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

To determine the hemodynamic effects of intravenous injection of calcium chloride, 26 patients were studied immediately after termination of extracorporeal circulation. Eighteen patients (Group A) had injection of a single bolus of CaCl2; in the other 8 patients (Group B), the bolus injection was followed by infusion of CaCl2 at a rate of 1.5 mg/kg/min for 10 minutes. Myocardial contractile element velocity (Vpm), aortic blood flow, electrocardiograms, and left ventricular, systemic arterial, pulmonary arterial, and left atrial pressures were recorded continuously. The baseline ionized calcium level after bypass was 3.6 +/- 0.6 mg/100 ml (normal range, 3.9 to 4.5 mg/100 ml); this increased to 5.4 +/- 0.5 mg/100 ml 1 minute after CaCl2 injection. The ionized calcium level was 4.7 +/- 0.6 mg/100 ml 6 minutes after CaCl2 injection in Group A, and was 5.9 +/- 0.2 mg/100 ml and 6.4 +/- 0.2 mg/100 ml at 6 and 10 minutes, respectively, in Group B. There was significant early hemodynamic improvement after CaCl2 injection, including increases in Vpm (p less than 0.001), cardiac index (p less than 0.001), mean blood pressure (p less than 0.01), and stroke volume index (p less than 0.001). A similar pattern of hemodynamic response was observed in both groups. Approximately 1 minute after CaCl2 injection, cardiac index returned to control level, Vpm and mean blood pressure remained elevated, and heart rate declined (p less than 0.01). Systemic vascular resistance gradually increased and was significantly elevated (p less than 0.05) in Group B at 3 minutes and in Group A at 6 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hemodynamic effects of calcium chloride injection following cardiopulmonary bypass: response to bolus injection and continuous infusion. 669 46

Ten normocalcemic critically ill patients who had experienced a decrease in cardiac index greater than or equal to 0.5 liter/min/m2 after incremental changes of PEEP received 7 mg/kg of CaCl2 as a slow iv bolus, followed by an infusion of 20 mg/kg CaCl2 over 60 min. Hemodynamic pressures and flow, oxygen uptake and transport, and blood chemistry variables were determined over a 120-min period. The results indicated that: (1) hemodynamic variables were not affected except for left ventricular stroke work index and mean blood pressure, which increased slightly; (2) both serum calcium and ionized calcium concentrations increased significantly, sometimes to dangerous levels; (3) colloid osmotic pressure and hemoglobin levels decreased slightly but consistently. In conclusion, CaCl2 administration failed to improve hemodynamic function depressed by PEEP. If CaCl2 can play a relevant role in the management of cardiovascular depression, further identification of appropriate doses and patients is necessary.
 ...
PMID:Calcium chloride administration in normocalcemic critically ill patients. 698 39

Effects of diltiazem, a calcium antagonist, on the cardiovascular system in the pentobarbital anesthetized dogs were investigated. Diltiazem (100 micrograms/kg and 300 micrograms/kg, i.v.) decreased blood pressure, heart rate and total peripheral resistance, while cardiac output and stroke volume were markedly increased. The max dp/dt of left ventricular pressure tended to increase with a dose of 100 micrograms/kg. Left ventricular end-diastolic pressure was slightly increased with a dose of 400 micrograms/kg. Rate pressure product was significantly reduced. Diltiazem (30 micrograms/kg and 100 micrograms/kg) increased pulmonary arterial flow together with the increase in both systolic and diastolic pulmonary arterial pressure. Diltiazem (100 micrograms/kg) increased common carotid, femoral and superior mesenteric arterial blood flow by 30 to 40%, whereas vertebral blood flow was increased by over 100%. The dose dependency in the vertebral blood flow was remarkable. Response of the vertebral artery to diltiazem was similar to that reported in the case of the coronary artery. In the His bundle electrogram, diltiazem increased the AH interval by about 10% at 100 micrograms/kg and 25% at 200 micrograms/kg, without changing the HV interval. Diltiazem-induced AH prolongation was completely depressed by epinephrine but only partially so by CaCl2. Thus, the effects of diltiazem on sinus rhythm and AV conduction in the anesthetized dog were more potent than the effects on cardiac contractility, although weaker than the effects of the vasodilating action. The vasodilator effects appear to be the primary action of diltiazem on the cardiovascular system.
 ...
PMID:[Effects of diltiazem on hemodynamics and His bundle electrogram in the anesthetized dog (author's transl)]. 723 61

Thrombin-induced phosphorylation of 47 kDa protein (P47) in platelets, a substrate of protein kinase C (PKC), was defective in stroke-prone spontaneously hypertensive rats (SHRSP) (Hypertens. 14, 304-315, 1989). Platelet PKC from SHRSP and Wistar Kyoto rats (WKY) was partially purified and Ca(2+)-sensitivity of PKC activity was examined to understand the defect in the protein phosphorylation. When the platelets from SHRSP and WKY were homogenized in a buffer containing 10 mM EGTA and 2 mM EDTA, approx. 80% of PKC was in the cytosol fraction. PKC in this fraction was purified by DE52 and hydroxyapatite column chromatography. Both platelet PKC preparations contained only PKC-alpha, and there was no significant difference in the Ca(2+)-dependency of activity between them. When the platelets from SHRSP and WKY were homogenized in a buffer containing 10 microM CaCl2, 90% of PKC was found to be bound to the membrane. PKC was extracted from the membrane with a buffer containing 2.5 mM EGTA and 2.5 mM EDTA, and purified by DE52 column chromatography. PKC from WKY platelets eluted as a single peak whereas that from SHRSP platelets eluted as two peaks (peak 1 and peak 2). Ca(2+)-sensitivity of peak 1 PKC was much lower than that of WKY PKC. In contrast, the Ca(2+)-sensitivity of peak 2 PKC appeared to be slightly higher than that of WKY PKC. The specific activity of peak 2 PKC was 4% to 5% of that of peak 1 and WKY PKC. These results suggest that there are two different types of PKC, normal and low Ca(2+)-sensitive in SHRSP platelets. Defective P47 phosphorylation in SHRSP platelets might be attributable to the occurrence of this low Ca(2+)-sensitive PKC.
 ...
PMID:The differences in Ca(2+)-sensitivity of protein kinase C in platelets from Wistar Kyoto rat and stroke-prone spontaneously hypertensive rat. 877 2

The major active constituent of Astragalus membranaceus, astragaloside IV, has been found to have properties of increasing coronary flow and cardioprotection. In this study, we examined the direct effects of astragaloside IV on vessel dilatation and contraction in isolated aortic rings from both normal and stroke-prone spontaneously hypertensive rats (SHR-SP) in vitro. The results demonstrated that astragaloside IV could antagonize vessel contractions induced by phenylephrine and potassium chloride in a concentration-dependent way. Astragaloside IV reduced CaCl2-induced contractions in Ca2+-free solution. Astragaloside IV also dilated aortic vessels in a dose-dependent manner, which was partially endothelium-dependent through the nitric oxide (NO) and cGMP pathways. The aorta from 6-month-old SHR-SP rats showed impaired endothelium function, and astragaloside IV dilated the vessels from the hypertensive rats to a lesser extent as compared with normal control rats. In the presence of perivascular fat tissue, the contractile responses induced by angiotensin II and phenylephrine were also attenuated by astragaloside IV. Collectively, this study provides functional evidence that astragaloside IV exerts vessel dilatation properties through the endothelium-dependent NO-cGMP pathway in normal and hypertensive rats. It blocks extracellular calcium influx and participates in vessel relaxation partly through phenylephrine and angiotensin II inhibition when perivascular fat is present.
 ...
PMID:Astragaloside IV dilates aortic vessels from normal and spontaneously hypertensive rats through endothelium-dependent and endothelium-independent ways. 1673 12

Hypertension is a common cardiovascular disease and can induce many complications, such as stroke and coronary heart disease. The purpose of the present study was to investigate the effect of ischemia/hypoxia on mesenteric artery vasomotor function in spontaneously hypertensive rats (SHR). Rat mesenteric arterial rings were cultured in modified ischemia-mimetic solution in a hypoxia incubator for a certain time period. Isometric tension changes of isolated mesenteric arterial rings were recorded continuously by a myograph system. The results obtained were as follows: In SHR group, the maximum contractions to KCl and phenylephrine (PE) were increased, and the maximum relaxation to acetylcholine (ACh) was decreased, compared to those in Wistar-Kyoto (WKY) rats group. Compared with SHR group and WKY with acute ischemia/hypoxia (WKY+H) group, SHR with acute ischemia/hypoxia (SHR+H) increased the maximum contractions induced by KCl and PE and inhibited the maximum relaxations by ACh. In SHR+H and SHR groups, the vasodilation induced by ACh was unaffected by N(G)-nitro-L-arginine methylester (L-NAME), whereas in WKY group, the relaxation to ACh was attenuated by L-NAME. CaCl2-induced contraction in depolarized rings in SHR+H group significantly shifted to the left compared with SHR group. In Ca(2+)-free K-H solution, the maximum contractions induced by PE and caffeine were increased in SHR+H group compared to those in WKY+H group; the PE- and caffeine-induced contractions were also enhanced in SHR group versus WKY group; the maximum contraction induced by PE was significantly increased in SHR+H group versus SHR group. These findings suggest that acute ischemia/hypoxia aggravates mesenteric artery dysfunction in SHR. The mechanism may be related to the decreased NO generation and increased sarcoplasmic reticulum Ca(2+) release.
 ...
PMID:[Effect of ischemia/hypoxia on mesenteric vasomotor function in spontaneously hypertensive rats and its possible mechanism]. 2219 49


<< Previous 1 2 3