Search PubMed⌕ Search

Biomedical subjects

B Reichart

Publications and source records attributed to B Reichart.

At least 271 records · Page 15Linked to original sources
PubMed1993

[Initial experience with the NOVACOR left heart assist system in transition for heart transplantation at the Grosshadern Clinic].

We recently used an electrically powered left ventricular assist device (NOVACOR Corp., Oakland, Calif.) to support the circulation of a 17-year-old man with profound circulatory impairment. He had been regularly listed for cardiac transplantation previously because of dilated cardiomyopathy, and decompensated acutely with severe biventricular failure before a suitable donor heart became available. Isolated left ventricular support with the NOVACOR system provided adequate haemodynamics and recovery of right ventricular, hepatic and renal function. After 2 days of support, orthotopic heart transplantation could be performed successfully. Five days after transplantation he developed a massive cerebral haemorrhage during a hypertensive crisis of which he recovered completely after neurosurgery without any residuals. He ist currently doing extremely well some 14 months after transplantation.

Adolescent↗
PubMed1993

Cardiac inotropic as well as coronary and pulmonary artery actions of epinine in human isolated tissues.

The present study was aimed to characterize the effects of epinine, the metabolite of the p.o. active dopamine derivate ibopamine in human cardiovascular tissues such as myocardium, coronary artery and pulmonary artery. Isometric force of contraction was studied in electrically driven papillary muscle strips from nonfailing (brain death), moderately failing (New York Heart Association class II-III, mitral valve replacement) and terminally failing human myocardium (New York Heart Association class IV, heart transplants) as well as in auricular trabeculae (aortocoronary bypass operation). Epinine increased force development in a concentration-dependent manner. In comparison to isoprenaline, epinine had a significantly lower potency but a similar efficacy to enhance force of contraction. Depending on the degree of myocardial failure, the effectiveness of epinine was reduced, whereas the potency was similar. Only in nonfailing myocardium, epinine increased force of contraction as effectively as Ca++. Prestimulation with forskolin or milrinone enhanced the potency of the epinine-mediated inotropic effect. In contrast, the beta-1-selective antagonist CGP 207.12A [2-hydroxy-5-(2-(hydroxy-3-(4-((1-methyl-4-trifluoromethyl)-1-H-imidazol -2-yl)-phenoxy)-propyl)-aminoethoxyl)-benzamide] and the beta-2-selective antagonist ICI 118.551 [erythro-(+-)-1-(7-methylindan-4-yloxy)-3- isopropylaminobutan-2-ol-hydrochloride] shifted the concentration-response curve of epinine significantly to the right, indicating action at both beta-2 and beta-1 adrenoceptors. Epinine exerted higher affinity at beta-2 compared to beta-1 adrenoceptors in radioligand binding experiments ([125I]iodocyanopinodolol). In human coronary artery rings and pulmonary artery rings epinine alone as well as epinine in the presence of propranolol initiated a concentration-dependent increase in tension development in precontracted (prostaglandin F2 alpha, 0.3 mumol/l) as well as in non-precontracted rings. These results suggest that epinine exerts no direct vasodilatory activity in human coronary and pulmonary arteries at concentrations which are capable to produce positive inotropic activity. The supposed beneficial effects of ibopamine in the treatment of heart failure may not be due to positive inotropic actions as the concentrations producing positive inotropy are much higher than the clinically observed plasma concentrations.

Adenylyl Cyclases↗
PubMed1993

Successful restoration of cell-mediated immune response after cardiopulmonary bypass by immunomodulation.

The objectives of this prospective randomized trial were to quantify immunosuppressive effects of cardiopulmonary bypass, to identify mechanisms responsible for postoperative immunosuppression, and to investigate the effects of immunomodulatory intervention on these mechanisms. Sixty patients were studied after cardiopulmonary bypass. Immunomodulatory therapy consisted of the cyclooxygenase inhibitor indomethacin, which blocks the downregulating agent prostaglandin E2, and thymopentin, which enhances T-lymphocytic activity. Twenty patients each received indomethacin either alone or combined with thymopentin. Twenty patients served as the control population. Our in vitro studies showed a decrease of CD4+ helper/inducer T cells and interleukin-2 receptor expression on T lymphocytes, while CD8+ suppressor/cytotoxic T cells and monocytes increased. Additionally, a depression of interleukin-1 and interleukin-2 synthesis as well as concurrent low gamma-interferon serum concentrations could be documented. These results indicate a downregulation of cell-mediated immune response. As an in vivo correlate of the immunomechanistic alterations, patients demonstrated an impaired delayed-type hypersensitivity response to an antigen skin test battery. These changes in immunoreactivity could be successfully counteracted by the combined immunomodulatory regimen, whereas sole indomethacin treatment could only partially restore depressed host defense parameters. With this study we could demonstrate for the first time that human lymphocytic interleukin-2 synthesis, which represents the key event among forward regulatory immune mechanisms, can be protected via in vivo immunoaugmentatory therapy and that this therapy can successfully counteract immunosuppressive effects of cardiopulmonary bypass.

Aged↗
PubMed1992

[Surgical therapy of congenital cardiovascular abnormalities. Palliation, correction, transplantation].

Thanks to new and further developments of surgical procedures, it has now become possible to provide surgical treatment for any form of congenital heart defect. For some procedures, however, long-term results are not yet available. In this review, currently accepted basic principles of modern surgical treatment of congenital heart disease are discussed. On the basis of the most common anomalies, the various surgical techniques (palliation, correction and heart transplantation) are considered.

Heart Defects, Congenital↗
PubMed1992

Allogeneic heart transplantation following xenogeneic bridging.

Xenografting seems to be a solution to bridge the time intervals when an essential allograft cannot be obtained. A subsequent allograft was never tried. Eight dogs (20-24 kg) of 2 years of age underwent right cervical heart transplantation. Donors were silver foxes (3-4 kg). The animals were treated by triple drug therapy consisting of cyclosporin A, methylprednisolone and azathioprine in clinical dosages. For control, six recipients received allogeneic heart transplantation (AHTP) and the identical immunosuppression. After rejection of the xenograft, a second allogeneic heart was anastomosed to the same right cervical vessels. Routine histology and immunohistology were performed. Thromboxane B2 and 6-keto-prostaglandin Fla were determined daily in peripheral blood. After final rejection sensitization of the recipient was controlled by haemagglutination tests. Survival times of the xenografts were 9.6 +/- 1.2. The subsequent hearts under the same therapy beat for 4.5 +/- 5.0 days. The average survival time of control hearts was 18 +/- 1.9 days. The five hyperacute second allografts showed signs of humoral rejection by absence of inflammation. The release of thromboxane B2 was different in hyperacute, accelerated or cellular rejection. In contrast to the long-functioning grafts, thromboxane B2 persisted during hyperacute rejection at a high level. However 6-keto-prostaglandin Fla showed no significant differences between long-time survivors and hyperacute rejecting hearts. After xenogeneic transplantation all recipients showed haemagglutinating titres between 1:4 and 1:16. Allogeneic grafts have different kinetics of rejection following xenogeneic heart transplantation (XHTP) compared with control hearts. Thromboxane B2 seems to be an important mediator in hyperacute rejection. This type of rejection is not associated with a change in 6-keto-prostaglandin Fla levels. These results indicate, that xenogeneic bridging under a common immunosuppressive regimen could lead to accelerated rejection of the following allograft. Under this condition clinical bridging is not advisable.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Changes in lymphocyte subsets and mitogen responsiveness following open-heart surgery and possible therapeutic approaches.

Septic multi-organ failure represents a common cause for operative mortality following open-heart surgery. One major reason might be the depression of cell-mediated immunity. The purpose of this prospective randomized trial was to quantify and specify the effects of open-heart surgery on cell-mediated immune mechanisms. In addition, the immunorestorative potential of a combined immunomodulatory therapy with the cyclooxygenase inhibitor indomethacin and the thymomimetic substance Thymopentin versus single drug administration of indomethacin was investigated. Twenty patients were given indomethacin for the first 5 postoperative days (group A). Another 20 patients also received Thymopentin perioperatively and on the second and fourth postoperative days (group B), while 20 patients underwent conventional therapy (group C). Cell-mediated immune response was quantified in vitro by measuring CD3+ T-lymphocytes and their subsets, CD4+ T-helper and CD8+ T-suppressor cells. Lymphocyte responsiveness to a specific (Antigen-Cocktail) and non-specific mitogen (phytohemagglutinin) provided information about the quality of cell-mediated immune response. On the first postoperative day CD3+ T-lymphocyte counts and Antigen-Cocktail-induced lymphocyte proliferation decreased significantly in all groups. The number of CD4+ T-Helper cells fell significantly only in groups A and C, while the decrease in group B was not statistically significant; the same applied to phytohemagglutinin-induced lymphocyte response. The CD4+/CD8+ ratio was significantly depressed only in group C, decreased slightly in group A and did not change as compared to baseline values in group B. All investigated parameters remained significantly depressed until the seventh postoperative day in group C.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Operation of acute dissecting aortic aneurysm in the 25th week of pregnancy using hypothermic extracorporeal circulation].

We report on a 24 + 2 weeks pregnant woman with Marfan's syndrome, who acutely developed a dissecting aortic aneurysm with aortic valve insufficiency. Emergency surgery was performed by using hypothermic extracorporeal circulation, whilst the aortic valve and ascending aorta were replaced by a synthetic graft. Foetal heart rates, continuously monitored by using Doppler ultrasound, were shown to be closely correlated with perfusion pressures. By applying perfusion pressures of 90-100 mmHg, we were able to maintain foetal heart rates of approximately 100/min. During the first postoperative day, the CTG was normal for gestational age and no contractions were noted. During the second postoperative night, the patient prematurely delivered a dead 820 g infant (Apgar score 0/0/0/0). In view of this case report, opportunities and problems associated with an application of extracorporeal circulation during pregnancy are discussed.

Adult↗
PubMed1992

Isolated presynaptic inotropic beta-adrenergic supersensitivity of the transplanted denervated human heart in vivo.

BACKGROUND: The regulation of contractility of the transplanted heart depends on circulating catecholamines resulting from cardiac denervation. Supersensitivity to circulating catecholamines may result from loss of presynaptic neuronal uptake or upregulation of postsynaptic beta-adrenergic receptors. METHODS AND RESULTS: Dose-response curves using the beta-adrenergic receptor agonists isoprenaline (no neuronal uptake) and epinephrine (neuronal uptake) were performed in vivo. The inotropic response was measured echocardiographically as the increase of fractional shortening (delta FS) and the increase of the systolic pressure/dimension ratio (delta P/D). The inotropic response to increasing doses of isoprenaline (5-20 ng/kg.min) was identical in 36 heart transplant recipients compared with 13 control subjects: delta FS during 20 ng/kg.min isoprenaline amounted to 18.2 +/- 6.2% versus 17.4 +/- 4.0% (NS) and delta P/D to 2.3 +/- 1.2 mm Hg/mm versus 2.2 +/- 0.5 mm Hg/mm (NS), respectively. A vagally mediated indirect negative inotropic effect in the innervated hearts was excluded by identical inotropic responses to isoprenaline in control subjects without and after atropine pretreatment. The inotropic response to increasing doses of epinephrine (10-40 ng/kg.min) was significantly augmented in 13 heart transplant recipients compared with 11 control subjects: delta FS during 40 ng/kg.min epinephrine amounted to 19.9 +/- 2.6% versus 8.6 +/- 2.0% (p less than 0.001) and delta P/D to 2.3 +/- 0.9 mm Hg/mm versus 0.6 +/- 0.3 mm Hg/mm (p less than 0.001), respectively. Pretreatment with desipramine (blockade of neuronal uptake) in control subjects resulted in a significantly increased inotropic response: delta FS during 40 ng/kg.min epinephrine amounted to 17.6 +/- 3.6% (p less than 0.001 versus untreated controls, NS versus heart transplant recipients) and delta P/D to 1.7 +/- 0.8 mm Hg/mm (p less than 0.001 versus untreated controls, NS versus heart transplant recipients). CONCLUSIONS: These findings provide evidence against a postsynaptic inotropic supersensitivity or subsensitivity of the beta-adrenergic receptor-effector system of the transplanted denervated human heart in vivo. However, a marked presynaptic inotropic supersensitivity is present because of denervation-associated loss of neuronal catecholamine uptake.

Adult↗
PubMed1992

[Incidence, prevention and therapy of cytomegalovirus and pneumocystis carinii infection after heart transplantation].

Diseases caused by cytomegalovirus (CMV) and pneumonia due to pneumocytis carinii (PCP) are problematic complications after allogeneic heart transplantation. Recipients of CMV-seropositive donors have a higher morbidity of CMV. By using an anti-CMV-immunoglobulin preparation in routine prophylaxis the incidence of CMV disease after heart transplantation could be reduced significantly. Ganciclovir 10 mg/kg is administered for treatment of CMV disease for at least 14 days. Recent investigations show that a prophylactic administration of ganciclovir after heart transplantation is safe, and it reduces the incidence of CMV-induced illness in CMV-seropositive patients. The incidence of PCP after heart transplantation varies according to the literature between 1 and 13%. The onset of the disease is located mostly between the third and the fifth month after heart transplantation. An effective prophylaxis can be achieved by low dose cotrimoxazole (960 mg at two days per week in adults) within the first six postoperative months. Cases of PCP are treated by cotrimoxazole or pentamidine and are associated with a mortality up to 60%.

Antibodies, Fungal↗
PubMed1992

[Return of circadian blood pressure and heart rate changes in patients with heart transplants].

A loss of the circadian rhythm pattern of blood pressure (BP) and heart rate, as well as the development of hypertension have been found after heart transplantation (Htx). To study whether a return of this rhythm occurs in the long-term after Htx, we used 24-h ambulatory monitoring to study 62 patients 5 days to 6.5 years after Htx. Patients were divided into two groups (Group 1: less than 6 months after Htx (n = 30), Group 2: 6 months or more after Htx (n = 32)). Group 2 had a higher BP and heart rate, as well as a significantly higher difference between systolic day and systolic night BP than group 1. There was also a significantly higher difference in heart rate between day and night values in group 2. The return of the circadian rhythm pattern in the longer term after heart transplantation may result from partial reinnervation of the heart, although other neurohumoral factors or concomitant medication may play a role.

Adrenergic beta-Agonists↗