Hypovolemic shock, pancreatic blood flow, and pancreatitis (original) (raw)
1988, International journal of pancreatology
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/rain 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 < 0.0l), 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.
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Hemorheological and Microcirculatory Relations of Acute Pancreatitis
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Acute pancreatitis still means a serious challenge in clinical practice. Its pathomechanism is complex and has yet to be fully elucidated. Rheological properties of blood play an important role in tissue perfusion and show non-specific changes in acute pancreatitis. An increase in blood and plasma viscosity, impairment of red blood cell deformability, and enhanced red blood cell aggregation caused by metabolic, inflammatory, free radical-related changes and mechanical stress contribute to the deterioration of the blood flow in the large vessels and also in the microcirculation. Revealing the significance of these changes in acute pancreatitis may better explain the pathogenesis and optimize the therapy. In this review, we give an overview of the role of impaired microcirculation by changes in hemorheological properties in acute pancreatitis.
Impaired venous return causes circulatory failure in experimental pancreatitic shock in dogs
Intensive Care Medicine, 1989
The haemodynamic effects in the early phase of canine acute experimental pancreatitis (AP) were studied using a cardiac catheterization technique. AP was induced in anaesthetized dogs with an infusion of trypsin-sodium-taurocholate into the pancreatic duct. The initial haemodynamic measurements were performed after the preparation of the animal and 5 min after the induction of AP. Thereafter, pressure and volume parameters were measured at 10 min intervals. AP induced significant increases in heart rate, dP/dtma x and mean arterial pressure, but a decrease in Vm~x 5 min after the induction of AP. After the initial phase, the heart rate remained significantly increased, while constant and significant decreases of stroke volume, cardiac output, enddiastolic volume and end-diastolic pressure developed. The parameters of the contractility of the left ventricle were not affected to the same extent. It is suggested that the circulatory failure observed in AP, characterised by a prompt reduction of cardiac output, was primarily due to a heavy reduction in preload. This supports the theory that cardiac output is primarily affected by impaired venous return with consequently decreased preload rather than by a loss of ventricular contractility. Hence, the existence of a myocardial depressant factor in the early phase of experimental AP does not gain support from the present results.
1988
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.
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