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Biomedical subjects

W Reichelt

Publications and source records attributed to W Reichelt.

72 records · Page 4Linked to original sources
PubMed1983

[Buprenorphine as a postoperative analgesic following halothane anesthesia. Hemodynamic and respiratory effects].

In 10 healthy patients, buprenorphine was given as the postoperative analgesic (dosage: peripheral venous injection of 5 microgram/kg BW) after traumatological interventions in the lower extremities, which had been performed under barbiturate-induced halothane anaesthesia. The haemodynamic investigations revealed that buprenorphine has only a minor effect on the high pressure system. In the area of the pulmonary circulation, there was a significant increase in mean pulmonary artery pressure from 15.9 mm Hg to 17.8 mm Hg (+12%), as well as an increase in pulmonary vascular resistance by 16.5%. These changes were most marked 30 to 60 min after the administration of buprenorphine. When 2-3 1 O2/min were administered, none of the patients had PaO2 values of less than 100 mm Hg. 60 min after the injection, the PaCO2 value increased from 33.7 mm Hg to a maximum of 43.9 mm Hg. In 3 patients, PaCO2 increased to more than 45 mm Hg. All patients with greater increases of PaCO2 also evidenced greater increases in the pulmonary vascular resistance. Altogether the haemodynamic changes after buprenorphine administration following halothane anesthesia were not very distinct. In individual cases, however, there were greater increases in PaCO2. The cause of this could involve the additive effects of premedication and anaesthesia medication, and possibly the pain level as well. Both the increase in pulmonary artery pressure and the increase in total pulmonary vascular resistance in these patients were due to hypercapnia (von Euler-Liljestrand mechanism).

Adolescent↗
PubMed1981

Total anomalous pulmonary venous connection: surgical treatment in 35 infants.

From 1973 through December 1980, 41 children with total anomalous pulmonary venous connection (TAPVC) were seen in our hospital, and 35 underwent surgery. The supracardiac type of TAPVC was found in 19 cases (46%), the intracardiac type in 6 infants (15%), the infracardiac type in 15 cases (37%), and the mixed type in one child (2%). Clinical and cardiac catheterization data demonstrated that children with the infracardiac type of TAPVC were referred very early in life and had the highest pulmonary artery pressures. Operation was performed in 35 cases, 15 of supracardiac, 6 of cardiac, 13 of infracardiac, and 1 of mixed type of TAPVC. Total in-hospital mortality was 39%, and was 28% in the operated children. The initial operative mortality of 71% in the years 1973 to 1975 has decreased to 18% in the last 5 years. Twelve of the surviving infants underwent re-catheterization showing excellent results. Only in one case, with additional aplasia of the left lung, did half-systemic pulmonary artery pressure persist. Corrective surgery offers the only chance of survival in most children with TAPVC. The operative risk can be reduced by increased surgical experience supported by optimal medical preparation of the patient. After adequate surgical correction long-term results appear to be excellent.

Age Factors↗
PubMed1981

[Prenalterol (CGP 7760 B), a new cardioselective beta 1-adrenoceptor-agonist (author's transl)].

The haemodynamic effects of the new selective beta 1-receptor-agonist prenalterol were investigated in two groups each of 8 patients. Dosages of 500 microgram/5 min and 100 microgram/1 min were given after direct closure of atrial septal defect under neuroleptanalgesia. Prenalterol 500 microgram/5 min increased cardiac index (37.5%), heart rate (19%), stroke index (16.2%), mean arterial pressure (26.5%) and dp/dtmax (84.5%) significantly. Total systemic resistance, total pulmonary vascular resistance and mean pulmonary pressure remained constant. Filling pressures of both ventricles decreased slightly but significantly. Maximal hemodynamic changes after infusion of 100 microgram/1 min prenalterol were half as great as with 500 microgram/5 min and occurred 3 min earlier. The haemodynamic action of prenalterol was rather long lasting. One hour after cessation of the drug-infusion there were still detectable haemodynamic effects. In contrast to investigations in awake patients there was a greater increase in heart rate, which is referred to influences on the vagal reflex caused by anaesthesia.

Adrenergic beta-Antagonists↗
PubMed1980

[The effects of dihydroergotamine on volume content and compliance of the extrathoracic capacitance vessels of man under anesthesia during extracorporeal circulation in hypothermia (author's transl)].

The influence of dihydroergotamine on volume content and compliance of the extrathoracic capacitance vessels during extracorporeal circulation was investigated. Compared with an untreated control group the compliance decreased (0.44 ml/mm Hg/kg b. wt.) and 490 ml of blood was mobilized and shifted from the circulation into the blood reservoir of the machine. Therefore DHE counteracts the effects of venous pooling.

Anesthesia, General↗
PubMed1980

[The effects of dihydroergotamine on the circulatory system of man during neurolept analgesia (author's transl)].

The effect of 0.015 mg/kg KHE i.v. on the circulatory system was investigated in 10 patients after closure of an atrial septal defect under neuroleptanalgesia. The arterial pressure increased due to an increase of total systemic resistance. The filling pressures of the right and the left ventricle increased while the stroke index remained unchanged. The maximal rate of rise of left ventricular pressure did not change despite the marked changes of pre- and afterload. The data support the drug mechanism of a volume shift from the peripheral to the central circulation. The possible reasons for the missing stroke index increase are discussed.

Adult↗
PubMed1980

[The effects of Akrinor on the extrathoracic capacitance vessels during extracorporeal circulation and on cardiac haemodynamics of anaesthetized man (author's transl)].

The circulatory effects of Akrinor were investigated in anaesthetized patients during extracorporeal circulation and following open heart surgery. Arterial pressure, cardiac index and the maximal rate of rise of left ventricular pressure increased, whereas the resistance to flow in both circuits and the cardiac filling pressures remained unchanged. The compliance of the extrathoracic capacitance vessels during extracorporeal circulation was unaltered compared with the control group, but the volume content was less after Akrinor (200 ml). If this volume is shifted to the intrathoracic compartment in the intact circulation, the amounts seems too small to explain the increase in cardiac index. This increase and the subsequent rise of the arterial pressure seemed to be due to increased myocardial contractility.

Anesthesia↗
PubMed1979

[Haemodynamic and vascular effects of dobutamine during and after open heart operations (author's transl)].

In cardiosurgical patients the haemodynamic effects of dobutamine 2.5 microgram/kg . min and 5 microgram/kg . min dobutamine were investigated during neuroleptanalgesia, intra- and immediately postoperatively. Intraoperative measurements were performed in 8 coronary surgical patients each after sternotomy and pericardiotomy, but before the aortocoronary venous bypass operation. The following haemodynamic parameters increased significantly: cardiac index (2.5 microgram/kg . min: 2.6 leads to 2.1 1/min . m2; 6 microgram/kg . min: 1.5 leads to 2.24 1/min . m2), heart rate (80 leads to 91 min-1; 86 leads to 107 min-1), stroke index (16%, 27%), mean arterial pressure (70 leads to 90 mm Hg; 70 leads to 93 mm Hg), mean pulmonary arterial pressure (8%; 14%), LV dp/dtmax (72%; 121%) and calculated myocardial oxygen consumption Eg (35%; 52%). Changes in right (PRA) and left ventricular filling pressure (PLVED), in total systemic resistance and total pulmonary vascular resistance were not significant. Postoperative measurement immediately after open heart operations (ASD-correction n = 5, aortocoronary venous bypass (n = 3) in neuroleptanalgesia too, showed the same haemodynamic results as intraoperatively before correction of coronary stenosis. Only a few premature ventricular beats were observed in 3 patients and there were no changes in S-T segments during dobutamine infusion. In another group of 15 patients selective vascular responses to an infusion of 10 microgram/kg . min dobutamine were examined during steady state cardiopulmonary bypass excluding heart and lungs from the circulation. No relevant direct influence on the arteriolar resistance vessels and the venous capacitance vessels were found. In a dose range of 2.5--5.0 microgram/kg . min dobutamine proved to be a potent inotropic agent causing almost no peripheral and relatively little positive chronotropic effects. But the increase in heart rate was more pronounced than in other clinical investigations in conscious patients, which might be due to an attenuation of vagal reflex by anaesthesia. The results indicate, that dobutamine may be a valuable drug in the treatment of intra- and postoperative low output syndromes especially in patients with coronary heart disease.

Adult↗
PubMedDate not supplied

Repetitive depletion and recovery of intracellular K+ in retinal Müller glial cells during whole-cell voltage-clamp.

A procedure was developed allowing repetitive depletion and recovery of K+ from the cell interior of Müller glial cells without patch pipette perfusion. To this end the whole-cell voltage-clamp technique using tight seal pipettes was applied to enzymatically isolated Müller cells of the guinea pig. When K+ was replaced by Cs+ and/or NMDG in the pipette solution voltage-activated outward currents could be generated similar to those found with normal K(+)-containing intracellular solution. This was the result of the distribution of K+ across the cell membrane due to the negative holding potential, i.e., K+ accumulated at the intracellular side of the cell membrane. This distribution should be favored by the low input resistance of Müller cells. K+ could also be removed from the cell interior by depolarizing voltage steps. Simultaneously, K+ influx had to be cut off by using a K(+)-free extracellular solution or blocking K+ channels using Ba2+. This procedure lead to reduction and eventually cessation of the K+ outward currents, indicating extinction of the intracellular K+ pool. The process is reversible, i.e., outward currents can be evoked again by depolarizing voltage steps after renewed application of extracellular K+ and/or removal of Ba2+. Hence, the intracellular K+ pool is filled up again. The described method was applied to demonstrate the dependence of the Müller cell Na+/glutamate transporter on the intracellular K+ concentration.

Animals↗
PubMedDate not supplied

Characterization of cystine uptake in cultured astrocytes.

Glutathione is involved in the maintenance of the structural and functional integrity of membrane proteins, in protection against free radicals and oxidative stress, and in the detoxification of xenobiotics. The cellular uptake of cystine is the rate limiting step in the biosynthesis of glutathione. The precise mechanism for such uptake is not clear as some reports indicate that the uptake occurs through a glutamate-cystine antiporter (system X(c)(-)), whereas, others suggest that it is taken up by the glutamate transporter (system X(AG)). Our studies in cultured astrocytes derived from neonatal rats showed that glutamate, D- and L-aspartate inhibited cystine uptake; that factors that increased intracellular glutamate levels, which would have enhanced the activity of the antiporter, did not stimulate cystine uptake; that the uptake was sodium dependent and partially chloride dependent; that the b(o,+) and ASC systems, which have been shown to carry cystine in some cells, did not mediate cystine uptake in astrocytes; that glutamate uptake blockers such as L-aspartate-beta-hydroxamate (AbetaH) and L-trans-pyrrolidine-2,4-dicarboxylate (PDC), as well as cystine uptake inhibitor L-alpha-aminoadipate (AAA) potently reduced cystine uptake. Additionally, deferoxamine (100 microM) as well as ammonium chloride (5 mM), both of which inhibit glutamate uptake, also inhibited cystine uptake. Taken together, our findings indicate that astrocytes take up cystine through a similar, if not identical, system used to take up glutamate. Interference of cystine uptake by astrocytes through the glutamate transport system may have profound effects on the redox state and the structural and functional integrity of the CNS.

Amino Acids↗