Why the study?
Does early cirrhosis of the liver alter vascular reactivity to norepinephrine in rats?
Does early cirrhosis of the liver alter vascular reactivity to norepinephrine in rats?
In early experimental cirrhosis, the peripheral vascular bed maintains its ability to constrict in response to norepinephrine, suggesting circulatory abnormalities are not due to vascular smooth muscle refractoriness.
Answers are grounded in this paper and cite their sources.
Preserved norepinephrine responsiveness in early cirrhosis rat models; leaves open vascular mechanisms of hypotension in human disease.
Vascular reactivity to norepinephrine was studied in rats with early cirrhosis of the liver and in control rats. Cirrhotic rats showed water and sodium retention but not ascites. Studies were performed in whole animals, isolated hindquarters, and isolated femoral arteries. Plasma catecholamine levels were measured by radioenzymoassay and their urinary metabolites by gas-liquid chromatography. Plasma norepinephrine was 331 +/- 49 pg/mL (mean +/- SEM) in control rats and 371 +/- 66 pg/mL in cirrhotic animals (p greater than 0.05). No differences in plasma epinephrine or dopamine were observed. Urinary excretion of catecholamine metabolites was increased in cirrhotic rats. These data suggest a moderate activation of the sympathetic nervous system. In basal conditions, cirrhotic rats showed lower mean arterial pressure than controls (101 +/- 4 vs. 116 +/- 4 mmHg (1 mmHg = 133.3 Pa); p less than 0.01). However, perfused hindlimb resistance was similar in cirrhotic and in control animals. In the whole animal and in the perfused hindquarter, the contractile response to norepinephrine was similar for control and for cirrhotic rats. The contractile response to norepinephrine exhibited by isolated femoral arteries was similar in those from cirrhotic and control rats. This indicates that the peripheral vascular bed has a well-maintained ability to constrict in response to norepinephrine, suggesting that circulatory abnormalities in early experimental cirrhosis are not caused by refractoriness of the vascular smooth muscle to norepinephrine.
No takes yet. Share an insight, caveat, or question.
Villamediana et al. (1988) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: