Effects of thoracic aortic occlusion and cerebrospinal fluid drainage on regional spinal cord blood flow in dogs: Correlation with neurologic outcome

Background alpha2-Adrenergic agonists produce analgesia primarily by a spinal action and hypotension and bradycardia by actions at several sites. Clonidine is approved for epidural use in the treatment of neuropathic pain, but its wider application is limited by hemodynamic side effects. This study determined the antinociceptive and hemodynamic effects of a novel alpha2-adrenergic agonist, MPV-2426, in sheep. Methods Forty sheep of mixed Western breeds with indwelling catheters were studied. In separate studies, antinociception to a mechanical stimulus, hemodynamic effects, arterial blood gas tensions, cerebrospinal fluid pharmacokinetics, and spinal cord blood flow was determined after epidural, intrathecal, and intravenous injection of MPV-2426. Results MPV-2426 produced antinociception with greater potency intrathecally (ED50 = 49 microg) than epidurally (ED50 = 202 microg), whereas intravenous administration had no effect. Intrathecal injection, in doses up to three times the ED95, failed to decrease systemic or central arterial blood pressures or heart rate, whereas larger doses, regardless of route, increased systemic arterial pressure. Bioavailability in cerebrospinal fluid was 7% after epidural administration and 0.17% after intravenous administration. Intrathecal MPV-2426, in an ED95 dose and three times this dose, produced a dose-independent reduction in thoracic and lumbar spinal cord blood flow. Conclusions MPV-2426 shares many characteristics of other alpha2-adrenergic agonists examined in sheep, but differs from clonidine and dexmedetomidine by lack of antinociception and minimal reduction in oxygen partial pressure after large intravenous and epidural injections. No hemodynamic depression was observed after intrathecal injection at antinociceptive doses. These results suggest this compound may be an effective spinal analgesic in humans with less hypotension than clonidine, although its relative potency to cause sedation was not tested in this study.

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Lumbar Drain

Mayo Clinic Critical and Neurocritical Care Board Review ◽

10.1093/med/9780190862923.003.0127 ◽

2019 ◽

pp. 907-911

Author(s):

Jamie J. Van Gompel

Keyword(s):

Spinal Cord ◽

Blood Flow ◽

Cerebrospinal Fluid ◽

Subarachnoid Hemorrhage ◽

Cord Blood ◽

Low Risk ◽

Communicating Hydrocephalus ◽

Spinal Cord Blood Flow ◽

Lumbar Drain ◽

Csf Leaks

Lumbar drainage has a major role in neurosurgical and neurocritical care procedures. Lumbar drain insertion is a simple and, when done well, low-risk procedure. A lumbar drain is often necessary in the management of perioperative cerebrospinal fluid (CSF) leaks, the most common use, but it may be beneficial for patients with subarachnoid hemorrhage and communicating hydrocephalus and for patients undergoing surgery involving the aorta with possible damage to the spinal cord. CSF removal optimizes spinal cord blood flow. This chapter describes lumbar drain insertion and some of the associated perils and pitfalls.

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Effects of Aortic Occlusion on Regional Spinal Cord Blood Flow and Somatosensory Evoked Potentials in Sheep

Neurosurgery ◽

10.1227/00006123-198711000-00012 ◽

1987 ◽

Vol 21 (5) ◽

pp. 668-675 ◽

Cited By ~ 11

Author(s):

Barry J. Kaplan ◽

William A. Friedman ◽

Nikolaus Gravenstein ◽

Rhonda Richards ◽

Richard F. Davis

Keyword(s):

Spinal Cord ◽

Blood Flow ◽

Evoked Potentials ◽

Cord Blood ◽

Somatosensory Evoked Potentials ◽

Aortic Occlusion ◽

Spinal Cord Blood Flow

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Transient Spinal Ischemia in Rat: Characterization of Spinal Cord Blood Flow, Extracellular Amino Acid Release, and Concurrent Histopathological Damage

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1994.75 ◽

1994 ◽

Vol 14 (4) ◽

pp. 604-614 ◽

Cited By ~ 75

Author(s):

Martin Marsala ◽

Linda S. Sorkin ◽

Tony L. Yaksh

Keyword(s):

Amino Acids ◽

Spinal Cord ◽

Blood Flow ◽

Cardiac Arrest ◽

Cord Blood ◽

Aortic Occlusion ◽

Spinal Ischemia ◽

Spinal Cord Blood Flow ◽

Glutamate Concentration ◽

Reperfusion Period

Extracellular concentrations of amino acids in halothane-anesthetized rats were measured using a microdialysis fiber inserted transversely through the dorsal spinal cord at the level of the lumbar enlargement in conjunction with HPLC and ultraviolet detection. After a 2-h washout and a 1-h control period, 20 min of reversible spinal cord ischemia was achieved by the inflation of a Fogarty F2 catheter passed through the femoral artery to the descending thoracic aorta. After 2 h of postischemic reperfusion, animals were transcardially perfused with saline followed by 10% formalin or 4% paraformaldehyde. The glutamate concentration in the dialysate was significantly elevated after 10 min of occlusion and returned to near-baseline during the first 30 min of reperfusion. Taurine was elevated significantly 0.5 h postocclusion and continued to increase throughout the 2 h of reperfusion. Glycine concentrations showed a tendency to be slightly above baseline during the reperfusion period. Glutamine concentrations modestly increased following 2 h of reperfusion. No significant changes in aspartate, asparagine, and serine were detected. In control animals no significant changes in any amino acids were detected. To assess the role of complete spinal ischemia on spinal glutamate release, studies were carried out using cardiac arrest. Twenty minutes after induction of cardiac arrest, the glutamate concentration was increased about 350–400%. In a separate group of animals, spinal cord blood flow (SCBF) and its response to decreased CO2 were measured using a laser probe implanted into the epidural space at the level of the L2 vertebral segment. SCBF decreased to 5–6% of the control during aortic occlusion. After reversible ischemia, marked hyperemia was seen for the first 15 min, followed by hypoperfusion at 60 min. Under control–preischemic conditions a decrease in arterial CO2 content caused a decrease in SCBF of about 25%. This autoregulatory response was almost completely absent when assessed 60 min after a 20-min interval of aortic occlusion. Histopathological analysis of spinal cord tissue from these animals demonstrated heavy neuronal argyrophilia affecting small and medium-sized neurons located predominantly in laminae III–V. These changes corresponded to signs of irreversible damage at the ultrastructural level. Occasionally, small areas of focal necrosis, located in the dorsolateral part of the dorsal horn and anterolateral part of the ventral horn, were found. The results are consistent with a role for glutamate in ischemically induced spinal cord damage and suggest that taurine elevation detected during the early reperfusion period may serve as an important indicator of irreversible spinal cord neuronal damage.

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