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Biomedical subjects

Q H Hogan

Publications and source records attributed to Q H Hogan.

At least 19 recordsLinked to original sources

A supraomohyoidal plexus block designed to avoid complications.

Interscalene blocks of the brachial plexus are used for surgery of the shoulder and are frequently associated with complications such as temporary phrenic block, Horner syndrome or hematoma. To minimize the risk of these complications, we developed an approach that avoids medially directed needle advancement and favors spread to lateral regions only: the supraomohyoidal block. We tested this procedure in 11 cadavers fixed by Thiel's method. The insertion site is at the lateral margin of the sternocleidomastoid muscle at the level of the cricoid cartilage. The needle is inserted in the axis of the plexus with an angle of approximately 35 degrees to the skin, and advanced in lateral and caudal direction. Distribution of solution was determined in ten cadavers after bilateral injection of colored solution (20 and 30 ml) and followed by dissection. In an eleventh cadaver, computerized tomography and 3D reconstruction after radio contrast injection was performed. In additional five cadavers we performed Winnie's technique with bilateral injection (20 and 30 ml). Concerning the supraomohyoidal block the injection mass reached the infraclavicular region surrounded all trunks of the brachial plexus in the supraclavicular region and the suprascapular nerve in all cases. The solution did not spread medially beyond the lateral margin of the anterior scalene muscle into the scalenovertebral triangle. Therefore, phrenic nerve, stellate ganglion, laryngeal nerve nor the vertebral artery were exposed to the injected solution. Distribution was comparable with the use of 20 and 30 ml of solution. Injections on five cadavers performing the interscalene block of Winnie resulted in an extended spread medially to the anterior scalene muscle. We conclude that our method may be a preferred approach due to its safety, because no structures out of interest were reached. Solution of 20 ml is suggested to be enough for a successful block.

Brachial Plexus↗

The efficacy of epinephrine or vasopressin for resuscitation during epidural anesthesia.

Cardiopulmonary resuscitation (CPR) during epidural anesthesia is considered difficult because of diminished coronary perfusion pressure. The efficacy of epinephrine and vasopressin in this setting is unknown. Therefore, we designed this study to assess the effects of epinephrine versus vasopressin on coronary perfusion pressure in a porcine model with and without epidural anesthesia and subsequent cardiac arrest. Thirty minutes before induction of cardiac arrest, 16 pigs received epidural anesthesia with bupivacaine while another 12 pigs received only saline administration epidurally. After 1 min of untreated ventricular fibrillation, followed by 3 min of basic life-support CPR, Epidural Animals and Control Animals randomly received every 5 min either epinephrine (45, 45, and 200 microg/kg) or vasopressin (0.4, 0.4, and 0.8 U/kg). During basic life-support CPR, mean +/- SEM coronary perfusion pressure was significantly lower after epidural bupivacaine than after epidural saline (13 +/- 1 vs 24 +/- 2 mm Hg, P < 0.05). Ninety seconds after the first drug administration, epinephrine increased coronary perfusion pressure significantly less than vasopressin in control animals without epidural block (42 +/- 2 vs 57 +/- 5 mm Hg, P < 0.05), but comparably to vasopressin after epidural block (45 +/- 4 vs 48 +/- 6 mm Hg). Defibrillation was attempted after 18 min of CPR. After return of spontaneous circulation, bradycardia required treatment in animals receiving vasopressin, especially with epidural anesthesia. Systemic acidosis was increased in animals receiving epinephrine than vasopressin, regardless of presence or absence of epidural anesthesia. We conclude that vasopressin may be a more desirable vasopressor for resuscitation during epidural block because the response to a single dose is longer lasting, and acidosis after multiple doses is less severe compared with epinephrine.

Anesthesia, Epidural↗

Anesthetic effects on mitochondrial ATP-sensitive K channel.

BACKGROUND: Volatile anesthetics show an ischemic preconditioning-like cardioprotective effect, whereas intravenous anesthetics have cardioprotective effects for ischemic-reperfusion injury. Although recent evidence suggests that mitochondrial adenosine triphosphate-regulated potassium (mitoK(ATP)) channels are important in cardiac preconditioning, the effect of anesthetics on mitoK(ATP) is unexplored. Therefore, the authors tested the hypothesis that anesthetics act on the mitoK(ATP) channel and mitochondrial flavoprotein oxidation. METHODS: Myocardial cells were isolated from adult guinea pigs. Endogenous mitochondrial flavoprotein fluorescence, an indicator of mitochondrial flavoprotein oxidation, was monitored with fluorescence microscopy while myocytes were exposed individually for 15 min to isoflurane, sevoflurane, propofol, and pentobarbital. The authors further investigated the effect of 5-hydroxydeanoate, a specific mitoK(ATP) channel antagonist, on isoflurane- and sevoflurane-induced flavoprotein oxidation. Additionally, the effects of propofol and pentobarbital on isoflurane-induced flavoprotein oxidation were measured. RESULTS: Isoflurane and sevoflurane induced dose-dependent increases in flavoprotein oxidation (isoflurane: R2 = 0.71, n = 50; sevoflurane: R2 = 0.86, n = 20). The fluorescence increase produced by both isoflurane and sevoflurane was eliminated by 5-hydroxydeanoate. Although propofol and pentobarbital showed no significant effects on flavoprotein oxidation, they both dose-dependently inhibited isoflurane-induced flavoprotein oxidation. CONCLUSIONS: Inhalational anesthetics induce flavoprotein oxidation through opening of the mitoK(ATP) channel. This may be an important mechanism contributing to anesthetic-induced preconditioning. Cardioprotective effects of intravenous anesthetics may not be dependent on flavoprotein oxidation, but the administration of propofol or pentobarbital may potentially inhibit the cardioprotective effect of inhalational anesthetics.

ATP-Binding Cassette Transporters↗

Painful neuropathy decreases membrane calcium current in mammalian primary afferent neurons.

Hyperexcitability of the primary afferent neuron leads to neuropathic pain following injury to peripheral axons. Changes in calcium channel function of sensory neurons following injury have not been directly examined at the channel level, even though calcium is a primary second messenger-regulating neuronal function. We compared calcium currents (I(Ca)) in 101 acutely isolated dorsal root ganglion neurons from 31 rats with neuropathic pain following chronic constriction injury (CCI) of the sciatic nerve, to cells from 25 rats with normal sensory function following sham surgery. Cells projecting to the sciatic nerve were identified with a fluorescent label applied at the CCI site. Membrane function was determined using patch-clamp techniques in current clamp mode, and in voltage-clamp mode using solutions and conditions designed to isolate I(Ca). Somata of peripheral sensory neurons from hyperalgesic rats demonstrated decreased I(Ca). Peak calcium channel current density was diminished by injury from 3.06+/-0.30 pS/pF to 2. 22+/-0.26 pS/pF in medium neurons, and from 3.93+/-0.38 pS/pF to 2. 99+/-0.40 pS/pF in large neurons. Under these voltage and pharmacologic conditions, medium-sized neuropathic cells lacked obvious T-type calcium currents which were present in 25% of medium-sized cells from control animals. Altered Ca(2+) signalling in injured sensory neurons may contribute to hyperexcitability leading to neuropathic pain.

Action Potentials↗

Hypoxia causes apnea during epidural anesthesia in rabbits.

BACKGROUND: Although pulmonary function is minimally changed by neuraxial blockade in most cases, ventilatory arrest may ensue in rare cases. The authors examined the mechanism of apnea in a rabbit model of sudden ventilatory arrest during the combination of epidural anesthesia and hypoxia. METHODS: Rabbits were studied during alpha-chloralose sedation and spontaneous ventilation through a tracheostomy tube. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Respiratory rate and tidal volume were measured by pneumotachograph. Responses were recorded during administration of oxygen at inspired oxygen concentrations of 11% for 2.5 min and 0% for 40 s, before and after either thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1.5%) or intramuscular lidocaine (15 mg/kg). In a third group of animals, epinephrine was given intravenously during epidural blockade to return mean arterial pressure to baseline values before hypoxia. In a fourth group of animals, which did not get lidocaine, sympathetic blockade and hypotension were produced with intravenously administered trimethaphan rather than epidural blockade. RESULTS: Thoracolumbar epidural anesthesia decreased mean arterial pressure from 76 +/- 4 mmHg (mean +/- SE) to 42 +/- 2 mmHg. Apnea during hypoxia occurred in 90% of these animals (nine of ten) but in only 11% of animals (one of nine) after intramuscularly administered lidocaine (P < 0.01). Treatment of epidural hypotension with epinephrine prevented apnea (zero of nine animals). Apnea during hypoxia occurred in 50% (three of six) of animals given trimethaphan. Apnea in all groups was sudden in onset, with no preceding decreases in respiratory rate or tidal volume. CONCLUSIONS: Epidural anesthesia results in a narrowed margin of safety for oxygen delivery to the brain and predisposes subjects to ventilatory arrest during hypoxia. This results from the combined effects of decreased blood oxygen content, which is due to decreased inspired oxygen concentration superimposed on circulatory depression due to neural blockade.

Anesthesia, Epidural↗

Lumbosacral cerebrospinal fluid volume is the primary determinant of sensory block extent and duration during spinal anesthesia.

UNLABELLED: BACKGROUND. Injection of local anesthetic into cerebrospinal fluid (CSF) produces anesthesia of unpredictable extent and duration. Although many factors have been identified that affect the extent of spinal anesthesia, correlations are relatively poor and the extent of spread remains unpredictable. This study was designed to determine whether variability in the volume of lumbosacral CSF among individuals is a contributing factor in the variability of spinal anesthesia. METHODS: Spinal anesthesia was administered to 10 healthy volunteers with 50 mg lidocaine in 7.5% dextrose. The technique was standardized to minimize variability in factors known to affect the distribution of spinal anesthesia. The extent of sensory anesthesia was assessed by pin-prick and by transcutaneous electrical stimulation. Motor blockade was assessed in the quadriceps and gastrocnemius muscles by force dynamometry. Duration of anesthesia was assessed by pinprick, transcutaneous electrical stimulation, and duration of motor blockade. Lumbosacral CSF volumes were calculated from low thoracic, lumbar, and sacral axial magnetic resonance images obtained at 8-mm increments. Volumes of CSF were correlated with measures of extent and duration of spinal anesthesia using the Kendall rank correlation test. RESULTS: Lumbosacral CSF volumes ranged from 42.7 to 81.1 ml. Volumes of CSF correlated with pin-prick assessments of peak sensory block height (P = 0.02) and duration of surgical anesthesia (as assessed by the duration of tolerance to transcutaneous electrical stimulation at the ankle (P < 0.05). CONCLUSIONS: Variability in lumbosacral CSF volume is the most important factor identified to date that contributes to the variability in the spread of spinal sensory anesthesia.

Adult↗

Effects of desflurane, sevoflurane and halothane on postinfarction spontaneous dysrhythmias in dogs.

BACKGROUND: Although desflurane (DES) and sevoflurane (SEV) have desirable features for use in patients with coronary artery disease, their effects on ventricular dysrhythmias following infarction are less known. We therefore examined the effects of DES and SEV upon spontaneous postinfarction ventricular dysrhythmias in dogs, and compared those effects to the well-established antidysrhythmic effects of halothane (HAL) in this model. METHODS: After institutional approval, the left anterior descending coronary artery was ligated in 16 adult mongrel dogs during isoflurane anesthesia. All dogs developed acute myocardial infarction and severe ventricular tachydysrhythmias. Twenty-two hours after infarction, dogs were anesthetized at 1.5 MAC with desflurane (10.8%) followed by sevoflurane (3.5%) in the treatment group (n = 10), or halothane (1.3%) in the other group (n = 6). Anesthetic gases were allowed to equilibrate for at least 20 min at each end-tidal concentration. At this time, the ECG was recorded for 9 min and evaluated for the number of ventricular ectopic and sinoatrial beats and summed duration of ventricular tachycardia. RESULTS: DES and SEV reduced the average rate of total ventricular ectopic beats by 40 +/- 4% and 42 +/- 4%, respectively. HAL decreased total ventricular ectopic rate by 59 +/- 6% and 62 +/- 5% after durations of anesthesia comparable to DES and SEV, respectively. Decreases in dysrhythmia in the presence of DES and SEV were significantly smaller than those produced by HAL after a comparable total duration of anesthesia. CONCLUSION: DES and SEV inhibit spontaneous postinfarction ventricular dysrhythmias, although attenuation of dysrhythmias was smaller than the inhibition during comparable doses of HAL.

Anesthesia, Inhalation↗

Neural blockade for diagnosis and prognosis. A review.

On the basis of the published material reviewed above, we conclude that there are many limitations that weaken the theoretic basis for neural blockade as a diagnostic or prognostic tool. In addition, these procedures in general lack thorough documentation of clinical usefulness. Reasonable employment of diagnostic neural blockade, therefore, requires not only care in technique and confirmation of effects, but also caution in interpretation and application of the results. This critical evaluation needs to be tempered, however, by two further observations. Experienced and observant clinicians have found these procedures may, on certain occasions, provide information that is helpful in guiding subsequent therapy, so we should not be in haste to dismiss the accumulated judgment of practitioners. Finally, the confusion and complexity that typifies diagnosis in chronic pain may justify the selective use of diagnostic blocks that make anatomic and physiologic sense, even if their validity is incompletely proved.

Anesthetics, Local↗

Epinephrine dysrhythmogenicity is not enhanced by subtoxic bupivacaine in dogs.

Since bupivacaine and epinephrine may both precipitate dysrhythmias, circulating bupivacaine during regional anesthesia could potentiate dysrhythmogenic effects of epinephrine. We therefore examined whether bupivacaine alters the dysrhythmogenicity of subsequent administration of epinephrine in conscious, healthy dogs and in anesthetized dogs with myocardial infarction. Forty-one conscious dogs received 10 micrograms.kg-1.min-1 epinephrine. Seventeen animals responded with ventricular tachycardia (VT) within 3 min. After 3 h, these responders randomly received 1 or 2 mg/kg bupivacaine or saline over 5 min, followed by 10 micrograms.kg-1.min-1 epinephrine. In the bupivacaine groups, epinephrine caused fewer prodysrhythmic effects than without bupivacaine. VT appeared in fewer dogs and at a later time, and there were more sinoatrial beats and less ectopies. Epinephrine shortened QT less after bupivacaine than in control animals. One day after experimental myocardial infarction, six additional halothane-anesthetized dogs received 4 micrograms.kg-1.min-1 epinephrine until VT appeared. After 45 min, 1 mg/kg bupivacaine was injected over 5 min, again followed by 4 micrograms.kg-1.min-1 epinephrine. In these dogs, the prodysrhythmic response to epinephrine was also mitigated by preceding bupivacaine. Bupivacaine antagonizes epinephrine dysrhythmogenicity in conscious dogs susceptible to VT and in anesthetized dogs with spontaneous postinfarct dysrhythmias. There is no evidence that systemic subtoxic bupivacaine administration enhances the dysrhythmogenicity of subsequent epinephrine.

Anesthetics, Local↗

Magnetic resonance imaging of cerebrospinal fluid volume and the influence of body habitus and abdominal pressure.

BACKGROUND: Although the cerebrospinal fluid (CSF) is the pathway of anesthetic delivery and the diluent for neuraxially administered drugs, little is known about its volume, including variability among individuals, longitudinal distribution, or influence of body habitus. Models made to investigate subarachnoid anesthetic distribution lack valid dimensions. CSF volume was measured in volunteers, and the effect of obesity and abdominal compression on CSF volume was evaluated using magnetic resonance imaging. METHODS: Low thoracic and lumbosacral axial magnetic resonance images of 25 healthy volunteers were obtained at 8-mm intervals by fast spin-echo sequence, which highlights CSF. A repeat image series was performed in 15 subjects during external abdominal compression. In two subjects, images were obtained without compression for the entire vertebral column. Dural sac and spinal cord areas were determined in a blinded fashion for each image using video/digital analysis. Area of the sac minus area of the cord constituted area of CSF and roots ("CSF/root"); this area multiplied by 8 mm resulted in CSF/root volume per section. RESULTS: There is great interindividual variability in CSF/root volume. From the T11-T12 disc to the sacral terminus of the dural sac, the mean volume for all subjects is 49.9 +/- 12.1 ml (mean +/- SD; range 28.0-81.1 ml). This volume was significantly less in relatively obese subjects (42.9 +/- 9.5 ml) than in nonobese subjects (53.5 +/- 12.9 ml). Abdominal compression decreased CSF/root volume by 3.6 +/- 3.2 ml. Sections through intervertebral foramina showed the biggest decrease with abdominal compression, with a lesser change in sections with veins and no change in the absence of these anatomic features. Total vertebral CSF/root volume in two subjects was 94.84 and 120.01 ml, respectively. CONCLUSIONS: CSF volume is widely variable between individuals. The decreased CSF volume that results from increased abdominal pressure, such as with obesity or pregnancy, may produce more extensive neuraxial blockade through diminished dilution of anesthetic. The mechanism by which increased abdominal pressure decreases CSF volume is probably inward movement of soft tissue in the intervertebral foramen, which displaces CSF.

Abdomen↗

Sympathetic and mesenteric venous responses to baroreceptor or chemoreceptor stimulation during epidural anesthesia in rabbits.

BACKGROUND: Baroreceptor and chemoreceptor reflexes maintain homeostasis through mechanisms that involve sympathetic activation. Because sympathetic control of the mesenteric veins plays a central role in hemodynamic responses to stress, the effects of epidural blockade on reflex responses to hypoxia and bilateral carotid occlusion (BCO) were examined by monitoring direct measures of splanchnic sympathetic neural traffic and mesenteric venous capacitance. METHODS: Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric venous diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Intraluminal venous pressure was monitored by a servo-null micropressure technique. Responses were recorded during repeated administration of three different stresses, F1O2 = 0% for 40 s, F1O2 = 11% for 2.5 min, and BCO for 60 s. Animals received either thoracolumbar epidural blockade (0.4 ml/kg lidocaine 1.5%; n = 7) or 15 mg/kg intramuscular lidocaine (n = 7). RESULTS: Hypoxia and BCO produced sympathetic stimulation and active constriction of mesenteric veins. Epidural anesthesia accentuated the mean arterial pressure decrease from F1O2 of 0%, caused the 11% response to F1O2 to become depressor instead of pressor, and decreased the pressor effect BCO. Sympathetic efferent nerve activity and venous diameter responses to hypoxia and BCO were attenuated or eliminated. CONCLUSIONS: The hemodynamic effects of hypoxia result from a combination of direct depression and reflex activation. Thoracolumbar epidural anesthesia in rabbits impairs compensatory reflexes invoked by chemoreceptor stimulation and eliminates response to baroreceptor stimulation. Loss of splanchnic control of mesenteric capacitance contributes to the inhibition of the hemodynamic response to hypoxia or BCO during epidural anesthesia in rabbits.

Anesthesia, Epidural↗

Neural blockade for upper-extremity pain.

Carefully performed and interpreted neural blockade can be a useful adjunct in both the diagnosis and treatment of painful syndromes of the upper extremity. Pain is a very difficult entity to quantify and diagnose specifically because of its subjective nature, vast differences between patients and their response to pain, and largely because of our inexact understanding of its physiology. Best results of block therapy require thorough understanding of these complexities and limitations, and a rational, careful examination of the data it provides.

Arm↗

Hypoxic contraction of isolated rabbit mesenteric veins. Contribution of endothelium and attenuation by volatile anesthetics.

BACKGROUND: Acute systemic hypoxia induces mesenteric venoconstriction in intact rabbits in part because of an increase in chemoreflex-mediated sympathetic efferent nerve activity. Inhaled anesthetics attenuate this reflex response. The direct effects of hypoxia on mesenteric veins are unknown. The purpose of the current study was to examine the effects of hypoxia on isolated rabbit mesenteric capacitance veins and to determine the effects of halothane, isoflurane, and enflurane on the responses to hypoxia. METHODS: Isometric tension was measured before, during, and after 10 min of hypoxia in the rings of either quiescent or norepinephrine contracted veins, with or without endothelium. Effects of various pharmacologic agents and volatile anesthetics on the responses to hypoxia were examined. RESULTS: Hypoxia augmented contractions to norepinephrine and phenylephrine only in endothelium-intact veins. The hypoxic response was inhibited by phentolamine (alpha-adrenoceptor antagonist) and abolished in the absence of extracellular Ca2+. There were no effects of propranolol (beta-adrenoceptor antagonist), ryanodine (a sarcoplasmic reticulum Ca2+ depleter), indomethacin (cyclooxygenase inhibitor), or nordihydroguaiaretic acid (lipoxygenase inhibitor). L-NAME (an inhibitor of nitric oxide synthase) enhanced basal sensitivity of veins to norepinephrine but had no effect on the response to hypoxia. Nicardipine (a blocker of voltage-gated calcium channels) depressed the hypoxic contraction by 86 +/- 5%, phosphoramidon (an inhibitor of endothelin-converting enzyme) by 82 +/- 8%, and BQ-123 (a specific endothelin-1 receptor antagonist) by 47 +/- 10%. Volatile anesthetics (1.0 MAC) inhibited responses to hypoxia in the absence as well as presence of L-NAME. CONCLUSIONS: These results suggest that in mesenteric capacitance veins of rabbits an intrinsic vascular mechanism contributes to endothelium-dependent hypoxic augmentation of contraction to alpha-adrenergic agonists that involve activation of endothelin-1, an endothelium-derived constricting factor. Inhibition of hypoxic contraction by volatile anesthetics is not mediated by endothelium relaxing factor.

Acetylcholine↗

Region of epidural blockade determines sympathetic and mesenteric capacitance effects in rabbits.

BACKGROUND: The mechanisms producing hemodynamic changes during epidural anesthesia are incompletely understood. The role of capacitance changes in the splanchnic venous bed can be clarified by comparing blocks of differing segmental distributions. Specifically, we speculated that blocks that include the innervation to the mesenteric circulation alter hemodynamics, sympathetic activity, and venous capacitance to a greater extent than blocks without blockade of sympathetic nerves to this critical vascular bed. METHODS: Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric vein diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Responses were compared after administration of epidural lidocaine using a dose and catheter level that limited anesthetic to lumbar levels (lumbar group) or thoracic levels (thoracic group). In addition, hemodynamic responses were recorded after thoracolumbar block in animals receiving alpha-chloralose but breathing spontaneously (spontaneous ventilation group) and in awake animals (awake group). RESULTS: Mean arterial pressure decreased 38.3 +/- 5.8% in the thoracic group but only 16.5 +/- 2.8 in the lumbar group. Sympathetic efferent nerve activity decreased in the thoracic group but increased in the lumbar group. An increase in vein diameter followed thoracic epidural anesthesia, but venoconstriction was observed after lumbar epidural block. The addition of intravenous sedation with alpha-chloralose did not increase the hypotensive effect of epidural anesthesia in this model. CONCLUSIONS: Block of sympathetic fibers to the splanchnic circulation with thoracic epidural lidocaine produces mesenteric venodilatation that contributes to hypotension in rabbits. A lesser decrease in blood pressure follows blocks limited to lower segments, because baroreceptor stimulation produces increased splanchnic sympathetic activity and mesenteric venoconstriction. Responses in this model are comparable with and without general anesthesia and mechanical ventilation. To minimize hemodynamic consequences, epidural blockade should ideally be confined to the fewest necessary segments, avoiding splanchnic innervation if possible.

Anesthesia, Epidural↗

Effects of epidural anesthesia on splanchnic capacitance.

Splanchnic veins play an important role in the active control of total body circulatory capacitance. The effects of epidural anesthesia on splanchnic venous capacitance have not previously been examined. A rabbit model using direct measures of mesenteric vein diameter and sympathetic efferent nerve activity was used to test the response to epidural lidocaine at three different doses and to intramuscular lidocaine at two doses. Epidural anesthesia produced hypotension, mesenteric venodilatation, and interruption of sympathetic activity. Maximal changes of these parameters were comparable in the three epidural dosage groups but were more prolonged with increasing dose. High-dose systemic lidocaine caused smaller changes in arterial pressure and sympathetic activity. Further experiments were done to investigate the mechanism of splanchnic venodilatation. Passive vein distension and effects of circulating lidocaine or catecholamines are not likely contributing factors. Blocks limited to thoracic segments, but including the origin of splanchnic preganglionic fibers, produce comparable mesenteric venodilatation and sympathetic interruption as extensive thoracolumbar blocks. Blocks limited to lumbar segments, however, showed mesenteric venoconstriction and increased splanchnic sympathetic activity. The variable responses in splanchnic capacitance with the onset of epidural anesthesia are the result of the competing influences of increased sympathetic activity from decreasing blood pressure and blockade of sympathetic fibers to the splanchnic veins.

Anesthesia, Epidural↗

Mechanism of mesenteric venodilatation after epidural lidocaine in rabbits.

BACKGROUND: Increased splanchnic venous capacitance has been observed during extensive thoracolumbar epidural anesthesia in rabbits, but the mechanism is not clear. The present study examines the contributions of intravascular pressure changes, catecholamine levels, neural input, and direct effects of lidocaine to mesenteric venodilatation. METHODS: Epidural catheters were inserted in rabbits anesthetized with alpha-chloralose. Vein diameter was measured by videomicrography from segments of ileum externalized in situ. Plasma epinephrine and norepinephrine levels were measured in animals receiving epidural blockade (0.4 ml/kg lidocaine 1.5%, n = 5) and in control animals given intramuscular lidocaine 15 mg/kg (n = 5). Intraluminal pressure was monitored during the onset of epidural anesthesia (0.4 ml/kg lidocaine 1.0%, n = 9) by a servo-null micropressure technique. The effect of inhibiting norepinephrine release from sympathetic nerves in the mesenteric veins was determined by using topical tetrodotoxin (n = 8) and by assessing the effect of topical lidocaine (10 and 100 micrograms/ml, n = 5) administered in the solution bathing the mesentery. RESULTS: Epidural injectate extended from T2 to L5. Plasma epinephrine decreased 68.3 +/- 4.4% (mean +/- SEM) with epidural anesthesia, and norepinephrine was lower after epidural block than after intramuscular lidocaine (1,868 +/- 290 pg/ml vs. 3,049 +/- 712 pg/ml). Mesenteric vein pressure decreased 35.3 +/- 3.5% and vein diameter increased 10.2 +/- 3.3% during epidural blockade. Tetrodotoxin caused mesenteric venodilatation (7.6 +/- 2.0%) and prevented venodilatation by subsequent epidural lidocaine. Topical lidocaine 10 micrograms/kg produced no change in vein diameter, but lidocaine 100 micrograms/ml increased it 3.5 +/- 1.3%. CONCLUSIONS: Splanchnic venodilatation during epidural anesthesia is an active process: a decrease in intravenous pressure concurrent with dilatation indicates that vein wall tension diminished. Significant dilatation with tetrodotoxin and lack of dilatation with subsequent epidural block point to a minor role for changes in circulating catecholamines. A direct effect of lidocaine does not contribute to splanchnic venodilatation except when circulating lidocaine concentrations reach very high levels.

Administration, Topical↗

Success rates in producing sympathetic blockade by paratracheal injection.

OBJECTIVE: Cervical paratracheal local anesthetic injections (stellate ganglion blocks) are performed to determine the sympathetic contribution to painful and other conditions of the head, neck, and arm. A block is useful for diagnosis only if the desired physiological effect is confirmed, but the frequency with which sympathetic function is successfully blocked is unclear. The goal of this study is to examine the rates of achieving various endpoints of sympathetic interruption by these injections, using commonly available measures of sympathetic change. DESIGN: Retrospective review. SETTING: Training center. PATIENTS: One hundred unselected consecutive blocks in 40 patients. INTERVENTION: Paratracheal sympathetic block at sixth cervical level. OUTCOME MEASURES: Bilateral hand temperature, ophthalmic changes. RESULTS: Horner's syndrome was successfully produced in 84 blocks and the ipsilateral hand warmed by > or = 1.5 degrees C in 60 blocks. However, the contralateral hand also warmed in 31 blocks so that ipsilateral warming exceeded contralateral warming in only 27 blocks, with diminished success by this criterion when the hand was warm before the block. CONCLUSIONS: We conclude that (a) identifying a Horner's syndrome and ipsilateral warming are not by themselves adequate to confirm selective sympathetic blockade; (b) selective sympathetic blockade of the arm is confirmed only if the temperature increase of the blocked side exceeds that of the contralateral side; and (c) cervical paratracheal blocks frequently fail to produce evidence of sympathetic interruption to the arm. Pathophysiological inferences based on these blocks should be made with caution and only with adequate documentation of physiological evidence of sympathetic blockade.

Anesthesia, Local↗