No abstract

SummaryOrotracheal intubation in mice is a complicated technique because of the peculiar oropharyngeal anatomy and the dif culty in visualizing the laryngis aditus. Here we report a new and simple method for rapid endotracheal intubation by using a small bore, straight bre-optic arthroscope. Under endoscope-assisted visualization of the laryngis aditus, a polyethylene cannula, inserted on a guide-wire in order to facilitate the introduction of the tip across the vocal cords, was advanced in the trachea. The success rate of intubation was 100%. We were also able to re-intubate the mice 4 and 8 weeks later without any major complications. We conclude that this method can be easily and safely used for studies where controlled pulmonary ventilation is necessary.

In the aortic banding-induced model of LVH: (i) the antihypertrophic effect of propranolol is independent of its beta-adrenergic blocking activity; and Iii) since disopyramide and D-propranolol also proved to be able to antagonize banding-induced LVH, the hypothesis is proposed that membrane-stabilizing activity, among the ancillary properties of propranolol, most likely accounts for the antihypertrophic effect of this drug.

We investigated the effects of isoflurane on the rabbit cardiovascular system at several end-tidal concentrations. Furthermore, because isoflurane has been reported to produce tachycardia while reducing sympathetic nervous activity and baroreflex function, we evaluated whether the chronotropic effects of isoflurane could be due to a vagal withdrawal. ECG, mean arterial pressure (MAP), and heart rate (HR) were obtained in rabbits the conscious, unsedated state and during isoflurane anesthesia by telemetric device. Measurements of pH, oxygen, carbon dioxide, plasma catecholamines, baroreflex sensitivity, and spectral analysis of HR variability were made in nonanesthetized and anesthetized animals. Isoflurane caused an increase in HR at 0.5, 1, and 1.5 minimum alveolar concentration (MAC) and a decrease in systolic and diastolic blood pressure (SBP, DBP) and MAP at 1 and 1.5 MAC. Biochemical analysis showed that isoflurane-mediated cardiovascular effects were not accompanied by any significant changes in plasma norepinephrine (NE) and epinephrine (Epi) levels. Neither were any significant differences in plasma catecholamine levels noted between anesthetized and awake animals. The analysis of spectral components of HR variability and baroreflex function indicated that isoflurane induced a marked reduction in the low- and high-frequency spectral power of HR variability and in baroreflex sensitivity. Tachycardia under isoflurane was suppressed dose dependently by the administration of clonidine or atenolol and was not influenced by bilateral vagotomy. Collectively, our results indicate that cardiovascular effects induced by isoflurane in smaller animals such as rabbits are similar to those observed in humans and other animal species. We showed that isoflurane-induced tachycardia is mainly the result of vagal withdrawal rather than a baroreflex response, even though a marginal role of baroreflex in heart response to higher concentrations of isoflurane cannot be excluded.

1 Cardiac hypertrophy is a homeostatic response to elevated afterload. Na þ /H þ exchanger (NHE) inhibition reduces the hypertrophic response in animal models of left ventricular hypertrophy (LVH) and myocardial infarction. We examined the effect of chronic treatment with cariporide, a selective inhibitor of Na þ /H þ exchanger isoform 1 (NHE-1), on left ventricular (LV) systolic and diastolic function under pressure overload conditions. 2 Male CD-1 mice were randomized to receive either a control diet or an identical diet supplemented with 6000 p.p.m. of cariporide. Cardiac pressure overload was induced by thoracic aortic banding. LV dimension and systolic and diastolic function were assessed in sham and banded mice by echocardiography and cardiac catheterization 2 and 5 weeks after surgery. Histological analysis was also performed. 3 After 2 weeks of pressure overload, the vehicle-treated banded mice (Veh-Bd) had enhanced normalized LV weight (about þ 50%) and normal chamber size and function, whereas cariporidetreated banded mice (Car-Bd) showed a preserved contractility and systolic function despite a marked attenuation of LVH. Diastolic function did not differ significantly among groups. After 5 weeks, the Veh-Bd developed LV chamber enlargement and systolic dysfunction as evidenced by a 16% increase in LV end-diastolic diameter, a 36% decrease in myocardial contractility, and a 26% reduction in percent fractional shortening. In contrast, Car-Bd showed an attenuated increase in LV mass, normal chamber size, and a maintained systolic function. A distinct histological feature was that in banded mice, cariporide attenuated the development of cardiomyocyte hypertrophy but not the attendant myocardial fibrosis. 4 In conclusion, the results of the present study indicate that (i) the hypertrophic response to pressure overload is dependent on NHE-1 activity, and (ii) at the 5-week stage, banding-induced deterioration of LV performance is prevented by NHE-1 inhibition. British Journal of Pharmacology (2004) 141, 526-532. doi:10.1038/sj.bjp.0705631 Keywords: Pressure overload; Na þ /H þ exchanger; cardiac remodeling; systolic function Abbreviations: BW, body weight; Car, cariporide; Car-Bd, cariporide-treated, banded mice; Car-Sh, cariporide-treated, shamoperated mice; CSA, cardiomyocyte cross-sectional area; Ees, end-systolic elastance; HR, heart rate; LVEDD, left ventricular end-diastolic diameter; LVEDP, left ventricular end-diastolic pressure; LV FS, left ventricular fractional shortening; LVSP, left ventricular systolic pressure; LVW/BW, left ventricular weight-to-body weight ratio; NHE-1, Na þ /H þ exchanger isoform 1; RWT, posterior-wall thickness-to-left ventricular end-diastolic diameter ratio; s s , end-systolic left ventricular wall stress; Veh-Sh, vehicle-treated, sham-operated mice; Veh-Bd, vehicle-treated, banded mice