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A Klee

Publications and source records attributed to A Klee.

At least 19 recordsLinked to original sources
PubMed1993

Evidence from comparative investigations that impaired platelet activation is not specific for stroke-prone spontaneously hypertensive rats.

BACKGROUND AND PURPOSE: Platelet behavior of Sprague Dawley (SD), Wistar (WI), Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), and stroke-prone spontaneously hypertensive rats (SHRSP) was studied in vivo to evaluate the importance of hypertension-related hemostatic disorders. METHODS: The study was based on the model of stimulus-induced pulmonary microembolization of labeled platelets. After injection of 51Cr-labeled homologous platelets into urethane-anesthetized rats, the organ distribution of the platelets was continuously monitored by gamma detectors. Count rates of two detectors--one placed above the animals' thoraxes (C1), the other above their abdomens (C2)-and the ratio of C1:C2 were calculated. The following platelet activators were applied intravenously: adenosine diphosphate (ADP; 50 micrograms/kg), collagen (100 micrograms/kg), and thrombin (50 IU/kg). RESULTS: All three substances caused a reversible pulmonary accumulation of the labeled platelets and hence an increase in C1/C2 (delta C1/C2%). ADP induced a shift of 75% in SD, 52% in WI, 32% in WKY, 30% in SHR, and 31% in SHRSP. Thrombin-mediated shift was 79% in SD, 64% in WI, 58% in WKY, 48% in SHR, and 54% in SHRSP. Collagen induced a shift of 85% in SD, 96% in WI, 84% in WKY, 56% in SHR, and 62% in SHRSP. CONCLUSIONS: Because indistinguishable results were observed in both hypertensive strains, we conclude that impaired platelet aggregation is not specific for SHRSP. Hence, it may not primarily be responsible for the increased occurrence of stroke in these animals.

Adenosine Diphosphate↗
PubMed1991

Effects of platelet activating factor on rat platelets in vivo.

Platelet activating factor (PAF) is not able to aggregate rat platelets in vitro. Due to the agonist effects of PAF on multiple cells, a possible role of PAF in the activation of rat platelets in vivo where different cells may influence each other was investigated. The pulmonary microembolization of 51Cr-labelled activated platelets was used as in vivo model. This model allowed us to monitor platelet behaviour by means of non-invasive methods. In contrast to results obtained in vitro, PAF activated rat platelets in vivo. The pulmonary microembolization of the platelets was dose-dependent and rapidly reversible. About 0.5 microgram/kg PAF caused a half-maximal rise of platelet-bound radioactivity in the thorax. Activation of the platelets by PAF was followed by extreme desensitization, so that a second injection of PAF did not provoke a significant response of the platelets. Platelet function was, however, not completely impaired because they still accumulated in the thorax after the application of ADP (50 micrograms/kg). That pulmonary entrapment had taken place was shown by a 3-fold increase in lung specific radioactivity. This was accompanied by a short-lasting thrombocytopenia. The PAF antagonist, WEB 2170 (30 micrograms/kg), significantly inhibited the microembolization of the platelets induced by PAF. Under in vitro conditions leukocytes purified from rat blood and activated by PAF were able to induce platelet aggregation. These results demonstrate that a PAF-specific activation of rat platelets is achievable in vivo which is probably mediated by other cells.

Adenosine Diphosphate↗
PubMed1991

Evaluation of pulmonary accumulation of 51chromium-labelled rat platelets following intravenous application of ADP and collagen.

We examined the effects of ADP- and collagen-induced pulmonary platelet embolism in the rat. Homologous 51Chromium-labelled platelets were used to monitor extracorporally the distribution of platelets in the circulation. For that purpose, collimated iodide scintillation detectors were placed above thorax (C1) and abdomen (C2). A dose-dependent increase in thoracic radioactivity, paralleled by a decrease in the abdomen, was observed after intravenous injection of ADP and collagen. This resulted in a shift of C1/C2, so that the effect of collagen was more pronounced (maximal increase of C1/C2 = 134%) than ADP (maximal increase of C1/C2 = 79%). The increase in thoracic radioactivity was caused by the uptake of platelets in the lung as was shown after administration of collagen (6-fold enrichment of labelled platelets). Lung platelet sequestration resulted in a dose-dependent thrombocytopenia. The ADP -and collagen-induced pulmonary platelet embolism reversibly provoked cardiovascular symptoms of shock: hypotension and bradycardia. Impaired gas exchange during platelet accumulation manifested itself in a reversible arterial hypoxaemia and hypercapnia, followed by a weak acidosis. We were able to inhibit ADP-dependent thoracic platelet accumulation by ticlopidine in a dose-related manner as well as collagen-induced thoracic platelet accumulation by acetylsalicylic acid. The results indicate that behaviour of homologous labelled rat platelets in vivo can easily be monitored, thus offering the opportunity to investigate the effects of antiaggregatory drugs on platelets in their natural environment.

Adenosine Diphosphate↗
PubMed1987

Transfer of functional opiate receptors from membranes to recipient cells by polyethylene glycol-induced fusion.

Opiate receptor-mediated inhibition of adenylate cyclase activity was elicited in membranes of C6BUI glioma cells and S49 cyc- lymphoma cells after fusion with opiate receptor-containing membranes derived from NG108-15 neuroblastoma x glioma hybrid cells. The fusion was induced by polyethylene glycol using procedures developed by Orly and Schramm [(1976) Proc. Natl. Acad. Sci. USA 73, 4410-4414]. Prior to fusion, the adenylate cyclase activity of the donor. NG108-15 cell membrane, was inactivated by N-ethylmaleimide treatment. Prostaglandin E1 receptors and the stimulatory GTP-binding protein Ns were transferred to the recipient cells along with opiate receptors. Thus, inhibitory receptors can be transferred to foreign adenylate cyclase systems just as stimulatory receptors had earlier been found to do. Furthermore, opiate receptors have been shown to function in non-neuronal cells.

Adenylyl Cyclase Inhibitors↗
PubMed1978

Clonidine in the prophylaxis of migraine.

The prophylactic effect of clonidine in a dosage of 0.05 mg twice daily was investigated in 49 patients using a double-blind, crossover trial carried out in four Departments of Neurology. Seventy-one patients were originally included but 22 patients withdrew, two of them due to side effects,the remainder because of inability to keep the requisite diary, lack of drug compliance or refusal to attend the checkups. Approximately equal numbers withdrew during the clonidine and placebo periods. There was no statistically significant difference between the number of migraine attacks or between the number of severe attacks (8 hours' duration or more) during the placebo and clonidine periods. This also applied to the patients with foodstuff-provoked migraine attacks. Sixty-three patients carried through a double-blind, crossover trial with capsules containing either 125 mg tyramine or placebo. There was no significant difference between the number of patients who developed attacks after the ingestion of placebo and the number who did so after the ingestion of tyramine. The same is true of the group with foodstuff-provoked migraine. As a rule side effects were few and mild. This study has not confirmed that clonidine has any pharmacological effect in prophylaxis of migraine.

Adult↗
PubMedDate not supplied

[Diagnostic and therapy of a severe fetal parvovirus-B19-infection with persistence of viral DNA in the mothers blood but inconspicuous serological tests. Case report].

In the 24th week of gestation we diagnosed a severe hydrops fetalis in a 25 year old VI gravid III para, who had contact to parvovirus B19 in the 14th week of gestation. Because of the severe anaemia of the fetus and the massively increased bilirubinoides in the amniotic fluid we decided at the same day to apply the first of four intrauterine transfusions. The serological patterns of maternal blood with highly positive parvovirus-B19-IgG and negative IgM suggested that an infection had occurred. Parvoviral DNA was found in maternal and fetal blood confirming the diagnosis of an acute intrauterine parvovirus-B19 infection. No viral DNA was detected in fetal ascites. IgM in fetal blood was negative. By means of four transfusions, the pregnancy could be prolonged until the 32 + 5th week of gestation while the ascites was declining. When rupture of membranes occurred, a cesarean section had to be performed due to contractions and presentation of the feet. The newborn's blood count exhibited a thrombocytopenia with normal haemoglobin and haematocrit. Five days after delivery, a blood exchange had to be done because of a hyperbilirubinaemia. After seven weeks, the child could be dismissed from hospital in good general status, with decreasing ascites, normal liver function and normal neurological status. The blood of the newborn was tested to be positive for IgG, while IgM-antibodies and parvovirus-B19-DNA were negative. The diagnosis of a parvovirus-B19 infection of a fetus with severe hydrops and anaemia could be verified by a positive proof for DNA in maternal blood, with negative IgM and highly positive parvovirus-B19-IgG and on the other hand highly positive viral DNA in fetal blood and in the amniotic fluid. 10 weeks after contact to parvovirus B19, i. e. in the 24th week of gestation, positive IgG- and negative IgM-antibodies were found in the mother's blood, whereas fetal complications were noticed. These data demonstrate that following an acute parvovirus-B19-infection of the mother IgM-antibodies can be proofed for 6 - 8 (- 10) weeks. On the other side parvovirus-B19-DNA in the mothers blood is detectable by means of PCR for 8 - 10 weeks and in some cases even more than 15 weeks.

Adult↗