[Difference of sensitivity of the peripheral and splanchnic circulations to vasodilator agents].
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To elucidate the relationship between the haemodynamic changes and glucagon in cirrhosis, we infused physiologic and supraphysiologic doses of this hormone in conscious rats with portal hypertension due to biliary cirrhosis. Cardiac output and splanchnic organ blood flows were measured by the radioactive microsphere method before and 30 min after glucagon infusion at doses of 2, 5 and 10 ng/min. Serum glucagon increased from a basal level of 92 +/- 17 pg/ml (mean +/- S.E.) to 399 +/- 89, 1151 +/- 136 and 2064 +/- 328 pg/ml, respectively, in sham-operated rats, and from 743 +/- 75 pg/ml to 1497 +/- 197, 1583 +/- 356 and 2957 +/- 649 pg/ml, respectively, in cirrhotic animals at 2, 5 and 10 ng/min doses. In both groups, cardiac output did not change after glucagon infusion at 2 and 5 ng/min doses, suggesting that factors other than glucagon are primarily responsible for the systemic hyperdynamic circulation in cirrhosis. Portal tributary blood flow increased significantly after glucagon infusion in sham-operated rats by 34 and 65% at doses of 5 ng/ml and 10 ng/ml, respectively, and in cirrhotic rats by 29% at a dose of 10 ng/ml. However, portal tributary blood flow did not change after glucagon infusion at the physiologic dose of 2 ng/min. This study shows that glucagon infused at a physiologic dose does not increase splanchnic blood flow, although it increases portal tributary blood flow at supraphysiologic doses. The discrepancy between blood glucagon levels and splanchnic haemodynamic responses suggests that glucagon plays only a minor role and that other factors are primarily responsible for the hyperdynamic state of the splanchnic circulation in rats with biliary cirrhosis.
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To evaluate the influence of the technical problems experienced when scanning transabdominally, a comparison was made between transabdominal and intra-abdominal Doppler parameters of the aorta and the splanchnic arteries. Peroperative color duplex sonography of the abdominal aorta and the splanchnic arteries was performed on 25 patients who were undergoing abdominal vascular reconstructive surgery under stabilized standardised anaesthesia. Doppler samples and diameter measurements were taken of the aorta, celiac, common hepatic, splenic, superior and inferior mesenteric arteries, both trans- and intra-abdominally. Significantly higher velocities were recorded in the celiac artery during intra-abdominal examinations. There was a trend toward higher recorded velocities in the other vessels. There was also a significant difference in the diameter measurements of most of the vessels. The trans- and intra-abdominal results were not always equivalent. The differences were not due to technical aspects. Transabdominal duplex sonography is difficult and may not be completely accurate in detecting quantitative flow parameters in the splanchnic arteries.
Gastrointestinal complications following cardiopulmonary bypass (CPB) are associated with high mortality rates. The identification of prolonged CPB time and calcium administration as independent predictors of gastrointestinal complications suggests decreased splanchnic perfusion as a possible mechanism. To test this hypothesis, we evaluated splanchnic organ perfusion during CPB and after calcium chloride administration. Mongrel dogs were studied under anesthesia and were cannulated for bypass. CPB was begun at 37 degrees C, and the heart was fibrillated and vented. After 30 min, CPB temperature was reduced to 25 degrees C for 1 h with the heart arrested through cold crystalloid cardioplegia. After rewarming to 37 degrees C for 30 min, the heart was cardioverted, and CPB was weaned off. Calcium chloride (10 mg/kg) or saline was administered. Organ blood flow was determined with radiolabeled microspheres at baseline, during CPB, and after weaning from CPB. Splanchnic organ blood flow did not decrease during any phase of CPB. Calcium chloride administration after CPB had no effect on splanchnic organ blood flow. While gastrointestinal injury may result from CPB, this study suggests that the mechanism of injury is not decreased by splanchnic organ perfusion during bypass. While calcium chloride can cause pancreatic injury, the responsible mechanism is not calcium-induced hypoperfusion.
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