Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The myocardial function and the central and peripheral circulation were studied after aortic valve replacement. All patients showed a similar postoperative pattern of response. During the operation, after termination of bypass, the mean arterial blood pressure (Pa,m) was low. The total peripheral vascular resistance (TPR) and pulmonary vascular resistance (PVR) were normal. Immediately after the operation Pa,m, TPR and PVR were higher than peroperatively. The cardiac index (CI) and stroke index (SI) were low, and the heart rate (HR) was high. At this stage the oesophageal temperature was increasing, but there was no shivering. Then followed a period in which Pa,m and TPR decreased, while CI and SI remained essentially unchanged. The oesophageal temperature reached its highest value 5 hours postoperatively. Peripheral warming began in the 3rd hour postoperatively and was completed in the 6th hour, when the peripheral temperature was 35 degrees C. The progressive peripheral warming, with peripheral cutaneous vasodilatation and slight reduction of the heart rate, took place without signs of increasing CI or SI. The left and right ventricular function, expressed as the relation between LVSWI and Pla,m, and RVSWI and Pra,m, respectively, varied postoperatively and showed no signs of improvement at the time of peripheral warming. Cardiac output and myocardial function seemed to be little affected by the obvious changes appearing during the systemic and peripheral vasodilatation in connection with central and peripheral warming.
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PMID:Circulatory adaptation after aortic valve replacement. A clinical study peroperatively and in the early postoperative period. 72 61

In anesthetized dogs we evaluated the influence of increased right ventricular (RV) pressures on left ventricular (LV) function by comparing the hemodynamic effects of increases in RV afterload (pulmonary arterial pressure) produced by positive end-expiratory pressure (PEEP) with those due to pulmonary arterial occlusion (PAO). Left atrial (Pla) and right atrial (Pra) pressures increased with PEEP and PAO [for Pla: 3.1 +/- 0.7 Torr (PEEP), 2.4 +/- 0.9 Torr (PAO); for Pra: 2.9 +/- 0.4 Torr (PEEP), 3.1 +/- 1.2 Torr (PAO)]. RV septal-free wall dimension (RVD) increased, and LV septal-posterolateral dimension (L2) decreased with both conditions [increases in RVD: 1.9 +/- 0.3 mm (PEEP), 2.2 +/- 0.5 mm (PAO); decrease in L2: 1.1 +/- 0.4 mm (PEEP), 0.9 +/- 0.3 mm (PAO)]. Extracorporeal bypass of the great veins did not alter these findings. LV function curves showed less stroke work at any Pla during PEEP, this being unaffected by vagotomy. When the RV was bypassed, there were no PEEP or PAO related changes in Pla or LV function. Thus diminished LV function with PEEP is probably due to the influence on the LV of a stressed RV in this situation.
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PMID:Influence of the right ventricle on canine left ventricular function with PEEP. 703 11

Although previous studies demonstrated beneficial effects of estrogen on cardiovascular function, the Women's Health Initiative has reported an increased incidence of coronary heart disease and stroke in postmenopausal women taking hormone replacement therapy. The objective of the present study was to identify a molecular mechanism whereby estrogen, a vasodilatory hormone, could possibly increase the risk of cardiovascular disease. Isometric contractile force recordings were performed on endothelium-denuded porcine coronary arteries, whereas molecular and fluorescence studies identified estrogen signaling molecules in coronary smooth muscle. Estrogen (1-1,000 nM) relaxed arteries in an endothelium-independent fashion; however, when arteries were pretreated with agents to uncouple nitric oxide (NO) production from NO synthase (NOS), estrogen contracted coronary arteries with an EC(50) of 7.3 +/- 4 nM. Estrogen-induced contraction was attenuated by reducing superoxide (O(2)(-)). Estrogen-stimulated O(2)(-) production was detected in NOS-uncoupled coronary myocytes. Interestingly, only the type 1 neuronal NOS isoform (nNOS) was detected in myocytes, making this protein a likely target mediating both estrogen-induced relaxation and contraction of endothelium-denuded coronary arteries. Estrogen-induced contraction was completely inhibited by 1 muM nifedipine or 10 muM indomethacin, indicating involvement of dihydropyridine-sensitive calcium channels and contractile prostaglandins. We propose that a single molecular mechanism can mediate the dual and opposite effect of estrogen on coronary arteries: by stimulating type 1 nNOS in coronary arteries, estrogen produces either vasodilation via NO or vasoconstriction via O(2)(-).
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PMID:Estrogen-induced contraction of coronary arteries is mediated by superoxide generated in vascular smooth muscle. 1616 67

The aim of this study was to test whether the simple ratio of right ventricular (RV) end-systolic pressure (Pes) to stroke volume (SV), known as the effective arterial elastance (Ea), provides a valid assessment of pulmonary arterial load in case of pulmonary embolism- or endotoxin-induced pulmonary hypertension. Ventricular pressure-volume (PV) data (obtained with conductance catheters) and invasive pulmonary arterial pressure and flow waveforms were simultaneously recorded in two groups of six pure Pietran pigs, submitted either to pulmonary embolism (group A) or endotoxic shock (group B). Measurements were obtained at baseline and each 30 min after injection of autologous blood clots (0.3 g/kg) in the superior vena cava in group A and after endotoxin infusion in group B. Two methods of calculation of pulmonary arterial load were compared. On one hand, Ea provided by using three-element windkessel model (WK) of the pulmonary arterial system [Ea(WK)] was referred to as standard computation. On the other hand, similar to the systemic circulation, Ea was assessed as the ratio of RV Pes to SV [Ea(PV) = Pes/SV]. In both groups, although the correlation between Ea(PV) and Ea(WK) was excellent over a broad range of altered conditions, Ea(PV) systematically overestimated Ea(WK). This offset disappeared when left atrial pressure (Pla) was incorporated into Ea [Ea * (PV) = (Pes - Pla)/SV]. Thus Ea * (PV), defined as the ratio of RV Pes minus Pla to SV, provides a convenient, useful, and simple method to assess the pulmonary arterial load and its impact on the RV function.
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PMID:Effective arterial elastance as an index of pulmonary vascular load. 1842 34

Induction of protein disulfide isomerase (PDI) is validated as a main mechanism by which 4-hydroxybenzyl alcohol (4-HBA), an active principle of Gastrodia elata Blume, reduces cerebral infarct volumes in a murine model of focal brain ischemia/reperfusion. In contrast to its position isomers, i.e. 3-hydroxybenzyl alcohol (3-HBA) and 2-hydroxybenzyl alcohol (2-HBA), and to aliphatic diols (1,4-butanediol and 1,5-pentanediol), 4-HBA administered intravenously at 25 mg/kg protected mice, significantly reducing total, cortical and sub-cortical infarct volumes by 42, 28 and 55%, respectively. All compounds, 4-HBA included, were devoid of antioedematous properties. Only the stroke protective 4-HBA, but neither 3-HBA nor 2-HBA, was capable of significantly inducing PDI in intact mouse brains. Stroke protection was fully prevented by bacitracin (500 mg/kg), a known inhibitor of PDI, which, without affecting basal brain PDI levels, altered the ability of 4-HBA to induce significantly PDI in intact brains. Taken as a whole, our data indicate that stroke protection induced by 4-HBA involves PDI as a key player, making this protein a valuable target to control brain injury disorders. The fact that 4-HBA, at doses up to 200mg/kg, was devoid of neurotoxicity in the rotarod test is also a decisive element to promote the neuroprotective use of this plant compound.
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PMID:Experimental stroke protection induced by 4-hydroxybenzyl alcohol is cancelled by bacitracin. 1942 93