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Biomedical subjects

J H Robert

Publications and source records attributed to J H Robert.

22 records · Page 2Linked to original sources

Steroids do not alter pancreatic blood supply in hypovolemic dogs: implications on steroid action in acute pancreatitis.

A recent report from our laboratory showed that pancreatic inflammation induced by hypovolemic shock can be explained to some extent by spoliation in pancreatic perfusion as revealed by electromagnetic flow determinations on the gastroduodenal artery (GDA). On the other hand, when given early in the course of hypovolemic shock, methylprednisolone sodium succinate (MPSS) alleviated pancreatic inflammation as evidenced by gross and histological findings. Five dogs (18-23 kg) were submitted to a 3-hour hypovolemic shock (mean arterial blood pressure, MABP = 50 mm Hg) and received during bleeding 35 mg/kg of MPSS over a 30 min period. Recordings of cardiac output (CO), MABP, regional blood flows in the GDA and superior mesenteric (SMA) arteries were taken every 15 min. The effect of MPSS was appreciated by comparing GDA flow variations in this group with those previously published of a control group comprised of 12 dogs submitted to 3 hours of hypovolemic shock without steroids; operative protocol was in all points similar in both groups. At no time were any significant changes noted when MPSS was added as far as CO and GDA flows were concerned. In other words, the beneficial action of steroids on hypovolemic pancreases cannot be explained by alteration in regional blood flow.

Acute Disease↗

Hypovolemic shock, pancreatic blood flow, and pancreatitis.

Electromagnetic blood flow determinations were carried out on the superior pancreatic duodena (SPDA), the splenic (SA) and the superior mesenteric (SMA) arteries and compared to cardiac output (CO, thermodilution technique) in 12 anesthetized dogs submitted to hypovolemic shock of various duration: 5 dogs underwent a one-hour and 7 a three-hour period of shock. A 50 mm Hg level of mean arterial blood pressure (MABP) was maintained throughout hypovolemia. Dogs were then reinfused. Control preshock values were 4.12 l/min for CO, 38.0 ml/min for SPDA, 405.9 ml/min for SA, and 963.6 ml/min for SMA. SPDA, SA and SMA flows expressed as % of CO amounted to 0.9, 9.8 and 23.4% respectively. No significant changes in SPDA and SMA flows were noted within the first hour of shock. However, from the end of the second hour on, both flows differed significantly (P less than 0.01), SMA increasing from -75.6% of its control value at the end of bleeding to -61.0%, and SPDA decreasing from -75.6 to -86.9%. Similar observations were made when respective flows were considered as % of CO. The SA behaved somewhat in an intermediate fashion. This relative spoliation in pancreatic blood supply as hypovolemia proceeds supports an ischemic etiology of acute pancreatitis (AP), which could account for some of the so-called idiopathic cases of AP.

Animals↗

Can serum and peritoneal amylase and lipase determinations help in the early prognosis of acute pancreatitis?

Serum and peritoneal amylase and lipase levels were determined at an early stage in 73 patients with acute pancreatitis confirmed by computed tomography (CT scan), surgery, and/or postmortem. Each patient was given an enzymatic score (ES), which reflects the predominance of the serum or peritoneal concentration of the two enzymes, as the case may be. This score can thus be either 0, 1, or 2; ES = 0 if neither enzyme is predominant in the peritoneal fluid, ES = 1 if amylase or lipase alone are predominant therein, and ES = 2 if both enzymes are predominant. This enzymatic score appears to be a good indicator of severity of disease, being as it is directly and significantly related to mortality rate, prognostic score as proposed by Ranson, and incidence of extrapancreatic spreads as demonstrated by CT scan. In 38 patients (including two fatalities) with an enzymatic score of 0 or 1, mortality was 5%, whereas in 35 patients (10 fatalities) with ES = 2, mortality was 29% (p less than 0.01).

Acute Disease↗