Blood cardioplegia reduces intraoperative ventricular fibrillation and transfusion requirements compared to crystalloid cardioplegia in canine mitral valve repair.

OBJECTIVE: Cardioplegic solutions are indispensable for open-heart surgeries, including mitral valve repair (MVR), a potentially curative treatment for myxomatous mitral valve disease in dogs. However, procedural methodologies are not fully established, and complications are yet to be comprehensively understood. Cardioplegic solutions contain various substances to protect the myocardium under temporal cardiac arrest. Nevertheless, ventricular fibrillation (VF) occurs as a common complication after releasing the crossclamp. Based on these backgrounds, the search for optimal cardioplegic solutions in dogs undergoing MVR is an urgent issue. This study aims to evaluate the occurrence of VF in dogs treated with blood cardioplegia (BCP) versus crystalloid cardioplegia (CCP) during MVR. ANIMALS: A total of 251 client-owned dogs who underwent MVR from November 2015 to November 2017 were included. METHODS: We retrospectively assessed the relationship between VF and type of cardioplegia (CCP or BCP) based on surgical records, including VF incidence, transfusion use, crossclamp time, and echocardiographic measurements. RESULTS: Logistic regression analysis showed that the CCP group was associated with the occurrence of VF (OR, 2.378; CI, 1.133-4.992; P = .022). In addition, the CCP group was associated with transfusion use (OR, 2.586; CI, 1.232-5.428, P = .022). There was no difference between the groups for the pre- and postoperative echocardiographic measurements. CLINICAL RELEVANCE: The BCP group had a lower incidence of VF and less transfusion use than the CCP group. This finding indicates that BCP may be a superior cardioplegic technique for MVR in dogs.

A new bipolar precordial electrocardiographic lead configuration for specific evaluation of atrial depolarization in healthy dogs.

OBJECTIVE: The Lewis lead is an EGC configuration used to detect atrial activity and its relationship with ventricular activity. However, no equivalent configuration has been proposed in veterinary medicine. Therefore, this study explored new bipolar lead configurations to evaluate atrial depolarization and investigated their characteristics by comparing them with conventional leads. The authors hypothesized that a lead with a high absolute value of the P wave (|P|) and a high ratio of the P wave to the QRS complex (|P|/|QRS|) might be an appropriate configuration. ANIMALS: 6 laboratory Beagles were used. PROCEDURES: Electrocardiograms were recorded using bipolar limb leads (I, II, III, aVL, aVF, and aVR) and unipolar precordial leads (C2, C3, C4, C5, C6, M1, M2, M5, M6, 1st-R, CV6LL, and V10) in the standing position. The new bipolar leads were attached in the following configuration: the negative electrode was attached to M6, and the positive electrode was sequentially applied to M1 and M2. The leads were named M6M1 and M6M2. RESULTS: The waveforms obtained using the new bipolar leads M6M1 and M6M2 showed significantly higher |P|/|QRS| and |P| values than those obtained using conventional limb leads and precordial leads. CLINICAL RELEVANCE: The new leads achieved a specific enhancement of atrial activity conducted at a reduced ventricular amplitude and increased atrial amplitude, similar to the Lewis lead in human medicine. These findings suggest that M6M1 and M6M2 could be supplemental lead configurations to identify P waves without amplifying the QRS waves compared to conventional methods.

Involvement of neurokinin-1 receptors in the autonomic nervous system in colorectal distension-induced cardiovascular suppression in rats.

Situational syncope, which includes rectally mediated reflexes, is defined as syncope induced by a specific situation. Its pathogenesis generally involves disorders of the autonomic nervous system. However, the mechanisms and preventive strategies are not yet well understood. Therefore, we hypothesized that a tachykinin neurokinin-1 receptor might be involved in the autonomic nervous system, and that a neurokinin-1 receptor antagonist could mitigate reflex syncope. This study used a rat model in which the reflex was induced by afferent vagal stimulation with colorectal distension (CRD). In the study, the rats were divided into three groups: non-CRD, CRD, and CRD with a neurokinin-1 receptor antagonist. First, we examined the effect of fosaprepitant, a neurokinin-1 receptor antagonist, on the circulatory response in this model. We then determined the brain regions that showed increased numbers of c-Fos immunoreactive cells in the respective groups. Our results suggest that the colorectal distension procedure reduced blood pressure and that fosaprepitant lowered this response. In addition, the number of c-Fos immunoreactive cells was increased in the caudal ventrolateral medullary region with colorectal distension, and this number was decreased by the administration of fosaprepitant. In conclusion, fosaprepitant might be involved in the vagal reflex pathway and potentially suppress the circulatory response to colorectal distension.

Canonical NF-κB p65, but Not p105, Contributes to IL-1ß-Induced IL-8 Expression in Cardiac Fibroblasts.

Cardiac fibroblasts participate in the inflammatory process of heart diseases as sentinel cells of the cardiac tissue. In this study, we investigated the effect of the proinflammatory cytokine, interleukin 1ß (IL-1ß), on the expression of interleukin 8 (IL-8), which contributes to the induction of innate immunity via the activation and recruitment of innate immune cells, such as neutrophils, to the site of inflammation in canine cardiac fibroblasts. IL-1ß mediates IL-8 mRNA expression and protein release in a dose- and time-dependent manner. The IL-ß-mediated IL-8 protein release and mRNA expression were inhibited by 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide, an inhibitor of the transcription factor, nuclear factor (NF)-κB. In cells treated with IL-1ß, NF-κB p65 and p105 were transiently phosphorylated, indicating the activation of NF-κB. However, IL-1ß failed to induce IL-8 mRNA expression in the cells transfected with p65 small interfering RNA (siRNA), but not in those transfected with p105 siRNA. These observations suggest that IL-1ß induces IL-8 expression via the activation of NF-κB p65 in canine cardiac fibroblasts.