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Biomedical subjects

H Löwe

Publications and source records attributed to H Löwe.

At least 19 recordsLinked to original sources

Deferoxamine (Desferal) improves the content of oxygen in myocardial tissues during recovery after hypoxia in isolated rabbit heart.

On isolated working right heart from rabbit tissue oxygen content as an indicator of function of oxygen transport and storage was observed by moderate hypoxia, hypoxia with deferoxamine (1) and iron infusion. In addition water content of myocardium as an indicator of metabolic damage was evaluated and the copper depletion was established. During the recovery the results presented a beneficial effect on the content of tissue oxygen which is due to 1. But the copper depletion was not changed. Possible connections are discussed.

Animals

Protection of the hypoxic myocardium by the bispyridine derivatives AWD 122-14 and milrinone: studies on isolated, working right rabbit hearts.

Isolated rabbit hearts were perfused via the aortic root with Muralt solution at a constant perfusion pressure of 52 mm Hg ("preload"). After passing the coronary system, the right ventricle pumps the perfusion medium against an "afterload" of 5.15 +/- 1.3 mm Hg through the arteria pulmonalis with a spontaneous heart rate of 131 +/- 11 beats/min. In this model, the right ventricle works under "physiological" conditions. The model was characterized by applying the parameters of Döring et al. The following parameters of this model were measured: RVPsyst. + diast., Qpulm., MVO2, HR, dp/dtmax, dp/dtmin. By applying the method of Neely et al. the external pressure work (w), the efficiency (e) and the coronary resistance (R) were calculated. After a short period of hypoxia of 5 min (the pO2 in the perfusion medium was decreased from 530 mm Hg to 160 mm Hg), the ventricle functions are reversibly depressed, and restored partially under reperfusion (15 min) of the myocardium in dependence of the hypoxia and reperfusion lesions. The application of 3 x 10(-6) mol/l of the two bispyridine derivatives AWD 122-14 and milrinone into the perfusion medium during the total experimental time protected the myocardium partially against the hypoxia and reperfusion lesions. This protecting activity can be shown in a better preserve and recovery of the ventricle functions (pulmonalis flow, external pressure work, efficiency). The application of 5 x 10(-8) mol/l nifedipine, a known protective substance, showed a lower activity in this model compared with the activity of the bispyridines.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

[Role of endogenous opioids in heart failure].

The peptidergic, endogenous opioid system counteracts exogenous and endogenous stress factors. The system will be activated by stress, e.g., also in case of heart failure. The endogenous opioids endorphin, met-enkephalin, leu-enkephalin, dynorphin, casomorphin, and others split from precursor proteins (250-265 amino acids) by a specific proteolytic cleavage. In clinical and experimental heart failure the plasma levels of endorphin and lipotropin are changed as an evidence of the activated opioid system. In patients with chronic heart failure the plasma levels of endorphin and lipotropin are decreased, which is discussed as an exhaustion of the opioid system. In the case of experimentally induced right-heart failure in dogs the plasma levels of endorphin and lipotropin are increased. Morphine antagonists (naloxone hydrochloride) which penetrate into the cerebral system improve the disturbed hemodynamics in dogs with a right-heart failure. The improving effects results from central actions since opiate antagonists, which cannot penetrate the blood-brain-barrier (naloxone methobromide) have no effect. The actions of opioid peptides will be induced by inhibition of the depletion and the reabsorption of catecholamines in synaptic storages (isolated atria from guinea pig). In cultures from cardiac myocytes (chicken ventricle cells) enkephalins induced positive inotropic effects via receptor mediated mechanisms. The results showed modulating activities of endogenous opioids against the effect of activated sympathetic activity.

Animals

The effect of amrinone on LDH release and perfusion pressure in isolated ischemic rabbit hearts.

Isolated rabbit hearts were perfused normoxically or ischemically using the technique of Langendorff. The hearts were perfused with a modified Krebs-Henseleit solution, perturbated with 95% O2/5% CO2 or in case of ischemia with N2 which replaced the O2. The perfusion rate was 25 ml/min under normoxic and 2.5 ml/min under ischemic conditions. The oxygen pressure was about 65 kPa in the normoxic and about 6 kPa in the ischemic medium. Reperfusion of ischemic hearts was realized in some cases normoxically. During the ischemic perfusion and reperfusion LDH was released time depended into the perfusion medium and the aortic inflow pressure increased. The LDH release and the increase of the inflow pressure are strong correlated. Both parameters direct to ischemic myocardial lesions. Amrinone applied as bolus in the start period of ischemia or as an infusion during the ischemic and reperfusion time limited the release of LDH and the increase of the inflow pressure. The results were discussed as a direct protecting effect of amrinone against a myocardial ischemic lesion, which is in correspondence with the improving effects of amrinone on the ischemia caused heart failure of canines in vivo, shown by Campbell et al.

Amrinone

Radical trapping and lipid peroxidation during myocardial reperfusion injury--radical scavenging by troxerutin in comparison to mannitol.

During ischemic perfusion and reperfusion of isolated rat hearts, OH and carbon-centered radicals were trapped in the perfusate. Both radicals were found to occur during LPO which was enhanced in the myocardium. The increase of LPO as well as of enzyme leakage were reduced by mannitol and the flavonoid troxerutin showing antioxidative action of greater than 500 and greater than 5 microM, respectively. The assumption is supported that radical-induced LPO is of pathogenetic relevance during myocardial reperfusion injury for which antioxidants could be of therapeutic advantage.

Animals

[The action of Cordemcura on the energy balance of the isolated rabbit heart].

The effect of Cordemcura, a new cardiotonic substance, was tested on retrograd perfused isolated rabbit hearts in comparison with equieffective doses of dopamine. The substances were applied continously via the perfusion medium in the following dosages: Cordemcura 3.34 X 10(-4) mol/l, 2.67 X 10(-3) mol/l; dopamine 3.9 X 10(-6) mol/l, 1.6 X 10(-5) mol/l). The effects of the substances were studied during normoxic and hypoxic perfusion. The heart rate was increased under normoxic perfusion of Cordemcura about 37.1% (3.34 X 10(-4) mol/l) and 17.9 (2.67 X 10(-3) mol/l). The oxygen consumption in relation to the performance of the hearts (contractility. heart rate) was increased by Cordemcura on 1.45 and 1.93 (3.34 X 10(-4) mol/l and 2.67 X 10(-3) mol/l) in the same way like by dopamine (1.30 and 2.66; 3.9 X 10(-6) mol/l and 1.6 X 10(-5) mol/l). The content of adenine nucleotides decreased in the hypoxic perfused hearts on nearly 20% of the control values. There was no difference between control, Cordemcura and dopamine treated hearts. Cordemcura increased the level of cAMP in the myocardium after 90 min of hypoxic perfusion in comparison with control hearts (control hearts 2.8 +/- 0.7 nmol/g protein; Cordemcura 4.7 +/- 0.8 nmol/g protein). In comparison to control hearts and dopamine treated hearts the hypoxic perfusion with Cordemcura resulted in a significant lower release of lactate dehydrogenase from the heart.

Aminopyridines

[The cardiovascular effect of Cordemcura on various animal models in vivo].

The cardiotonic activity of Cordemcura was investigated in anesthetized pigs, cats, and rats. Hemodynamic measurements were made under normal conditions and under drug-induced heart failure (hexobarbital, isoproterenol). Cordemcura caused significant positive inotropic effects with rapid onset and relatively short duration of action (0.2-3.2 mg/kg i. v.). In the pig dp/dtmax was increased by 31.4% (p less than 0.02) at 1.6 mg/kg, in the cat by 34.2% (p less than 0.05) at 0.5 mg/kg, and in the rat by 14.4% (ns) at 0.5 mg/kg. The inotropic response was associated with a significant reduction of total peripheral resistance (TPR) (pig: -21.4%, p less than 0.02; cat: -13.7), and relatively small changes in heart rate, cardiac output, and blood pressure. Under drug-induced heart failure there was no further increase in the cardiotonic activity of Cordemcura. The hemodynamic effects of Cordemcura were compared with the effects of dopamine (5-100 micrograms/kg i. v.) and ouabain (10-40 micrograms/kg i. v.).

Aminopyridines

Calculation of a mean functional diameter of capillaries of isolated rabbit hearts and changes of this diameter during hypoxia. Pathophysiological and pharmacological studies.

Isolated rabbit hearts were perfused aerobically (45 min) and hypoxically (105 min), using a modified Langendorff technique. The mean functional diameter of capillaries (MFDC) was calculated from the perfusion rate per minute and the inflow resistance by the model of Hagen-Poiseuille. The MFDC expresses the mean lumen of all capillaries of the heart, regardless of the different behaviour of the capillaries in the different regions of the myocardium. The MFDC decreased very rapidly after the onset of a hypoxia from 3.5 +/- 0.3 micron to about 70% of the initial diameter within 5-10 min (p less than 0.01) and then in a slower range within the following 70 min to about 44% of the initial diameter. The release of lactate dehydrogenase (LDH) from the hypoxic myocardium was detectable after 45 min of hypoxia and rose drastically after 60 min of hypoxia in our model. The decrease of the MFDC as well as the release of LDH from the hypoxic myocardium can be diminished by application of O-(beta-hydroxyethyl)-rutoside or 10 mM mannitol to the hypoxic perfusion medium. Both substances have antioxidant activities. It is discussed that the injury of the microvasculature is an early process during hypoxia, which can potentiate the hypoxic changes of the myocardial cells by additional diminution of the supply with oxygen and substrates. The protecting activities of substances with antioxidant actions to hypoxic myocardium were supported.

Adenosine

Absolute and relative myocardial ischemia by isoproterenol overdosage.

Administration of greater than or equal to 10 mg/kg isoproterenol in rats absolutely diminished local myocardial blood flow within 0.5 min continuing up to 45 min. The blood flow reduction was followed by an increased lactate content and a decrease of both the intracellular redox potential and the content of high energy phosphates in the myocardium. The graduation of the initial lactate accumulation in different myocardial regions corresponds to the myocardial distribution of the infarct-like necroses occurring 24 h later. The very early alterations are comparable with an absolute (blood flow reduction), irreversible, and acute ischemia. In the dose range from 0.05 to 1 mg/kg of isoproterenol, an acceleration of the local myocardial blood flow was caused which, however, was accompanied by ischemia-like disturbances, too. Therefore, this condition is considered as a relative ischemia, an increased but insufficient blood supply.

Animals

[Formation of crystal-like ribosomal aggregates in smooth muscle cells of the guinea pig ileum following incubation in vitro].

The formation of crystal-like aggregates of ribosomes with a ribosome-ribosome distance of 45--50 nm in degenerated smooth muscle cells from guinea pig ileum was described. The ribosome aggregates were formed under the influence of tissue incubation for 15--60 minutes at room temperature (25 degrees C) To our knowledge, this is the first observation of crystal-like ribosome aggregates in adult mammalian tissue.

Animals