7 research outputs found
Spatiotemporal characteristics of atrial fibrillation electrograms: a novel marker for arrhythmia stability and termination
Background: Sequentially mapped complex fractionated atrial electrograms (CFAE) and dominant frequency (DF) sites have been targeted during catheter ablation for atrial fibrillation (AF). However, these strategies have yielded variable success and have not been shown to correlate consistently with AF dynamics. Here, we evaluated whether the spatiotemporal stability of CFAE and DF may be a better marker of AF sustenance and termination.
Methods: Eighteen sheep with 12 weeks of "one-kidney, one-clip" hypertension underwent open-chest studies. A total of 42 self-terminating (28–100 s) and 6 sustained (>15 min) AF episodes were mapped using a custom epicardial plaque and analyzed in 4-s epochs for CFAE, using the NavX CFE-m algorithm, and DF, using a Fast Fourier Transform. The spatiotemporal stability index (STSI) was calculated using the intraclass correlation coefficient of consecutive AF epochs.
Results: A total of 67,733 AF epochs were analyzed. During AF initiation, mean CFE-m and the STSI of CFE-m/DF were similar between sustained and self-terminating episodes, although median DF was higher in sustained AF (p=0.001). During sustained AF, the STSI of CFE-m increased significantly (p=0.02), whereas mean CFE-m (p=0.5), median DF (p=0.07), and the STSI of DF remained unchanged (p=0.5). Prior to AF termination, the STSI of CFE-m was significantly lower (p<0.001), with a physiologically non-significant decrease in median DF (−0.3 Hz, p=0.006) and no significant changes in mean CFE-m (p=0.14) or the STSI of DF (p=0.06).
Conclusions: Spatiotemporal stabilization of CFAE favors AF sustenance and its destabilization heralds AF termination. The STSI of CFE-m is more representative of AF dynamics than are the STSI of DF, sequential mean CFE-m, or median DF
Prostaglandins E2 And F2α as Inflammatory and Vasoactive Mediators in Black Walnut Heartwood Extract-Induced Equine Laminitis
Standing flank laparotomy for colic: 37 cases
Background:
Standing flank laparotomy can be an alternative to ventral midline laparotomy in horses with colic. Standing flank laparotomy avoids general anaesthesia, provides excellent access to some regions of the abdominopelvic cavity and costs less than ventral midline laparotomy.
Objective:
To report a series of cases of peritoneal and intestinal diseases other than SC diseases managed with standing flank laparotomy.
Study design:
Retrospective case series.
Methods:
Records from equids with colic subjected to standing flank laparotomy at five hospitals (2003-2020) were reviewed. Descriptive data analysis was performed.
Results:
Thirty horses (sixteen survived to discharge), six ponies (four survived) and one donkey (euthanised) were subjected to standing flank laparotomy via the left flank (n = 31), right flank (n = 2) or both flanks (n = 4). The primary disease affected the peritoneum (0/5 survived), SI (5/9 survived) and caecum and/or LC (15/23 survived). Enterotomy was performed in four animals (all survived). Partial typhlectomy was performed in one horse (euthanised). Resection-anastomosis of the SI or LC was performed in three animals (one survived). Three animals had intraoperative complications that negatively affected the outcome: Two ponies had intolerance to abdominopelvic exploration; one mare had spontaneous exteriorisation of a long segment of the SI leading to a large tear in the mesentery. In seven cases, severe/extensive lesions found during standing flank laparotomy warranted immediate euthanasia. The survival rate was 54%. All owners were satisfied with the decision to perform standing flank laparotomy.
Main limitations:
The retrospective design, lack of a control group, small number of cases and lack of standardised protocols between hospitals.
Conclusions:
Although ventral midline laparotomy is the standard of care for horses with colic, standing flank laparotomy is a viable approach for some types of colic. Systemic administration of analgesics may not produce sufficient peritoneal analgesia, which can lead to intolerance to abdominopelvic exploration during standing flank laparotomy in horses with colic and may negatively affect the outcome
Effect of voltage-gated and capacitative calcium entry blockade on agonist-inducted construction of equine laminar blood vessels
Objective—To characterize the relative contributions of voltage-gated and capacitative Ca²⁺ entry to agonist-induced contractions of equine laminar arteries and veins. Animals—16 adult mixed-breed horses. Procedures—Laminar arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Concentration-response curves were obtained for the vasoconstrictor agonists phenylephrine, 5-hydroxytryptamine (5-HT), prostaglandin F2α (PGF2α), and endothelin-1 (ET-1) either in the absence of extracellular Ca²⁺ or in the presence of the voltage-gated Ca²⁺ channel inhibitor diltiazem or the putative inhibitor of capacitative Ca2+ entry, trifluoromethylphenylimidazole. Results—In the absence of extracellular Ca2+, maximal responses of veins to 5-HT, phenylephrine, ET-1 and PGF2α were reduced by 80%, 50%, 50%, and 45%, respectively; responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 95%, 90%, and 20%, respectively. Although diltiazem did not affect the maximal responses of veins to any agonist, responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 40%, 50%, and 27%, respectively. Trifluoromethylphenylimidazole did not affect maximal responses of veins, but did reduce their contractile responses to low concentrations of ET-1 and PGF2α. Conclusions and Clinical Relevance—Results suggested that the contribution of extracellular Ca²⁺ to laminar vessel contractile responses differs between arteries and veins and also between contractile agonists, voltage-gated Ca²⁺ entry is more predominant in laminar arteries than in veins, and capacitative Ca²⁺ entry has a minor role in agonist-induced contractile responses of laminar veins.John F. Peroni, James N. Moore, Erik Noschka, Tristan H. Lewis, Stephen J. Lewis, Tom P. Robertso
Evaluation of activation of protein kinase C during agonist-induced constriction of veins isolated from the laminar dermis of horses
Effects of Rho-kinase and Src protein tyrosine kinase inhibition on agonist-induced vasoconstriction of arteries and veins of the equine laminar dermis
Objective — To determine the effects of inhibition of Rho-kinase or Src-family protein tyrosine kinases (srcPTK) on agonist-induced contractile responses in equine laminar arteries and veins. Sample Population — Laminar arteries and veins obtained from 13 adult mixed-breed horses. Procedures — Laminar vessels were mounted on myographs and exposed to phenylephrine (PE), 5-hydroxytryptamine (5-HT), prostaglandin F2α (PGF2α), and endothelin-1 (ET-1) with or without the Rho-kinase inhibitor Y-27632 (10μM), srcPTK inhibitor PP2 (10μM), or a negative control analogue for PP2 (PP3; 10μM). Results — Responses to PE were reduced by use of Y-27632 in laminar vessels (approx inhibition, 55%). However, Y-27632 reduced responses to 5-HT to a greater degree in veins than in arteries (approx inhibition of 55% and 35%, respectively). The Y-27632 also reduced responses of laminar veins to ET-1 by approximately 40% but had no effect on maximum responses of laminar arteries to ET-1, although a rightward shift in the concentration response curve was evident. Addition of PP2 reduced responses to PE, 5-HT, and PGF2α in laminar veins by approximately 40%, 60%, and 65%, respectively, compared with responses after the addition of PP3; PP2 had no effect on responses to ET-1. In laminar arteries, PP2 reduced 5-HT–induced contractions by approximately 50% but did not affect responses to PE or ET-1. Conclusions and Clinical Relevance — Results of the study were consistent with activation of Rho-kinase being important during agonist-induced constriction in laminar vessels, activation of srcPTK being an agonist-dependent event, and more prominent roles for Rhokinase and srcPTK in veins than in arteries.Tom P. Robertson, James N. Moore, Erik Noschka, Tristan H. Lewis, Stephen J. Lewis, John F. Peron