of the dorsal columns is lost as evidenced by sensory-evoked potentials, which were absent during and for 3 h after compression in lambs [22,23]. Despite differences in mechanism and site of SCI, these investigators also demonstrated an immediate decrease in MAP (111 ± 2 at baseline to 87 ± 2 30 min post SCI) which was sustained for the 2.5-h monitoring period.…”

“…* P < 0.05 for comparisons to baseline; # P < 0.05 for comparisons between groups much of which can be attributed to differences in anesthesia, characteristics of the SCI (level, severity, and mechanism) as well as species [25][26][27][28]. Studies employing anesthetics with cardiac depressant and vasodilatory effects, such as pentobarbital, halothane, and ether have reported lower cardiac output and blood pressure after SCI [22,23,25] compared to those using ketamine or chloralose [20,29]. The relatively mild hypotension seen in our study did not require treatment and may have been due, in part, to the use of fentanyl as the main anesthetic, which is devoid of effects on cardiac contractility and systemic vascular resistance [30].…”

“…Although our study is the first to examine hemodynamics after cervical SCI in an immature animal, Hitchon et al have performed a series of experiments in 3-monthold lambs weighing 20 ± 5 kg (approximately 1/3 of mature adult weight) in which they measured systemic hemodynamics and spinal cord blood flow following lower thoracic (T13) compressional SCI induced by inflating an epidural balloon for 40 (incomplete) or 80 (complete) min [22,23]. This injury mechanism differs from classical traumatic SCI in that blood flow falls to near zero during compression and is followed by hyperemia, suggestive more of an ischemic mechanism, whereas after traumatic contusional SCI hyperemia does not occur.…”

“…Experimental studies of the acute hemodynamic effects of SCI have been performed primarily in adult animal models [17][18][19][20][21][22][23]. These studies have demonstrated an immediate increase in blood pressure, heart rate (HR), and cardiac output usually lasting for 5-15 min, followed by prolonged periods of hypotension, bradycardia, escape rhythms, and variable changes in cardiac output.…”