[Cardiovascular complications of pancreatis diseases]. / Pancreasbetegségekhez társuló cardiovascularis eltérések.

Under physiological conditions, the pancreas scarcely influences the function of the cardiovascular system, although the hormones produced in the healthy pancreas (insulin, glucagon and somatostatin) affect the myocardial contractility in pharmacological doses. Among the diseases of the pancreas, the pancreatic tumours (insulinoma, glucagonoma and vipoma), furthermore the acute and chronic pancreatitis involve cardiovascular complications, which influence the outcome of the disease. Although the clinical picture is dominated by the metabolic changes of the excessively produced hormones in pancreatic tumours, the cardiac and vascular effects of the hormones may be considerable. In acute necrotizing pancreatitis, enzymes released from the pancreas and inflammatory mediators transform acute necrotizing pancreatitis into "multiple organ disease"; one of the important forms of this disease is the cardiovascular shock syndrome. One of the best-known complications of chronic pancreatitis is the pancreoprive diabetes mellitus, and beside that other, nonspecific cardiac alterations (e.g. ECG-changes) may occur.

Acute myocardial infarction enhances the portal venous histamine level in dogs.

OBJECTIVE AND DESIGN: The aim of our experiments was to determine the plasma histamine level in the portal venous (VP) blood during acute coronary occlusion and reperfusion. SUBJECTS: 27 adult mongrel dogs of either sex were randomized for three groups: sham-operated controls, occlusion group (group O) and reperfusion group (group R). TREATMENT: The left circumflex coronary artery (LCx) was proximally occluded and the occlusion was maintained during 6 h (group O), or after a 60-min occlusion the LCx was reperfused (group R). The portal vein was cannulated to take blood samples for hormone measurements. METHODS: The plasma histamine concentrations were measured with the radioenzymatic method. RESULTS: The VP plasma histamine level was significantly increased 60 min after the LCx occlusion in groups O (99.9 +/- 40.2 vs. 252.9 +/- 100 pg/ml, mean +/- SD) and R (101.2 +/- 55.1 vs. 179.8 +/- 96 pg/ml), and remained high in group O (240.4 +/- 81 pg/ml), while 2 h after LCx reperfusion it had decreased to the basic level. There was no correlation between the hemodynamic parameters and the portal vein plasma histamine levels. CONCLUSIONS: Histamine is released into the gastrointestinal tract during acute myocardial ischemia and reperfusion, but the release of the vasoactive drug has no effect on systemic hemodynamics.

Cardiac manifestations in primary Sjögren's syndrome.

OBJECTIVE: To determine cardiac manifestations in primary Sjögren's syndrome (SS). METHODS: Echocardiographic examination was undertaken in 64 patients (62 women, two men) with primary SS (54 definite (DSS) and 10 probable (PSS)) who had systemic symptoms. Twenty one healthy women volunteers of similar age acted as controls. RESULTS: Acute exudative pericarditis occurred in only one patient. An echogenic pericardium was demonstrated in 21 patients (19 DSS, two PSS) (33%) who had a previous symptom free pericarditis, but in none of the controls. Pulmonary pressure was significantly greater in the patients than in the controls (31 (SD 8) mm Hg compared with 24 (7) mm Hg), but there was no significant difference between the DSS and PSS groups. Left ventricular (LV) systolic function was similar in patients and controls. Twenty two patients (20 DSS, two PSS) and one control subject were excluded from LV diastolic function evaluation because of conditions likely to influence the parameters. Of the remaining 42 patients with SS (34 DSS, eight PSS), 21 (17 DSS, four PSS) had impaired diastolic function, confirmed by several diastolic parameters. LV diastolic dysfunction and echogenic pericardium occurred independently of each other, and there was no correlation between the occurrence of these silent cardiac abnormalities and the clinical and laboratory findings. CONCLUSIONS: Obvious cardiac involvement is rare in primary SS, but clinically silent manifestations (symptom free pericarditis and LV diastolic dysfunction) are common. The clinical and prognostic significance of these changes cannot yet be defined.

Noninvasive monitoring of hemodynamic changes in acute pancreatitis in rabbits.

Hemodynamic parameters of experimental acute necrotizing pancreatitis (AP) were monitored by means of echocardiography in rabbits. Left ventricular (LV) systolic and diastolic parameters were determined before and 1, 3, 6, 12, 18, and 24 hr after injection of taurocholic acid in the pancreatic duct in AP animals. Temporary LV dilatation was observed 6 hr after the AP induction [LV end-diastolic (ED) diameter from 1.16 +/- 0.04 to 1.22 +/- 0.04 cm, P < 0.05, ED volume from 2.98 +/- 0.34 to 3.57 +/- 0.75 ml, P < 0.05] without decrease in systolic function. Cardiac output (CO) and stroke volume (StV) was increased in both groups 3 hr after the operation (from 0.53 +/- 0.15 to 0.71 +/- 0.06 L/min, P < 0.05 in AP), but in the AP animals it remained high. However, 24 hr after AP induction, both the CO and the StV were decreased significantly. The LV diastolic function was impaired 1 hr after AP induction, but had recovered after 12 hr. In conclusion, an early diastolic impairment followed by LV enlargement could be noninvasively observed in experimental AP in rabbits.