Woodrow W. Wendling

The use of somatosensory evoked potentials to determine the relationship between patient positioning and impending upper extremity nerve injury during spine surgery: a retrospective analysis.

Somatosensory evoked potential (SSEP) monitoring is used to prevent nerve damage in spine surgery and to detect changes in upper extremity nerve function. Upper extremity SSEP conduction changes may indicate impending nerve injury. We investigated the effect of operative positioning on upper extremity nerve function retrospectively in 1000 consecutive spine surgeries that used SSEP monitoring. The vast majority (92%) of upper extremity SSEP changes were reversed by modifying the arm position and were therefore classified as position-related. The incidence of position-related upper extremity SSEP changes was calculated and compared for five different surgical positions: supine arms out, supine arms tucked, lateral decubitus position, prone arms tucked, and the prone “superman” position. The overall incidence of position-related upper extremity SSEP changes was 6.1%. The lateral decubitus position (7.5%) and prone superman position (7.0%) had a significantly more frequent incidence of position-related upper extremity SSEP changes (P < 0.0001, Z-test for Poisson counts) compared with other positions (1.8%–3.2%). No patient with a reversible SSEP change developed a new postoperative deficit in the affected extremity. SSEP monitoring is of value in identifying and reversing impending upper extremity peripheral nerve injury.

Methylmethacrylate monomer produces direct relaxation of vascular smooth muscle in vitro

Methylmethacrylate bone cement is associated with severe hypotensive reactions during surgery and anesthesia. The purpose of this in vitro study was to determine if methylmethacrylate monomer could produce hypotension by acting directly on vascular smooth muscle.

The effects of N-methyl-D-aspartate agonists and antagonists on isolated bovine cerebral arteries

This pharmacologic study examines the direct cerebrovascular effects of N-methyl-D-aspartate (NMDA) receptor agonists and antagonists to determine whether large cerebral arteries have NMDA receptors. Bovine middle cerebral arteries were cut into rings to measure isometric tension development in vitro. Two competitive agonists, L-glutamate and NMDA, each had negligible effects on ring tension in the absence of exogenous vasoconstrictors. L-glutamate (in high concentrations) produced direct relaxation of potassium (K+)-constricted arteries, but the relaxation was not selective for L-glutamate, D-glutamate, or mannitol. Relaxation with L-glutamate was abolished when it was isosmotically substituted in the K+-rich medium. NMDA (in the absence or presence of glycine) and two competitive antagonists, 2-amino-5-phosphopentanoic acid (AP5) and (+/-)-3-(s-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), each had little effect on the tone of arteries preconstricted with potassium or the stable thromboxane A2 analog U-46,619. Three noncompetitive antagonists (S(+)-ketamine, dizocilpine, and dextrorphan) and their stereoisomers (R(-)-ketamine, (-)MK-801, and levorphanol) each produced dose-dependent relaxation of K+- or U-46,619-constricted arteries; relaxation was not selective for the (+) or (-) stereoisomers. These results suggest that large cerebral arteries lack NMDA receptors mediating constriction or relaxation. All noncompetitive antagonists dilated cerebral arteries, but by mechanisms that were not stereospecific. (Anesth Analg 1996;82:264-8)

Ketamine directly dilates bovine cerebral arteries by acting as a calcium entry blocker.

This in vitro study was performed to determine the role of calcium in ketamine-induced cerebral vasodilation. Isolated bovine middle cerebral arteries were cut into rings to measure isometric tension development or into strips to measure radioactive 45Calcium (45Ca) uptake. Ketamine produced direct relaxation of arterial rings; the relaxation was attenuated in Ca(2+)-deficient media. Ketamine produced dose-related relaxation of arteries preconstricted with potassium, a stable thromboxane A2 analogue, or endothelin. Endothelial stripping with Triton X-100 had no effect on subsequent ketamine-induced relaxation. In Ca(2+)-deficient media containing potassium or the stable thromboxane A2 analogue, ketamine produced competitive inhibition of subsequent Ca(2+)-induced constriction. Ketamine blocked potassium- and thromboxane A2-stimulated 45Ca uptake in a dose-dependent manner, but had no effect on basal 45Ca uptake, the externally bound 45Ca content, or the volume of the 3H-sorbitol space. These results indicate that ketamine can directly dilate cerebral arteries by acting as a calcium channel antagonist; ketamine inhibits 45Ca uptake through both potential-operated (potassium) and receptor-operated (thromboxane A2) channels in cerebrovascular smooth muscle.

Effects of calcium antagonists on isolated bovine cerebral arteries: inhibition of constriction and calcium-45 uptake induced by potassium or serotonin.

The purpose of this study was to determine the mechanisms by which organic calcium channel blockers inhibit cerebral vasoconstriction. Isolated bovine middle cerebral arteries were cut into rings to measure contractility or into strips to measure radioactive calcium (45Ca) influx and efflux. Calcium channel blockers (10(-5) M verapamil or 3.3 X 10(-7) M nifedipine) and calcium-deficient solutions all produced near-maximal inhibition of both potassium- and serotonin-induced constriction. In calcium-deficient solutions containing potassium or serotonin, verapamil and nifedipine each blocked subsequent calcium-induced constriction in a competitive manner. Potassium and serotonin significantly increased 45Ca uptake into cerebral artery strips during 5 minutes of 45Ca loading; for potassium 45Ca uptake increased from 62 to 188 nmol/g, and for serotonin from 65 to 102 nmol/g. Verapamil or nifedipine had no effect on basal 45Ca uptake but significantly blocked the increase in 45Ca uptake induced by potassium or serotonin. Potassium, and to a lesser extent serotonin, each induced a brief increase in the rate of 45Ca efflux into calcium-deficient solutions. Verapamil or nifedipine had no effect on basal or potassium-stimulated 45Ca efflux. The results demonstrate that verapamil and nifedipine block 45Ca uptake through both potential-operated (potassium) and receptor-operated (serotonin) channels in bovine middle cerebral arteries.

N-methyl-D-aspartate (NMDA) antagonists--S(+)-ketamine, dextrorphan, and dextromethorphan--act as calcium antagonists on bovine cerebral arteries.

Ketamine, an intravenous anesthetic and a major drug of abuse, is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist. Ketamines enantiomer, S(+)-ketamine, acts stereoselectively on neuronal NMDA receptors. The purpose of this in vitro study was to compare the direct effects of S(+)-ketamine, 2 other noncompetitive NMDA receptor antagonists (dextrorphan and dextromethorphan), and the calcium entry blocker nimodipine on the cerebral vasculature, using bovine middle cerebral arteries as an experimental model. Arterial rings were mounted in isolated tissue chambers equipped with isometric tension transducers to obtain pharmacologic dose-response curves. In the absence of exogenous vasoconstrictors, the NMDA antagonists or nimodipine had negligible effects on cerebral arterial tone. When rings were preconstricted with either potassium or the stable thromboxane A2 mimetic U46619, the NMDA antagonists and nimodipine each produced dose-dependent relaxation. Prior endothelial stripping had no effect on subsequent drug-induced relaxation of K+-constricted rings. In Ca2+-deficient media containing either potassium or U46619, the NMDA antagonists and nimodipine each produced competitive inhibition of subsequent Ca2+induced constriction. In additional experiments, arterial strips were mounted in isolated tissue chambers to directly measure calcium uptake, using 45calcium (45Ca) as a radioactive tracer. The NMDA antagonists and nimodipine each blocked potassium-stimulated or U46619-stimulated 45Ca uptake into arterial strips. These results indicate that S(+)-ketamine, dextrorphan, and dextromethorphan, like nimodipine, directly dilate cerebral arteries by acting as calcium antagonists; they all inhibit 45Ca uptake through both potential-operated (potassium) and receptor-operated (U46619) channels in cerebrovascular smooth muscle.

Vascular effects of etomidate administered for electroencephalographic burst suppression in humans.

Although its status as a neuroprotectant is controversial, etomidate is often employed for pharmacologic cerebral protection in aneurysm surgery. One purported advantage of etomidate over thiopental is its hemodynamic stability. This study examined the cardiovascular effects of etomidate given for electroencephalographic (EEG) burst suppression during cerebral aneurysm clipping in humans and the direct effects of etomidate on arteries in vitro. The charts of intracranial aneurysm surgery patients were retrospectively reviewed to determine the dose of etomidate employed, the frequency of concurrent vaspressor administration, and whether hemodynamic changes were associated with etomidate use. Against a background of balanced anesthesia, the dose of etomidate to induce burst suppression was 0.73 +/- 0.49 mg/kg (mean +/- SD) and the maintenance dose was 48 +/- 30 microg/kg/min. Etomidate produced an immediate decrease in mean arterial pressure that was sustained in patients who did not receive vasopressor support. During etomidate administration, 48% of patients (10 of 21) received some form of vasopressor support such as phenylephrine or ephedrine, and 62% of patients (13 of 21) receiving isoflurane had the anesthetic discontinued or its inspired concentration decreased. Etomidate in vitro produced dose-dependent relaxation of human internal mammary arterial rings that had been preconstricted by potassium or norepinephrine. Etomidate, in EEG burst suppression doses, decreases mean arterial pressure in anesthetized patients undergoing cerebral aneurysm surgery. One mechanism of etomidate-induced hypotension may be direct relaxation of vascular smooth muscle, because etomidate directly dilates preconstricted human arteries in vitro.

Intravenous vitamin K1 prior to orthotopic heart transplantation : effects in vivo and in vitro

Background: Vitamin Kj is used to reverse warfarins anticoagulant action. It is unclear whether intravenous vitamin K1 is safe or efficacious prior to urgent cardiac surgery.