Louie Wang

Intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension.

Sympathetic hyperactivity during sudden intracranial hypertension leads to cardiovascular instability, myocardial dysfunction, and neurogenic pulmonary edema. Because spinal anesthesia is associated with sympatholysis, we investigated the protective effects of intrathecal lidocaine in a rodent model. Halothane-anesthetized rats were given a 10-&mgr;L intrathecal injection of saline (n = 10) or lidocaine 1% (n = 6). A subdural balloon catheter was inflated for 60 s to produce intracranial hypertension. Hemodynamics were monitored, and hearts and lungs were harvested for histological examination. In Saline versus Lidocaine-Treated rats, peak mean arterial blood pressure during balloon inflation was 115 ± 4 mm Hg versus 78 ± 8 mm Hg (P < 0.05), mean arterial blood pressure 30 min after balloon deflation was 47 ± 2 mm Hg versus 67 ± 3 mm Hg (P < 0.05), and lung weight was 1.54 ± 0.03 g versus 1.41 ± 0.04 g (P < 0.05), respectively. Cardiac dysrhythmias and electrocardiographic changes were more frequent in the Saline-Treated group (P < 0.05). Saline-Treated rats had extensive, hemorrhagic pulmonary edema, whereas the Lidocaine-Treated rats had only patchy areas of lung abnormality. Histological changes in the myocardium were rare, and no difference was found between the two groups. We conclude that intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension.

A demand-based assessment of the Canadian anesthesia workforce — 2002 through 2007

PurposeThe number of anesthesia providers required by the Canadian health care system remains controversial. Questions persist regarding both the adequacy of the current supply and what the future demand will be. The purpose of this study was to quantify the number and adequacy of anesthesia providers in 2002, and predict the same for the year 2007.MethodsAll licensed health care facilities potentially employing anesthetic services were identified. On February 1st, 2002 a questionnaire was mailed to each institution. On April 1st, a second mailing was sent to non-responders. Those facilities that did not respond to either mailing were contacted by telephone.ResultsResponses were obtained from 831 of 891 (93%) health care facilities. Four hundred and twenty-six of the facilities employed anesthetic services. There were 1,610 operating rooms (ORs) in use daily and 2,134 full-time equivalent (FTE) anesthesia providers were available to the institutions surveyed. Respondents identified an immediate need for 228 additional FTEs. Hospitals with less than five ORs or five FTEs reported higher vacancy rates than hospitals with greaterthan five ORs orfive FTEs (P < 0.0001). Ontario (n = 85) and Quebec (n = 69) had the largest absolute deficits of FTEs and significantly greater odds of vacancies than western provinces (Ontario OR = 1.84, Quebec OR = 2.50). The projected need for 2007 was an additional 560 FTEs.ConclusionThis is the first study to survey a national census of “consumers” of anesthetic services: Canadian health care facilities. The results indicate substantial current and worsening future shortages of anesthesia providers in Canada.RésuméObjectifLe nombre de prestateurs d’anesthésie réclamé par le système de soins de santé du Canada demeure controversé. Des questions subsistent sur le nombre suffisant des effectifs actuels et la demande dans l’avenir. Nous avons voulu quantifier le nombre et la capacité des prestateurs d’anesthésie en 2002 et prédire ces mêmes données pour 2007.MéthodeTous les établissements de santé autorisés à offrir des services anesthésiques ont été recensés. Le premier février 2002, un questionnaire a été posté à chaque institution. Le premier avril, un second envoi a été fait aux non-répondants. Ceux qui n’ont répondu à aucun questionnaire ont été joints par téléphone.RésultatsNous avons obtenu des réponses de 831 sur 891 (93%) établissements de santé. Des services d’anesthésie étaient offerts dans 426 centres. Il y avait 1 610 salles d’opération (SO) utilisées chaque jour et l’équivalent à temps plein (ETP) de 2 134 prestateurs d’anesthésie disponibles pour les institutions sondées. Les répondants ont déterminé un besoin immédiat de 228 ETP supplémentaires. Les hôpitaux de moins de cinq SO ou cinq ETP avaient des taux plus élevés d’inoccupation que les hôpitaux de plus de cinq SO ou cinq ETP (P < 0,0001). L’Ontario (n = 85) et le Québec (n = 69) avaient les déficits absolus les plus importants d’ETP et des risques d’inoccupation plus signifcativement élevés que les provinces de l’Ouest (Ontario SO = 1,84, Québec SO = 2,50). Les besoins projetés pour 2007 étaient l’ETP supplémentaire de 560.ConclusionC’est le premier recensement national des «consommateurs» de services d’anesthésie: les établissements de santé du Canada. Il indique des pénuries actuelles substantielles de prestateurs d’anesthésie au Canada qui vont s’aggraver dans l’avenir.

Involvement of excitatory amino acid pathways in the expression of precipitated opioid withdrawal in the rostral ventrolateral medulla: an in vivo voltammetric study

Previous studies have shown that catecholaminergic neurons in the rostral ventrolateral medulla (RVLM) become hyperactive during opioid withdrawal. In the present study, the role of excitatory amino acid pathways in the expression of opioid withdrawal in the RVLM was examined by using differential pulse voltammetry (DNPV) to measure changes in the catecholamine oxidation current (CA.OC) following naloxone challenge in rats treated with acute or chronic morphine. Acute morphine (10 micrograms i.c.v.) significantly reduced the CA.OC signal in the RVLM and the mean arterial pressure to 37.1 +/- 6.6% and 21.1 +/- 3.5% below baseline, respectively. Naloxone (1 mg kg-1 i.v.) reversed the morphine effect and produced a significant increase in the CA.OC signal to 25.6 +/- 15.2% above baseline. In animals treated with chronic morphine (10 micrograms h-1 i.c.v., 5 days), naloxone (1 mg kg-1 i.v.) produced a significant increase in the CA.OC signal to 54.2 +/- 16.5% above baseline. Both the nonselective excitatory amino acid antagonist, gamma-D-glutamylglycine (DGG, 200 micrograms i.c.v.) and the selective NMDA antagonist, D(-)-amino-7-phosphonoheptanoic acid (D-APH, 25 micrograms i.c.v.) attenuated the naloxone-induced increase in the CA.OC by 50.7% and 46.0% respectively. In morphine naive animals, DGG and D-APH depressed the CA.OC by 42.8 +/- 8.7% and 17.7 +/- 9.8%, respectively. To the extent that the CA.OC is an index of neuronal activity, these results suggest that RVLM hyperactivity during morphine withdrawal is dependent, in part, upon activation of NMDA receptors.

Central dexmedetomidine attenuates cardiac dysfunction in a rodent model of intracranial hypertension

PurposeTo determine if central sympathetic blockade by dexmedetomidine, a selective alpha2 adrenergic receptor agonist, prevents cardiac dysfunction associated with intracranial hypertension (ICH) in a rat model.MethodsFollowing intracisternal administration of dexmedetomidine (1 μg · μl−1, 10 μL volume) or the stereoisomer levomedetomidine (1 μg· μL−1, 10 μL volume) in halothane-anesthetized rats, a subdural balloon catheter was inflated for 60 sec to produce ICH. Intracranial pressure, hemodynamic, left ventricular (LV) pressures and electrocardiographic (ECG) changes were recorded. Plasma and myocardial catecholamines and malondialdehyde (MDA) levels were measured.ResultsAfter levomedetomidine administration, subdural balloon inflation precipitated an increase in mean arterial pressure (149 ± 33% of baseline), heart rate (122 ± 19% of baseline), LV systolic pressure (LVP), LV end-diastolic pressure (LVEDP), LV developed pressure (LVDP), LV dP/dtmax and rate pressure product (RPP) (132 ± 19%, 260 ± 142%, 119 ± 15%, 126 ± 24% and 146 ± 33% of baseline value, respectively). ICH decelerated LVP fall (τ), as t increased from 7.75 ± 1. 1 to 14.37 ± 4.5 msec. Moreover, plasma norepinephrine levels were elevated ( 169 ± 50% of baseline) and there was the appearance of cardiac dysrhythmias and other ECG abnormalities. This response was transient and cardiac function deteriorated in a temporal manner. Intracisternal dexmedetomidine prevented the rise in plasma norepinephrine, blocked the ECG abnormalities, and preserved cardiac function. Moreover, dexmedetomidine attenuated the rise in MDA levels.ConclusionsThe results demonstrate that dexmedetomidine attenuates cardiac dysfunction associated with ICH. Our results provide evidence for the role of central sympathetic hyperactivity in the development of cardiac dysfunction associated with ICH.RésuméObjectifDéterminer si !e biocage sympathique central par ia dexmédétomidine, un agoniste sélectif des récepteurs alpha2 adrénergiques, prévient ia dysfonction cardiaque associée à l’hypertension intracrânienne (HIC) chez un modèle rat.MéthodeAprès l’administration intradstemale de dexmédétomidine (1 μg · μL−1, volume de 10μL) ou du stéréoisomère lévomédétomidine (1 μg · μL−1, volume de 10 μL) chez des rats anesthésiés à l’halothane, un cathéter sous-dural à ballonnet a été gonflé pendant 60 s pour produire une HIC. La pression intracrânienne, l’hémodynamique, les pressions ventriculaires gauches (VG) et les changements électrocardiographiques (ECG) ont été enregistrés. Les niveaux plasmatiques et myocardiques de catécholamines et de malondialdéhyde (MDA) ont été mesurés.RésultatsAprès l’administration de lévomédétomidine, le gonflement du ballonnet sous-dural a précipité une hausse de la tension artérielle moyenne (149 ± 33 % des mesures de base), de la fréquence cardiaque (122 ± 19 % de la base), la tension systolique VG (TVG), la tension télédiastolique VG (TTDVG), la tension développée du VG (TDVG), dP/dtmax VG et le produit tension-fréquence cardiaque PJF (132 ± 19%, 260 ± 142 %, 119 ± 15 %, 126 ± 24% et 146 ± 33% des valeurs de base, respectivement). L’HIC a décéléré la chute de la TVG (τ), à mesure que t augmentait de 7,75 ± 1,1 à 14,37 ± 4,5 msec. De plus, les niveaux plasmatiques de norépinéphrine étaient élevés (169 ± 50 % de la base) et des dysrythmies cardiaques sont apparues avec d’autres anomalies ECG. La réaction a été une détérioration transitoire de la fonction cardiaque d’une manière temporelle. La dexmédétomidine intracisternale a empêché l’élévation de norépinéphrine plasmatique, bloqué les anomalies ECG et préservé la fonction cardiaque. La dexmédétomidine a diminué la hausse des niveaux de MDA.ConclusionLes résultats démontrent que la dexmédétomidine atténue la dysfonction cardiaque associée à HIC. Ils mettent en évidence le rôle de l’hyperactivité sympathique centrale dans le développement de dysfonction cardiaque associée à l’HIC.

Morphine decreasesin vivo catechol activity in the rostral ventrolateral medulla

ConclusionDecreased neck extension assessed at the bedside is a predictor of unanticipated difficult intubation. Neck extensions of < 5 cm, in conjunction with the Mallampati airway classification, should become a routine part of airway assessment.

Mannitol but not dantrolene prevents myocardial dysfunction following intra-cranial hypertension in rats.

Cardiac complications stemming from intra‐cranial hypertension may result from impaired intra‐cellular Ca2+ homeostasis. The aim of this study was to examine the effects of dantrolene, a blocker of sarcoplasmic reticulum (SR) Ca2+ release, on myocardial dysfunction associated with intra‐cranial hypertension in rats. Dantrolene (10 mg) with and without 15% mannitol was administered to halothane‐anesthetized rats prior to induction of intra‐cranial hypertension by subdural balloon inflation. Its effects were compared to 3% and 15% mannitol and 5% Pentaspan®. Dantrolene with mannitol or 15% mannitol alone prevented the transient intra‐cranial hypertension‐induced hyperdynamic response and ensuing circulatory collapse that was found in animals pre‐treated with 3% mannitol solution or pentaspan. Moreover, hemodynamic function was preserved irrespective of TnI cleavage. However, only animals treated with high dose 15% mannitol exhibited lower lipid peroxidation content in the heart. In contrast, pre‐treatment with dantrolene alone did not prevent the cardiac complications associated with intra‐cranial hypertension. In conclusion, 15% mannitol attenuated the cardiopulmonary complications associated with intra‐cranial hypertension. Dantrolene without mannitol was without effect. Since mannitol exhibits free radical scavenging properties, protection could be the result of a decrease in oxidative stress after intra‐cranial hypertension.

Activation of the Rostral Ventrolateral Medulla in an Acute Anesthetized Rodent Strychnine Model of Allodynia

UNLABELLED After the administration of intrathecal strychnine, allodynia is manifested as activation of supraspinal sites involved in pain processing and enhancement of cardiovascular responses evoked by normally innocuous stimuli. The objective of this study was to investigate the effect of strychnine-induced allodynia on adrenergic neuronal activity in the C1 area of the rostral ventrolateral medulla (RVLM), a major site involved in cardiovascular regulation. The effect of intrathecal strychnine (40 microg) or saline followed by repeated hair deflection to caudal lumbar dermatomes in the urethane-anesthetized rat was assessed by measuring voltammetric changes in the RVLM catechol oxidation current (CA x OC), mean arterial pressure (MAP), and heart rate (HR). After the administration of intrathecal strychnine, hair deflection evoked a significant and sustained increase in the RVLM CA x OC and MAP (peak 146.4%+/-5.6% and 159%+/-18.4% of baseline, respectively; P < 0.05). There was a nonsignificant increase in HR (peak 128%+/-8.2%). In the absence of hair deflection, there was no demonstrable change. Intrathecal saline-treated rats failed to demonstrate changes in RVLM CA x OC, MAP, or HR. In the present study, we demonstrated that, after the administration of intrathecal strychnine, innocuous hair deflection evokes temporally related neuronal activation in the rat RVLM and an increase in MAP. This suggests that the RVLM mediates, at least in part, the cardiovascular responses during strychnine allodynia. IMPLICATIONS Neural injury-associated pain, as manifested by allodynia, is resistant to conventional treatment. In a rat model of allodynia, we demonstrated activation of the brain region involved in sympathetic control. Innovative therapies that target this region may be successful in managing this debilitating condition.

Introduction of an anesthesia assistant increased the efficiency of an operating room

METHODS An OR nurse was recruited to function solely as the AA. The AA performed the preoperative nursing checklist, assisted with induction and emergence, and set up anesthesia equipment between cases. There was one week of education and training prior to the start of the 4 week study. Using a prospective, crossover study design, a gynecology OR utilized the AA for 2 weeks while data was simultaneously collected for the control arm in the orthopedic OR. After 2 weeks the AA crossed over to the orthopedic OR and control data was simultaneously collected for the gynecology OR during this time. Demographic and time data were recorded and time differences were analyzed using a Student t-test. General linear modeling was used in multivariable analysis. Alpha less than 0.05 were used for all statistical tests.