Influence of influenza viral infection on airway smooth muscle activity.

The contractility of airway smooth muscle (ASM) plays an important role in pathophysiology of several bronchial disorders. Increased contraction of ASM during asthma and respiratory viral infection has been attributed to the release of mediators acting through different receptors. In the present study, influence of influenza type A virus (H1N1) infection has been examined on ASM responsiveness to various bronchoactive agents e.g. adenosine, histamine, 5-hydroxytryptamine (5-HT) and isoproterenol in an organ bath set up for isolated tissue preparation. The contractile effect of adenosine, histamine and 5-HT was enhanced, however, relaxant response of isoproterenol was attenuated with the duration following viral exposure. The most prominent response was observed 48 to 72 hr after infection and tissues from multiple exposure to virus infected animals showed the maximum contractile response. Results demonstrated the deleterious effect of viral infection on ASM function and the findings will be helpful in understanding the mechanism of influenza virus induced bronchoconstriction.

Hypotensive effect of intracerebroventricular injection of norepinephrine and its modulation by alpha and beta adrenergic blockers in conscious rabbits.

The present study was designed to investigate the role of central adrenoceptors in the hypotensive effect of intracerebroventricular (ICV) injection of norepinephrine (NE) in conscious rabbits. Experiments were carried out on 19 adult rabbits (oryctolagus cuniculus) of either sex. A dose-dependent hypotensive response to ICV injection of NE was observed with no significant change in heart rate. The hypotensive response of NE was blocked 74.2 +/- 0.7% by yohimbine (alpha-2 adrenergic blocker), and 25.0 +/- 0.5% by metoprolol (beta-1 adrenergic blocker). NE response was not affected either by prazosin or butoxamine (alpha-1 and beta-2 adrenergic blockers respectively). The results suggest that the dose-dependent hypotensive response of ICV administered NE is mediated through alpha-2 and beta-1 central adrenoceptors.

Cardiovascular responses to phenylephrine during acute experimental anaemia in anaesthetized cats.

Experiments were performed on anaesthetized artificially ventilated cats to study the effects of phenylephrine (PE) on cardiovascular responsiveness, before and after induction of experimental anaemia. Acute anaemia was induced by replacement of blood by dextran in three steps of 20% each of total estimated blood volume. The effect of PE (20 micrograms/kg) was investigated at four stages: control and after 1st, 2nd and 3rd exchanges of blood. Induction of anaemia produced a significant increase in heart rate (HR) and cardiac output (CO) and a decrease in right atrial pressure (RAP). No significant change in mean arterial pressure (MAP), LV dP/dt max and blood gas tension was observed. Administration of bolus dose of PE produced a rapid rise in MAP, LVdP/dt max, and a decrease in HR without a change in the RAP. The pattern of response to PE was similar after induction of acute anaemia, however the magnitude of the response was significantly reduced. The attenuation in the response to PE was related to the fall in the haematocrit (HCT) level. This shows that induction of experimental anaemia, produced an increase in CO due to an increase in HR and SV and the effect of PE on cardiovascular responsiveness was significantly attenuated. The reduced sensitivity to PE during acute anaemia could be due to many factors such as inadequate O2 supply, effect of local vasodilating agents or some other cardiotonic agents which are known to contribute to vascular responsiveness.

Cardiovascular responses to phenylephrine and sodium nitroprusside during acute coronary occlusion in dogs.

The effects of administration of pressor agent phenylephrine (PE) and depressor agent, sodium nitroprusside (SNP) (10-40 micrograms/kg) on arterial blood pressure (ABP) and heart rate (HR) were investigated during acute occlusion of left anterior descending coronary artery (LAD) in anaesthetized, artificially ventilated dogs with and without the influence of selective blockade of autonomic nervous system (ANS). ABP response to PE was significantly (P < 0.05) attenuated following 4 hrs of LAD occlusion in all the four groups of animals. SNP response at higher dose (40 micrograms/kg) was also significantly (P < 0.05) attenuated 4 hrs after LAD occlusion in ANS intact, beta-blocked and atropinized groups. The bradycardia response to PE after LAD occlusion was abolished in vagotomized group while in the other three groups, it was significantly attenuated following 4 hrs of LAD occlusion. The tachycardia response to SNP was significantly (P < 0.05) attenuated 4 hrs after LAD occlusion in ANS intact and atropinized animals. The response was abolished in beta-blocked animals and no significant change occurred (P > 0.05) in vagotomized group. This study suggests that the cardiovascular reflex effects of PE and SNP are significantly attenuated following acute LAD occlusion. Blocking any of the components of ANS changed this responsiveness.