Repeated Administration of the Cannabinoid WIN Alters the Isoflurane-Sparing Effect of Morphine and Dexmedetomidine.

The impacts of morphine and dexmedetomidine on the MAC of isoflurane were studied in rats constantly medicated with the cannabinoid WIN 55,212-2. METHODS: Prior to the administration of morphine, the MAC was measured in both untreated rats (MAC (ISO)) and those treated with a cannabinoid (MAC (ISO + CANN)). The effects of morphine (MAC (ISO + MOR)) and dexmedetomidine (MAC (ISO + DEX)) on untreated rats and rats treated for 21 days with the cannabinoids (MAC (ISO + CANN + MOR)) and (MAC (ISO + CANN + DEX) were also studied. RESULTS: MAC (ISO) was 1.32 ± 0.06, and MAC (ISO + CANN) was 1.69 ± 0.09. MAC (ISO + MOR) was 0.97 ± 0.02 (26% less than MAC (ISO)). MAC (ISO + CANN + MOR) was 1.55 ± 0.08 (8% less than MAC (ISO + CANN)), MAC (ISO + DEX) was 0.68 ± 0.10 (48% less than MAC (ISO)), and MAC (ISO + CANN + DEX) was 0.67 ± 0.08 (60% less than MAC (ISO + CANN)). CONCLUSIONS: Medication with a cannabinoid for 21 days augmented the MAC of isoflurane. The sparing effect of morphine on isoflurane is lower in rats constantly medicated with a cannabinoid. The sparing effect of dexmedetomidine on the minimum alveolar concentration of isoflurane is greater in rats repeatedly medicated with a cannabinoid.

Minimum Alveolar Concentration of Isoflurane in Rats Chronically Treated with the Synthetic Cannabinoid WIN 55,212-2.

The minimum alveolar concentration MAC of isoflurane was measured in rats chronically treated with WIN 55,212-2. METHODS: The MAC of isoflurane was determined in 24 male rats from expiratory samples at time of tail clamping under the following conditions: without treatment MAC(ISO), in rats treated for 21 days with WIN 55,212-2 MAC(ISO + WIN55), and in rats 8 days after stopping treatment with WIN 55,212-2 (MACISO + WIN55 + 8D). RESULTS: The MAC(ISO) was 1.32 ± 0.06. In the MAC(ISO + WIN55) group, the MAC increased to 1.69 ± 0.09 (28%, p-value ≤ (0.0001). Eight days after stopping treatment with WIN55, the MAC did not decrease significantly, 1.67 ± 0.07 (26%, p-value ≤ 0.0001). CONCLUSIONS: The administration of WIN 55,212-2 for 21 days increases the MAC of isoflurane in rats. This effect does not disappear 8 days after discontinuation of treatment with the synthetic cannabinoid.

Cardiovascular effects of constant rate infusions of lidocaine, lidocaine and dexmedetomidine, and dexmedetomidine in dogs anesthetized at equipotent doses of sevoflurane.

This study evaluated the cardiovascular effects of a constant rate infusion (CRI) of lidocaine, lidocaine and dexmedetomidine, and dexmedetomidine in dogs anesthetized with sevoflurane at equipotent doses. Treatments consisted of T1-Lidocaine [loading dose 2 mg/kg body weight (BW), IV, and CRI of 100 µg/kg BW per min] at 1.4% end-tidal of sevoflurane (FESEV); T2-Dexmedetomidine (loading dose 2 µg/kg BW, IV, and CRI of 2 µg/kg BW per hour) and FESEV 1.1%; and T3-Lidocaine-Dexmedetomidine using the same doses of T1 and T2 and FESEV 0.8%. Constant rate infusion of lidocaine did not induce any cardiovascular changes; lidocaine and dexmedetomidine resulted in cardiovascular effects similar to dexmedetomidine alone. These effects were characterized by a significant (P < 0.001) decrease in heart rate, cardiac output, cardiac index, oxygen delivery, and pulmonary vascular resistance index, and a significant (P < 0.001) increase in mean and diastolic arterial pressure, systemic vascular resistance index, pulmonary arterial occlusion pressure and oxygen extraction ratio, compared with baseline values. In conclusion, a CRI of lidocaine combined with dexmedetomidine produces significant cardiovascular changes similar to those observed with dexmedetomidine alone.

Effets cardiovasculaires des infusions constante de taux de lidocaïne, lidocaïne et dexmédétomidine, et dexmédétomidine chez chiens anesthésier at équipotent doses de sevoflurane. L'objet de cette etude a été la evaluation des effets cardo-vasculaires de la perfusion à debit continue (CRI) de lidocaïne, lidocaïene et dexmédétomidine, et dexmédétomidine en chiens anesthésiés avec sévoflurane dans équipotentiel dose. Les traitemets consistèrent á T1-Lidocaïne [dose de charge de 2 mg/kg, IV, et perfusion à debit continue (CRI) de 100 µg/kg/min] en 1,4 % en fin d'expiration du sévoflurane (FESEV); T2-Déxmédetomidine (dose de charge de 2 µg/kg, IV, et perfusion à debit continue (CRI) de 2 µg/kg/h) et FESEV 1,1 % et T3-Lidocaïne-Dexmédétomidine en utilisant la même dose de T1 et T2 et FESEV 0,8 %. Perfusion à debit continue (CRI) de lidocaïne ne induit pas aucun échange cardio-vasculaire; lidocaïne et dexmédétomidine resulta dans effets cardio-vasculaires similaires a dexmédétomidine seule. Ces effets caracterices par significative décroissance (P < 0,001) en fréquence cardiaque, le débit cardiaque, index cardiaque, la libération de l'oxygène, pulmonaire indice de résistance vasculaire, et significative accroissement de la moyenne a la pression artériele diastolique (P < 0,001), indice de résistance vasculaire systémique, et l'extraction d'oxygène. En somme, la perfusion à debit continue (CRI) de lidocaïne produit significative échange cardio-vasculaire similaire à ceux observe en itilisant seulement dexmédétomidine.(Traduit par les auteurs).