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Anaesthetized Rabbits (anaesthetized + rabbits)

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Medical Sciences	50%

Selected Abstracts

Mechanisms of genioglossus responses to inspiratory resistive load in rabbits

ACTA PHYSIOLOGICA, Issue 3 2002
N. P. ALEKSANDROVA
ABSTRACT The purpose of the present study has been to determine whether pharyngeal dilator muscles participate in inspiratory load compensatory responses and if so, to elucidate role of upper airway mechanoreceptors in these responses. The experiments were performed on anaesthetized rabbits. Each animal was tested in three ways by the imposition of inspiratory resistive load: (1) at upper airways via face mask, (2) at the tracheostomic cannula placed below larynx (all upper airway receptors were `bypassed') and (3) at the mouth after the section of the hypoglossus nerves (motor denervation of genioglossus muscle). The inspiratory load applied to the upper airways evoked significant increases in integrated genioglossus activity (to 129 ± 14.7% of control) and its inspiratory duration (to 113 ± 5% of control) already within the first loaded breath (P < 0.05). The increases in the inspiratory activity of musculius genioglossus were relatively greater than the simultaneous increases in the activity of the diaphragm. Motor denervation of the pharynx dilator muscles (including m. genioglossus) increased airway resistance to 184 ± 19% of control (P < 0.05) and induced obstructive alterations in the breathing pattern during unloaded breathing: decrease in maximal inspiratory flow (,13%) and increase in the level of negative oesophageal pressure (+14%) and the peak diaphragm activity (+6%). After nervi hypoglossus sections additional increases in motor and pressure outputs were required in order to maintain unaltered ventilation at the same degree of loading as before denervation. The results indicate that the pharyngeal dilator muscles have a role in compensation of added inspiratory load. Activation of these muscles facilitate the load compensating function of `pump' muscles by decreasing airway resistance. Tracheostomy did not reduce the genioglossus response to inspiratory loading, ruling out any role for upper airways receptors in the genioglossus response to inspiratory load compensations. [source]

5-Hydroxytryptamine-induced microvascular pressure transients in lungs of anaesthetized rabbits

ACTA PHYSIOLOGICA, Issue 2 2001
N. Sen
We determined lung microvascular pressure transients induced by 5-hydroxytryptamine (5HT), by the micropuncture technique. We mechanically ventilated anaesthetized (halothane 0.8%), open-chested rabbits, in which we recorded pulmonary artery (PA), left atrial (LA) and carotid artery pressures and cardiac output. For 4-min periods of stopped ventilation, we constantly inflated the lung with airway pressure of 7 cmH2O, then micropunctured the lung to determine pressures in arterioles and venules of 20,25 ,m diameter. An intravenous bolus infusion of 5HT (100 ,g), increased total pulmonary vascular resistance by 59%. Prior to 5HT infusion, the arterial, microvascular and venous segments comprised 30, 50 and 19% of the total pulmonary vascular pressure drop, respectively. However 14 s after 5HT infusion, the PA-arteriole pressure difference (arterial pressure drop) increased 46%, while the venule-LA pressure difference (venous pressure drop) increased >100%. The arteriole,venule pressure difference (microvascular pressure drop) was abolished. The increase in the arterial pressure drop was maintained for 4.8 min, whereas the increased venous pressure drop reverted to baseline in <1 min. We conclude that in the rabbit lung in situ, a 5HT bolus causes sustained arterial constriction and a strong but transient venous constriction. [source]

Tetrodotoxin-induced conduction blockade is prolonged by hyaluronic acid with and without bupivacaine

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2004
M. F. Stevens
Background:, In isolated nerves, tetrodotoxin (TTX) blocks nerve conduction longer than bupivacaine. In vivo, however, both substances block nerve conduction to an equal duration, presumably because the hydrophilic TTX binds only weakly to the perineural tissue. High molecular weight hyaluronic acid (HA) prolongs the action of local anaesthetics several-fold. We tested whether admixture of HA enhances the binding of TTX to the perineural tissue and thus induces an ultralong conduction block after a single application. Methods:, In 12 anaesthetized rabbits, the minimal blocking concentrations of TTX, TTX and HA (TTX/HA) and bupivacaine with HA (bupivacaine/HA) were determined by blocking the natural spike activity of the aortic nerve. In 18 other animals, equipotent concentrations of either TTX, TTX/HA or TTX/bupivacaine/HA were applied topically to the aortic nerve. After disappearance of the spike activity, the wound was closed to simulate the clinical situation of a single shot nerve block. The time until recovery of spike activity was determined. The nerves were examined for signs of neurotoxicity 24 h after the application of the drugs. Data are presented as means ± SD and compared by ANOVA and Student's t -test for unpaired data. Results:, The conduction block by TTX/bupivacaine/HA (10.1 ± 1.9 h) or TTX/HA (9.3 ± 1.0 h) was significantly longer than that of plain TTX (7.9 ± 1.0 h). Neurotoxicity was not observed. Conclusions:, Both HA and HA/bupivacaine prolong the TTX-induced conduction blockade of the aortic nerve of rabbits in vivo. No signs of neurotoxicity were observed. [source]

Pharmacological profile of SL 59.1227, a novel inhibitor of the sodium/hydrogen exchanger

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2000
Janine Lorrain
The NHE1 isoform of the Na+/H+ exchanger plays an important role in the regulation of intracellular pH and in cardiac cell injury caused by ischaemia and reperfusion. SL 59.1227 is a novel imidazolypiperidine Na+/H+ antiport inhibitor which is structurally unrelated to previously described acylguanidine inhibitors such as cariporide. Recovery of pHi following an intracellular acid load was measured in CCL39-derived PS120 variant cells, selectively expressing either NHE1 or NHE2 isoforms of the Na+/H+ exchanger. pHi recovery was potently and selectively slowed by SL 59.1227 in NHE1-expressing cells (IC50 3.3±1.3 nM) versus NHE2-expressing cells (2.3±1.0 ,M). The respective IC50 values for cariporide were 103±28 nM (NHE1) and 73±46 ,M (NHE2). In anaesthetized rats following left coronary artery occlusion (7 min) and reperfusion (10 min) SL 59.1227 (10,100 ,g kg,1 min,1 i.v.) inhibited ischaemia-mediated ventricular tachycardia (71,100%) and reperfusion-induced ventricular fibrillation (75,87%) and prevented mortality. Bolus i.v. administration of SL 59.1227 (1 mg kg,1) produced anti-arrhythmic effects when administered either before or during ischaemia. Cardiac infarct size was determined in anaesthetized rabbits following left coronary artery occlusion (30 min) and reperfusion (120 min). Infarct size measured as a percentage of the area at risk was 36.2±3.4% (control group) versus 15.3±3.9% (SL 59.1227 0.6 mg kg,1 i.v.). SL 59.1227 is the first example of a potent and NHE1-selective non-acylguanidine Na+/H+ exchanger inhibitor. It possesses marked cardioprotective properties. British Journal of Pharmacology (2000) 131, 1188,1194; doi:10.1038/sj.bjp.0703671 [source]