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Plasma levels of ANP (pg/ml; radioimmunoassay) as a parameter for postischemic dysfunction and levels of Troponin T (TnT) (ng/ml; ELISA test) as a parameter for postischemic cellular damage were determined in 15 patients with coronary artery disease (CAD) (mean age: 58 +/- 6.1 years; 13 m, 2 w; with no history of myocardial infarction and no signs for congestive heart failure) prior to, during and after extracorporal circulation (ECC). Under standardized conditions during the ECC basic parameters concerning the cardial hemodynamic (heart rate (HR); systolic (RRsys, mmHg), diastolic pressure (RR dia, mmHg) central venous pressure (CVP, mmHg); left atrial pressure (LAP, mmHg); left ventricular enddiastolic pressure (LVEDP, mmHg)) and ECG monitoring blood samples were performed: 1) prior to operation (op); 2) prior to CPB; 3) 1 h CPB; 4) 5 min after CPB; 5) 1 h after CPB; 6) 6 h postoperative (postop); 7) 24 h postop; 8) 48 h postop; 9) 10 days postop. Also the left atrial diameter (LAD, mm) and the left ventricular enddiastolic diameter at Q (LVEDD, mm) pre- and postop were documented with m-mode echocardiography (Echo) and ejection fraction (EF, %) was calculated. The bypass operations were performed with intermittent aortic cross-clamping with open venae cavae (CVP: 0-5 mmHg) and moderate hypothermia. For the determination of ANP levels and TnT levels in arterial and venous blood, a double-antibody (AB) radioimmunoassay and an ELISA test were used. Concerning the patients with CAD there was a maximal increase of ANP from preoperative 90 +/- 10 (M +/- SEM) pg/ml (p < 0.05) up to intraoperative 380 +/- 38 pg/ml. Ten days postop, the ANP level was with 262 +/- 33 pg/ml still increased threefold in comparison to the preoperative level. TnT showed an increase from preoperative 0.02 +/- 0.01 ng/ml up to intraoperative 3.44 +/- 0.47 ng/ml. Ten days postop the TnT concentration was at the preoperative level with 0.13 +/- 0.11 ng/ml. Five minutes after bypass up to 48 h postop, ANP and TnT levels were correlated (p < 0.05, r = 3.4). There was an increase of the LAD from preoperative 42.2 +/- 1.1 mm up to 46.8 +/- 1.2 mm (p < 0.05) 10 days postop as determined by m-mode echo. LVEDD and EF changed from preoperative 51.1 +/- 0.9 mm and 73 +/- 2% to 54.5 +/- 1.2 mm and 65 +/- 4% 10 days postop. The significant increase of TnT (172-fold) indicates the cellular, myocardial injury, caused by the operation without signs in ECG recordings and no signs of congestive heart failure. The significantly increased ANP level up to the 10th day postop indicate sa very sensitive prolonged, postischemic dysfunction, which is not compensated 10 days postop.

The clinical clues of sudden arterial hypertension, acute pain in the side, proteinuria, hematuria, abdominal bruits and renal failure are suspicious for spontaneous dissection of the renal arteries, even in the absence of one or more of the above-mentioned symptoms. To confirm the diagnosis and to provide appropriate therapy, immediate renal arteriography is mandatory, otherwise acute loss of renal tissue may occur. We report on one patient with spontaneous dissection of the renal arteries.

210 patients receiving antihypertensive treatment underwent non-invasive ambulatory blood-pressure monitoring for the first time. 44 suffered from chronic renal failure, 51 had been renal transplanted, 36 had chronic glomerulonephritis, 36 had renovascular hypertension, and 43 had essential hypertension with severe end-organ damage. We analyzed the Circadian rhythm and the rate of insufficient antihypertensive treatment. While mean daytime systolic and diastolic blood pressure were not different between groups, patients with chronic renal failure, renal transplant or glomerulonephritis showed a very high rate (95-72%) of absent nighttime blood-pressure reduction. In patients with renovascular hypertension or complicated essential hypertension there was a lower rate (69-40%) of absent nighttime blood pressure reduction. The ambulatory blood-pressure monitoring led to a modification of antihypertensive treatment in 78% of patients because of nighttime hypertension. We think that ambulatory blood-pressure monitoring is an essential tool for physicians treating patients with renal disease or complicated essential hypertension.

Plasma levels of human atrial natriuretic peptide (ANP) were measured in 10 patients with mild essential hypertension (EH) (WHO I). The renin-angiotensin-aldosterone-(RAA) system and ANP were investigated in a sequential study without treatment and under administration of a cardioselective beta-blocker (betaxolol). We analyzed the RAA system and ANP under conditions of volume loading induced by 2000 ml saline and volume depletion induced by 40 mg furosemide iv. Volume depletion induced a stimulation of the RAA-system but the ANP levels decreased from 87 +/- 13.6 to 55 +/- 7.6 pg/ml. Volume loading induced a suppression of the RAA-system but caused a rise of ANP from 47 +/- 12 pg/ml to 133 +/- 30 pg/ml. Under application of betaxolol the RAA system was suppressed and ANP levels were increased, but physiological volume regulation was maintained. Although blood pressure and heart rate were lowered under administration of betablockers, the ANP levels were increased. These results suggest that increased ANP in plasma under administration of betaxolol may play a role in compensatory mechanisms in response to beta-adrenergic blockade.

There have been only a few investigations that have considered renal disease or any disturbance of renal function in the calculation of risk in cardiac surgery. Risks of cardiac surgery have to be considered for renal disease without direct connection to heart disease (e.g., infections of the kidney and of the urinary tract, primary and secondary glomerulonephritis, parenchymal renal disease, and impaired renal function of unknown origin), as well as in renal disease with concomitant influence on heart and kidney (e.g., infective endocarditis, arterial hypertension, systemic disease of heart and kidney such as with diabetes mellitus, disturbance of kidney function or electrolyte balance due to heart failure). In most cases, the problem is solved by therapeutic intervention and postponement of cardiac surgery. A limited or negative operative indication is found with untreatable infection of the kidney or urinary tract, with untreatable nephrotic syndrome, in advanced renal disease with heart transplantation, as well as in case of severe arterial hypertension with possible organ complications, and in advanced diabetes mellitus with ESRD and multiorgan involvement. After cardiac surgery, acute renal failure represents a critically important complication. Primary therapeutic procedures must include prophylaxis of hemodynamic unstable situations, as well as prophylaxis of infectious complications. Cardiac surgery in dialysis patients and post-transplant patients is basically possible and only has a slightly increased risk compared to patients with normal renal function. Seventy-seven dialysis patients were operated (49 aorto-coronary bypass operations, 19 single-valve and multiple-valve replacements, five patients with valve replacement and aorto-coronary bypass, and four other cardiac surgical operations). Only in valve replacement, was mortality significantly higher than in renal healthy persons, the main causes of death being cerebrovascular complications and septicemia.

After suicidal ingestion of 9 g Propafenone, a 31-year-old woman showed unconsciousness, cerebral convulsions, respiratory depression, sinus arrest, ventricular tachycardia and recurrent atrioventricular block. The maximum Propafenone plasma level was 4,702 ng/ml. Only 67.2 mg of Propafenone were eliminated within 4 h of hemoperfusion. Successful therapy could be achieved by symptomatic intensive care treatment. Additionally, 2 X 25 ml of 20%-saline solution were infused. In this case no efficacy of hemoperfusion in the treatment of Propafenone intoxication could be documented.

The physiological role of inactive renin, especially the question of whether and how a conversion to active renin takes place in vivo, remains controversial. In order to show the dynamic alterations from inactive to active renin following acute ACE-inhibition, both forms of renin were investigated in both renal veins and the peripheral circulation of 20 patients with essential hypertension and 20 patients with renovascular hypertension before and 1 h after 25 mg of captopril. Active and inactive renin were determined indirectly as plasma renin activity (PRA, unit: ng/ml x h). In vitro activation of inactive renin was achieved with trypsin (1 mg/ml plasma), followed by a further determination of PRA (= total renin). Subtraction of the active renin from the total renin yields the amount of inactive renin. In patients with essential hypertension, the mean values of active renin increase equally in both renal veins (1.4 and 1.3 before, 1.9 and 1.8 after captopril) and the peripheral circulation (0.9 and 1.3) (p less than 0.002), whereas the inactive renin decreases correspondingly. Renal veins: 7.6 and 8.2 before, 7.2 and 7.6 after captopril; peripheral circulation: 7.7 before and 7.0 after captopril (p less than 0.05). In all patients with renovascular hypertension, there is basally a marked lateralization of active renin (6.4 vs 3.5; p less than 0.01) and inactive renin (20.5 and 18.9, p less than 0.03) towards the side of the ischemic kidney. After captopril, the values for total renin and active renin increase (p less than 0.001), and the side difference for active renin becomes still more pronounced (33.0 vs 14.2; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Digitalis therapy is frequently accompanied by adverse drug reactions. Severe digitalis intoxications are still a problem. Therapeutical methods, which could be used in the case of a life threatening digoxin intoxication, are known, but not yet generally available. Hemodialysis has only a minor effect on digoxin excretion. This study was planned to test the hypothesis that hemoperfusion across dextran-cocoated charcoal or the resin Amberlite XAD 4 could be more effective in the therapy of digoxin intoxications. The ability of hemoperfusion to eliminate digoxin was tested in a patient who had to undergo treatment beacuse of a severe bromcarbamide intoxication. Additionally we compared the effect of several modifications on this method in 12 dogs, which had received 0.05 mg/kg body weight per day for three days prior to the experiment. Although hemoperfusion across Amberlite XAD 4 may eliminate as much digoxin as normal human kidneys during the few hours of treatment, the amount of digoxin removed after all is only a small percentage of the total body pool. Thus compared to the risks of hemoperfusion as an invasive treatment its effect is small. According to our results, hemoperfusion cannot be recommended as a standard therapy of severe digoxin intoxications.