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Hepatic microvascular effects of terbutaline in experimental cardiogenic shock in rats.

1. Experimental myocardial infarction was produced in rats by direct electrical cauterization of the myocardium of left ventricle. This produced cardiogenic shock with the accompanying haemodynamic changes of low cardiac output, low mean arterial pressure, raised central venous pressure and an absence of cardiac arrhythmias. 2. The liver microcirculation was observed using in vivo television microscope method. The diameter and erythrocyte flow velocity in the liver sinusoids were measured quantitatively. 3. During experimental cardiogenic shock 80% of the liver sinusoids were constricted; the remaining 20% showed dilatation. In all these liver sinusoids the erythrocyte flow velocity was only 50% of the pre-shock level. 4. Intravenous injection of the selective beta 2-adrenoceptor agonist terbutaline (0.15 mg/kg) restored the systemic arterial pressure to pre-shcok levels and partially raised the cardiac output. In the liver microcirculation terbutaline restored both constricted and dilated liver sinusoids to pre-shock calibres, but only partially raised erythrocyte flow velocity. 5. It is proposed that during experimental cardiogenic shock, terbutaline produces dilatation in the terminal liver microcirculation by opening sphincters of liver sinusoids and restores sinusoid diameters to pre-shock calibres. Therefore, terbutaline has the capacity to decrease peripheral resistance and unload the circulation during cardiogenic shock.[1]

References

  1. Hepatic microvascular effects of terbutaline in experimental cardiogenic shock in rats. Koo, A., Tse, T.F., Yu, D.Y. Clin. Exp. Pharmacol. Physiol. (1979) [Pubmed]
 
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