Hemodynamic and thermoregulatory effects of xylazine-ketamine mixture persist even after the anesthetic stage in rats / Efeitos hemodinâmicos e termorregulatórios da mistura cetamina-xilasina persistem mesmo após o período anestésico em ratos

The xylazine-ketamine mixture (KX) is an anesthetic approach commonly administered to assess cardiovascular function in rodents. This study aimed to examine if the cardiovascular and thermoregulatory effects of KX could persist after the anesthetic state ceased in rats. Male Wistar rats were anesthetized with K (50mg/kg) X (10mg/kg) through the intra-peritoneal route. Hemodynamic and thermoregulatory repercussions were evaluated in animals in awake state, during an anesthetic depth and after complete recovery of anesthetized state. KX was efficient to significantly induce deep anesthesia in all rats after 10min. A complete recovery of anesthetized state was observed only after 210min. Compared with preanesthetic state and control animals that received no drug, KX induced a significant reduction of systolic and diastolic blood pressure at 10min. Hypotension was more prominent at 150min. The heart rate was also significantly reduced after 10 min of KX and the highest magnitude of bradycardia was observed at 30min. In addition, rectal temperature was markedly decreased at 30min of KX and the higher reduction occurred at 150min. The hemodynamic and thermoregulatory effects of KX were maintained even after complete anesthetic recovery.

Objetivou-se com este estudo avaliar a persistência dos efeitos cardiovasculares e termorregulatórios da associação cetamina e xilasina (CX) mesmo após o período anestésico em ratos. Ratos Wistar machos foram anestesiados com cetamina 50mg/kg e xilasina 10mg/kg, por via intra-peritoneal. As repercussões hemodinâmica e termorregulatória foram avaliadas com os animais acordados, durante o período anestésico e após recuperação completa da anestesia. A CX foi eficiente em induzir significante regime anestésico em todos os ratos após 10min. A recuperação completa do estado de anestesia foi observada somente após 210min. Comparado com o estado pré-anestésico e com animais controles, que não receberam anestesia, a CX induziu significativa redução das pressões sistólica e diastólica aos 10min. A hipotensão foi mais evidente aos 150min após CX. A frequência cardíaca também foi significativamente reduzida com 10min de CX e a bradicardia foi mais acentuada aos 30min. A temperatura retal foi reduzida aos 30min, sendo mais acentuada após 150min de anestesia. Os efeitos hemodinâmicos e termorregulatórios da CX persistem mesmo após completa recuperação anestésica.

Drag reduction by polyethylene glycol in the tail arterial bed of normotensive and hypertensive rats

This study was designed to evaluate the effect of drag reducer polymers (DRP) on arteries from normotensive (Wistar) and spontaneously hypertensive rats (SHR). Polyethylene glycol (PEG 4000 at 5000 ppm) was perfused in the tail arterial bed with (E+) and without endothelium (E-) from male, adult Wistar (N = 14) and SHR (N = 13) animals under basal conditions (constant flow at 2.5 mL/min). In these preparations, flow-pressure curves (1.5 to 10 mL/min) were constructed before and 1 h after PEG 4000 perfusion. Afterwards, the tail arterial bed was fixed and the internal diameters of the arteries were then measured by microscopy and drag reduction was assessed based on the values of wall shear stress (WSS) by computational simulation. In Wistar and SHR groups, perfusion of PEG 4000 significantly reduced pulsatile pressure (Wistar/E+: 17.5 ± 2.8; SHR/E+: 16.3 ± 2.7 percent), WSS (Wistar/E+: 36; SHR/E+: 40 percent) and the flow-pressure response. The E- reduced the effects of PEG 4000 on arteries from both groups, suggesting that endothelial damage decreased the effect of PEG 4000 as a DRP. Moreover, the effects of PEG 4000 were more pronounced in the tail arterial bed from SHR compared to Wistar rats. In conclusion, these data demonstrated for the first time that PEG 4000 was more effective in reducing the pressure-flow response as well as WSS in the tail arterial bed of hypertensive than of normotensive rats and these effects were amplified by, but not dependent on, endothelial integrity. Thus, these results show an additional mechanism of action of this polymer besides its mechanical effect through the release and/or bioavailability of endothelial factors.

Determination of myocardial infarction size in rats by echocardiography and tetrazolium staining: correlation, agreements, and simplifications

Triphenyltetrazolium chloride (TTC) staining and echocardiography (ECHO) are methods used to determine experimental myocardial infarction (MI) size, whose practical applicability should be expanded. Our objectives were to analyze the accuracy of ECHO in determining infarction size in rats during the first days following coronary occlusion and to test whether a simplified single measurement by TTC correctly indicates MI size, as determined by the average value for multiple slices. Infarction was induced in female Wistar rats by coronary artery occlusion and MI size analysis was performed after the acute (7th day) and chronic periods (after 4 weeks) by ECHO matched with TTC. ECHO and TTC showed similar values of MI size ( percent of left ventricle perimeter) in acute (ECHO: 33 ± 11, TTC: 35 ± 14) and chronic (ECHO: 38 ± 14, TTC: 39 ± 13 periods), and also presented an excellent correlation (r = 0.92, P < 0.001). Although measurements from different heart planes showed discrepancies, a single measurement acquired from the mid-ventricular level by TTC was a good estimate of MI size calculated by the average of multiple planes, with minimal disagreement (Bland-Altman test with mean ratio bias of 0.99 ± 0.07) and close to an ideal correlation (r = 0.99, P < 0.001). In the present study, ECHO was confirmed as a useful method for the determination of MI size even in the acute phase. Also, the single measure of a mid-ventricular section proposed as a simplification of the TTC method is a satisfactory prediction of average MI extension.