Search PubMed⌕ Search

Biomedical subjects

Ulrich Sunderdiek

Publications and source records attributed to Ulrich Sunderdiek.

5 recordsLinked to original sources

Evidence for palliative enlargement of the right ventricular outflow tract in severe tetralogy of Fallot.

OBJECTIVE: If the pulmonary artery (PA) tree in patients with Fallot's tetralogy (TOF) is extremely hypoplastic, a shunt procedure may be difficult and not desirable because of side-effects. Moreover, the failing catch-up growth of the pulmonary annulus is well known. In patients with a severe form of TOF, we performed palliative transannular patching of the right ventricular outflow tract. The early and long-term follow-up was evaluated. METHODS: Eleven patients (93 days (10-245 days); 3.5+/-0.7 kg (2.5-4.3 kg)) had highly symptomatic TOF (Hb: 18+/-2g/dl, SO2: 68+/-11%); angiographic diameters: RPA: 4.1 mm (2.5-6.4 mm), LPA: 3.4 mm (1.6-7.0 mm), PA trunc: 4.4 mm (2.5-7.0 mm). All 11 underwent transannular enlargement of the right ventricular outflow tract without closure of the ventricular septum defect. A PA index (cross-sectional area of the pulmonary arteries to BSA) was used to compare pre- and postoperative data. For follow-up, the patients were repetitively examined clinically and echocardiographically. RESULTS: Preoperative PA index was 87+/-40 mm2/m2 (normal: 330+/-35 mm2/m2). Postpalliation angiograms (age: 10-14 months) demonstrated a significant catch-up growth in nine patients (PA index from 99+/-40 to 310+/-54 mm2/m2) and inadequate growth in two patients (PA index 63 and 115 mm2/m2). Perioperative mortality was zero. Ten patients (43 months; 6-105 months) underwent elective repair. Six patients received pulmonary homograft valves (6-15 years after repair) because of severe pulmonary valve insufficiency and severe RV dilation. COMPLICATIONS: One patient died 10 months postpalliation due to pneumonia, one patient received a pacemaker after repair and died (2 months post-repair) due to pacemaker failure, a 5-year-old patient died 1 month after repair due to sepsis. All eight long-term survivors (12-17 years) are in excellent clinical condition. Echocardiography revealed good RV function and near normal diameters at peak systolic pressures between 25 and 50 mmHg. Only one patient developed brady-arrhythmia; a pacemaker was implanted 8 years after repair and 2 years after homograft implantation. CONCLUSIONS: In a very severe form of TOF, palliative right ventricular outflow tract construction may provide the potential for complete repair. In the presented high-risk patient group, mortality was not related to the hypoplastic pulmonary arteries. Obviously, all patients need pulmonary valve implantation in the long run.

Constriction, Pathologic↗

[Protective effects of a delta-opioid-receptor agonist and an oxygen radical scavenger on postischemic hearts].

BACKGROUND AND PURPOSE: The cardioprotective effects of delta-opioid receptor agonists is mediated-at least in part-via oxygen radicals. Mannitol that is used in cardiac surgery because of its osmotic properties exerts its beneficial effects on stunned myocardium via scavenging hydroxyl radicals. The effects of a delta-opioid receptor agonist (D-Ala2-D-Leu5-Enkephalin [DADLE]), the radical scavenger mannitol and their combination on postischemic dysfunction in rabbit hearts were investigated. METHODS: Isolated, blood-perfused rabbit hearts were subjected to a 20-min global, normothermic, no-flow ischemia that was followed by a 60-min reperfusion. Systolic and diastolic ventricular function as well as coronary blood flow (CBF) were assessed. The hearts were assigned to one of four groups: 1. placebo (n = 6); 2. DADLE (n = 8; 430 nM); 3. mannitol (n = 7; 8.6 mM); 4. DADLE + mannitol (n = 7). RESULTS: Ischemic contracture in the DADLE and the mannitol group was significantly smaller compared with the placebo group. Contracture was smallest in the DADLE + mannitol group. The postischemic function in the placebo group was drastically reduced (p < 0.05), while it was best preserved in the DADLE + mannitol group. CBF and MVO(2) were changed similarly in all groups (n. s.). The external efficiency was significantly higher in the groups with DADLE and/or mannitol than in the placebo group. Both DADLE and mannitol exhibit cardioprotective properties. Combination of both substances exerts an additive, positive effect on the ischemic contracture. Noteworthy, the protective effects of DADLE during reperfusion were not antagonized by the oxygen radical scavenger mannitol. On the other hand, DADLE + mannitol did not augment the protective effects of the single substances during reperfusion, except for the isovolumic LVP(max). CONCLUSION: Both substances improve the postischemic systolic and diastolic function and the relation between cardiac work and oxygen needed for this work. Thus, both substances offer promising properties in the clinic.

Analgesics, Opioid↗

[The isolated rabbit heart: comparison between five different modifications].

BACKGROUND: The isolated heart as an experimental model has been firmly established for more than 100 years. MATERIAL AND METHODS: In this study, five modifications are compared: 1. modified Langendorff apparatus (LA) with modified Krebs-Henseleit (KH) solution a) not containing bovine serum albumin (BSA; n = 13) and b) containing BSA (n = 16), 2. LA with KH solution containing BSH and bovine erythrocytes (n = 14), 3. LA with support rabbit (n = 6), and 4. "working heart" preparation with KH solution, BSA and bovine erythrocytes (n = 16). In the latter modification, no balloon was inserted into the left ventricular cavity, i. e., systemic and coronary circuits were not separated from each other. After completion of the preparation and 20-min stabilization, hemodynamic and metabolic data were assessed while the hearts were contracting in the ejecting mode. Thereafter, protocols for different studies were performed that are not presented here. However, the stability of the modifications within their individual protocols is reported. RESULTS: The results suggest that hearts perfused with KH solution are well suited for short protocols. In spite of the additional costs and time, blood perfusion is required for long-lasting protocols or if changes in coronary flow are to be investigated. CONCLUSIONS: The working heart exhibits both the best function and stability at a relatively low experimental expenditure. Yet, it is not suited for studies where perfusion pressure needs to be changed independent of arterial pressure.

Animals↗

Preconditioning: myocardial function and energetics during coronary hypoperfusion and reperfusion.

BACKGROUND: Ischemic preconditioning (IP) is gaining more acceptance as a protective method in beating heart surgery. Yet it remains controversial whether preconditioning can attenuate myocardial dysfunction during reperfusion after severe coronary hypoperfusion. We examined this issue and also the issue of whether this protection is mediated by adenosine A1 receptors. METHODS: In isolated, blood-perfused rabbit hearts, the effects of IP (3 minutes of no flow ischemia and 8 minutes of reperfusion) during 30 minutes of coronary hypoperfusion and 60 minutes of reperfusion were investigated. In two groups (n = 8 each) with and without (control group) preconditioning, ventricular function was assessed by load-insensitive measures: slope of the end-systolic pressure-volume relation (Emax), slope of the stroke work/end-diastolic volume relation (Mw), and end-diastolic pressure-volume relation. External efficiency was calculated, and contractile efficiency was assessed using the reciprocal of the myocardial oxygen consumption-pressure-volume area relationship. To investigate the possible role of adenosine, the adenosine A1 receptor antagonist DPCPX (2.5 micromol/L) was administered before preconditioning in a third group (n = 7). RESULTS: The effects of hypoperfusion on systolic function, diastolic function (dP/dtmin, end-diastolic pressure-volume relation), external efficiency, and contractile efficiency were similar in both the IP and control groups. Lactate efflux was significantly reduced after preconditioning (p = 0.02). During reperfusion, recovery of systolic function and coronary flow were significantly improved in the IP group compared with controls: aortic flow, 85% versus 63% (p = 0.01); dP/dtmax, 91% versus 67% (p = 0.001); pressure-volume area, 97% versus 68% (p = 0.01); Emax, 74% versus 62% (p = 0.03); and Mw, 94% versus 84% (p = 0.04). Release of creatine kinase was reduced in the IP group, 9.6 +/- 1.3 U x 5 min(-1) x 100 g(-1) wet weight, versus controls, 12.7 +/- 2.7 U x 5 min(-1) x 100 g(-1) wet weight (p = 0.04). During reperfusion, contractile efficiency (p = 0.03) and external efficiency (p = 0.02) recovered better in preconditioned than in untreated hearts. Recovery was less pronounced in the DPCPX group compared with the IP group (p, not significant). CONCLUSIONS: The results, derived from load-insensitive measures, confirm that IP provides protection after episodes of severe hypoperfusion by attenuating systolic dysfunction without improving diastolic dysfunction and reduces the severity of anaerobic metabolism as well as ischemic injury. Contractile efficiency and external efficiency both indicate improved energetics after IP (oxygen utilization by the contractile apparatus). The protective effect, at least in part, is mediated by adenosine A1 receptors.

Animals↗