Analgesic, cardiorespiratory effects and motor block characteristics of epidural levobupivacaine alone or in combination with methadone or dexmedetomidine in bitches undergoing unilateral total mastectomy.

The aim of this study was to evaluate the latency, extent of analgesia, and duration of motor block of levobupivacaine alone and combined with methadone or dexmedetomidine after epidural administration during and after mastectomy in dogs. Twenty-four mature, mixed-breed female dogs were randomly divided into three experimental groups with eight animals each, according to the agents used in lumbosacral epidural analgesia: levobupivacaine 0.75% alone (1.5mg/kg - control group), levobupivacaine 0.75% (1.5 mg/kg) + methadone 1% (0.3 mg/kg), or levobupivacaine 0.75% (1.5 mg/kg) + dexmedetomidine 0.05% (3 µg/kg). During surgery, cardiorespiratory parameters were evaluated. Rescue analgesia was given when there were signs of nociception and was necessary in all three treatment groups. Since all animals received rescue analgesia during the surgery and immediately post-surgery, the duration of the sensitive block were not evaluated. The extent of sensory block was between the 12º and 13º thoracic vertebrae for the control group, 7º thoracic vertebra to 5º lumbar vertebra (methadone group), and 8º thoracic vertebra to 4º lumbar vertebra for the dexmedetomidine group. Methadone or dexmedetomidine combined with levobupivacaine increased the extent of the sensory block and the duration of the motor block in bitches when administered via the epidural route.

A complex CLCN1 variant associated with hereditary myotonia in a mixed-breed dog.

Hereditary myotonia (HM) is characterized by delayed muscle relaxation after contraction as a result of a mutation in the CLCN1 gene. We describe here a complex CLCN1 variant in a mixed-breed dog with clinical and electromyographic signs of HM. Blood samples from the myotonic dog, as well as from his male littermate and parents, were analyzed via amplification of the 23 exons encoding CLCN1. After sequencing the CLCN1 gene, a complex variant was found in exon 6 c.[705T>G; 708del; 712_732del], resulting in a premature stop codon in exon 7 and a protein that was 717 amino acids shorter than the normal CLC protein. The myotonic dog was identified as homozygous recessive for the complex CLCN1 variant; its parents were heterozygous, and its male littermate was homozygous wild-type. Knowledge of the CLCN1 mutations responsible for the development of hereditary myotonia allows greater clarification of this condition.

PCR-RFLP molecular confirmation of color dilution alopecia in dogs in Brazil.

Color dilution alopecia (CDA) is a dermatopathy observed exclusively in animals having a diluted coat color. In dogs, color dilution occurs as a result of a single-nucleotide variation (SNV) c.-22G > A in the melanophilin gene. We standardized a PCR-restriction-fragment length polymorphism (PCR-RFLP) technique to identify this mutation and determine its frequency in dogs in Brazil. The standardized PCR-RFLP technique could efficiently identify the SNV c.-22G > A in the melanophilin gene, with mutated allele frequencies of 0.1, 0.1, and 0.0875 in Dachshund, Miniature Pinscher, and Yorkshire Terrier breeds, respectively, with no statistical difference among the breeds (p = 0.252). The mutation was identified in 2 homozygous Dachshund dogs with alopecia, confirming the clinical characteristic of CDA. The standardization of a simpler and more accessible molecular technique for recognition of the SNV c.-22G > A in the melanophilin gene allows identification of heterozygous (phenotypically normal) dogs that can be excluded from reproduction, to avoid the birth of dogs with diluted coat color and consequently CDA.