Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 30 patients with congenital or acquired heart disease the haemodynamic effects of diazepam (Valium) 0.3 mg/kg were investigated during surgical procedures under neuroleptanalgesia. The following parameters were measured or calculated: Heart rate (HR), arterial pressure (-Part, Psyst, Pdiast), pulmonary artery pressure (-PAP), right (-PRA) and left atrial pressure (-PLA), left ventricular pressure (PLV), left ventricular enddiastolic pressure (PLVED), left ventricular peak dp/dt (dp/dtmax), cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke index (SI), total systemic resistance (TSR), total pulmonary resistance (TPR), work index of the right (RVWI) and left ventricle (LVWI). In comparison with a control group (n = 36) diazepam caused a decrease in arterial pressure cardiac index, stroke index, right and left atrial pressure and dp/dtmax. This, however, was mainly attributable to vasodilatation and not to a negative inotropic effect, which is of only minor importance with diazepam. These haemodynamic changes resulted in a reduction in myocardial oxygen consumption. Diazepam is a valuable drug in neuroleptanalgesia, when an increase in blood pressure can not be controlled by fentanyl or droperidol.
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PMID:[Diazepam (valium). Changes in haemodynamics, myocardial oxygen consumption and vascular tone (author's transl)]. 69 81

In 36 patients with acquired heart disease effects of 0.15 mg/kg piritramide on hemodynamics, inotropic state and myocardial oxygen consumption were investigated during and after cardiac surgery (basic neuroleptanalgesia). It could be demonstrated, that piritramide is not inducing any negative inotropic effects compared to a control group (n = 36) and a fentanyl group (0.003 mg/kg, n = 31). There were only small changes in HR, SV, PRA and PLA. A slight decrease in Part, PLV, and arterial perfusion pressure during extracorporeal circulation is interpreted as a peripheral vasodilatation. The resulting decrease in heart work caused a significant decrease in myocardial oxygen consumption (-18%), which is of special advantage in patients with coronary heart disease.
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PMID:[Comparative clinical investigations on the cardiovascular effects of piritramide (dipidolor) and fentanyl (author's transl)]. 724

In 52 patients with acquired heart disease haemodynamic effects of 0,2 mg/kg and 1,0 mg/kg morphine were investigated during surgical procedures under neuroleptanalgesia. The following parameters were measured or calculated: heart rate (HR), arterial pressure (Part, Psyst, Pdiast), pulmonary artery pressure (PAP), right (PRA) and left atrial pressure (PLA), left ventricular pressure (PLV), left ventricular end-diastolic pressure (PLVED), left ventricular peak dp/dt (dp/dtmax), cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke index (SI), total systemic resistance (TSR), total pulmonary resistance (TPR), work index of the right (RVWI) and left ventricle (LVWI). Myocardial oxygen consumption (EG) was calculated according to the method of Bretschneider. There was almost no change in cardiac index and stroke index. In comparison to a control group (n=36) morphine caused a dose-dependent decrease in arterial pressure and in arterial perfusion pressure during extracorporeal circulation. This, however, was mainly attributable to vasodilatation and not to a negative inotropic effect. In accordance with the changes in haemodynamics there was a remarkable decrease in myocardial oxygen consumption (EG: -21.1%; 1,0 mg/kg morphine).
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PMID:[Haemodynamic effects of morphine in man (author's transl)]. 728 4

13C cross-polarization/magic angle spinning (CP/MAS) NMR and (1)H T(1rho) experiments of poly(L-alanine) (PLA), poly(L-valine) (PLV), and PLA/PLV blends have been carried out in order to elucidate the conformational stability of the polypeptides in the solid state. These were prepared by adding a trifluoroacetic acid (TFA) solution of the polymer with a 2.0 wt/wt % of sulfuric acid (H(2)SO(4)) to alkaline water. From these experimental results, it is clarified that the conformations of PLA and PLV in their blends are strongly influenced by intermolecular hydrogen-bonding interactions that cause their miscibility at the molecular level.
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PMID:A study of conformational stability of poly(L-alanine), poly(L-valine), and poly(L-alanine)/poly(L-valine) blends in the solid state by (13)C cross-polarization/magic angle spinning NMR. 1194 39

Cadmium and lead are heavy metals that have been shown to induce vascular disorders such as atherosclerosis in experimental animals. However, little is known about the mechanisms by which cadmium and lead induce vascular toxicity. The toxicity was investigated using a culture system of vascular endothelial and smooth muscle cells. Cadmium destroys the monolayer of endothelial cells and the cytotoxicity is protected by zinc and copper without metallothionein induction. On the other hand, lead does not exhibit cytotoxicity but inhibits the repair of endothelial monolayers after wounding by a lower response to endogenous basic fibroblast growth factor mediated by suppression of the synthesis of perlecan, a large heparan sulfate proteoglycan. In addition, cadmium and lead reduce endothelial fibrinolytic activity by induction of plasminogen activator inhibitor type 1 synthesis and by inhibition of tissue-type plasminogen activator, respectively. In vascular smooth muscle cells, cadmium and lead can promote their proliferation and influence proteoglycan synthesis and fibrinolysis in different manners. These results indicate that cadmium and lead have specific toxicities in the proliferation, fibrinolysis, and extracellular matrix formation of vascular endothelial and smooth muscle cells.
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PMID:[Cell biology of heavy metal toxicity in vascular tissue]. 1504 28