Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0393754 (HSA)
 2,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of nimodipine in decreasing mortality and morbidity of subarachnoid haemorrhage (HSA) is evaluated in 51 patients admitted to the Neurological and Neurosurgery Departments of the Santa Maria Hospital. Reductions of 2 x (0.65, 6.39) of the incidence of ischemia in the total group and of 2.1 x (0.58, 7.79) of mortality in the sub-group with initial severity of less than 4 points of the Hunt score were observed relatively to a comparable group of patients previously admitted who did not receive nimodipine. Randomized clinical trials that tested the effect of nimodipine in the context of HSA are reviewed.
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PMID:[Nimodipine in subarachnoid hemorrhage]. 195 Jun 63

Induction of anesthesia with isoflurane in combination with fentanyl, thiopentone, nitrous oxide and pancuronium was studied in nine patients scheduled for coronary artery bypass grafting. Ejection fraction (EF) of the left ventricle was monitored with a single crystal probe linked to a microcomputer, after injection of 200 MBq Tc 99m-HSA. Stroke volume index determined by thermodilution and EF were used to calculate left ventricular end-diastolic volume index (LVEDVI). The degree of ischemia was numerically scored as evaluated from the ECG (modified V5 lead). The study protocol covered seven periods from awake before induction to 5 min after intubation. EF decreased moderately during intubation (P less than 0.05). Systemic vascular resistance index (SVRI) was decreased (P less than 0.05) at all times except during intubation when it was unchanged compared to control. LVEDVI decreased during induction (P less than 0.05), while left ventricular filing pressure remained unchanged. Heart rate did not change. Systolic arterial pressure decreased from 147 mmHg (19.6 kPa) to about 100 mmHg (13.3 kPa) during induction (P less than 0.05). Two patients were given vasoconstrictors because of low arterial pressure. The mean ischemic score did not change. One patient, however, had signs of progressive ischemia. In this patient isoflurane administration was stopped after the last recording and the ECG normalized within 20 min.
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PMID:Isoflurane and intravenous anesthesia used for induction before coronary artery bypass grafting. 278 47

Right ventricular (RV) systolic and diastolic functions were assessed in patients with previous anteroseptal myocardial infarction to ascertain the influence of interventricular septal ischemia on RV function. Gated right ventriculography with continuous infusion of krypton-81 m was performed in 12 normal subjects and 28 patients with infarction but without significant stenosis of the right coronary artery. Furthermore, RV contractile reserve by postextrasystolic potentiation was evaluated by gated radionuclide ventriculography with 99mTc-HSA. The patients with anteroseptal infarction were divided into two groups by the presence or absence of three hours' redistribution in the septal region on exercise thallium-201 myocardial scintigraphy. Two indices of systolic function (ejection fraction and the peak ejection rate) and three indices of diastolic function (1/3 diastolic filling rate, the peak filling rate and time to the peak filling rate) were derived from the right ventricular time-activity curve and its derivative curve. There was no difference in systolic function among normal subjects and patients with or without redistribution. However, diastolic function was impaired only in the patients without redistribution. The RV contractile reserve in the patients without redistribution was less than in those with it. Thus, RV systolic function was maintained in the patients with anteroseptal infarction, but contractile reserve deteriorated only in severe septal ischemia. Similarly, diastolic function was maintained in mild septal ischemia, but impaired in severe septal ischemia. We concluded that RV systolic and diastolic functions are closely related to interventricular septal ischemia.
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PMID:[Right ventricular systolic and diastolic functions assessed by 81mKr scintigraphy and relation to ventricular septal ischemia]. 345 54

Acute lesions of the gastroduodenal mucosa may result from gastric mucosal ischemia with subsequent cellular dysfunction, capillary leakage and increased susceptibility to mucosal damage. A new technique for measuring the effect of hypovolemic shock and gastric mucosal permeability is presented. Piglets were injected intravenously with human serum albumin labelled with 100 micro Ci of iodine-131 (131I-HSA). Serial blood and gastric samples were obtained for gamma counting during the control, hypovolemic shock and resuscitative periods. Increased gastric acid secretion and clearance of labelled serum albumin occurred after resuscitation from hypovolemic shock. The authors believe that increased capillary permeability and defective gastric mucosal cell function due to ischemia contribute to these changes.
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PMID:Radiotracer assessment of gastric mucosal permeability after hypovolemic shock. 736 60

The authors examined the effect of delayed high-concentration albumin therapy on ischemic injury in a highly reproducible model of middle cerebral artery (MCA) occlusion in rats. Male Sprague-Dawley rats weighing 270 to 320 g were anesthetized with halothane and subjected to 120 minutes of temporary MCA occlusion induced by means of a poly-L-lysine-coated intraluminal nylon suture inserted retrograde via the external carotid artery into the internal carotid artery and MCA. The agent (20% human serum albumin [HSA]) or control solution (sodium chloride 0.9%) was administered intravenously at a dosage of 1% of body weight immediately after suture removal following a 2-hour period of MCA occlusion. The animals' neurological status was evaluated during MCA occlusion (at 60 minutes) and daily for 3 days thereafter. The brains were perfusion-fixed, and infarct volumes and brain edema were determined. The HSA significantly improved the neurological score compared with saline at 24 hours after MCA occlusion. The rats treated with HSA also had significantly reduced total infarct volume (by 34%) and brain edema (by 81%) compared with saline-treated rats. There was a strong correlation between hematocrit level and brain edema (p < 0.01), and between total infarct volume or brain edema and neurological score at 24, 48, and 72 hours postinjury (p < 0.0002). These results strongly support the beneficial effect of delayed albumin therapy in transient focal ischemia and indicate its possible usefulness in treating patients with acute ischemic stroke.
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PMID:Effect of delayed albumin hemodilution on infarction volume and brain edema after transient middle cerebral artery occlusion in rats. 932 48

The effects of intestinal ischemia and reperfusion (I/R) on small intestinal mucosal endothelial and epithelial barrier integrity and phagocytic function were assessed in rats subjected to 20- or 40-min mesenteric ischemia and a 3-h reperfusion. The results showed that human serum albumin (125I-HSA) flux through the endothelial layer to the interstitial space increased as did 125I-HSA clearance from blood to the gut lumen and 131I-HSA flux from the gut lumen to the interstitial space in rats with I/R. E. coli adhering to microvilli, invading and passing into the microvessels, were noted on the small intestinal mucosa in animals subjected to 40-min ischemia and a 3-h reperfusion. Phagocytic function increased, especially in the small intestinal wall, lungs, liver, and spleen in the groups with I/R, correlating with the length of ischemia. The results imply that both endothelial and epithelial barrier integrity is impaired in the early phase after I/R and that the epithelial barrier more effectively restricts macromolecular leakage compared with the endothelial barrier. I/R impairs the intestinal barrier not only by causing tissue hypoxia but also by activating the phagocytic system and aggravating barrier damage, which finally may result in bacterial translocation and remote organ dysfunction.
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PMID:Phagocytic and intestinal endothelial and epithelial barrier function during the early stage of small intestinal ischemia and reperfusion injury. 1071 78

PNA+Tempol, albumin containing conjugated (polynitroxyl albumin; PNA) and free (4-hydroxyl-2,2,6,6-tetramethyl-piperidinyl-1-oxyl; Tempol) nitroxide may protect against injury caused by reactive oxygen species. Therefore, the actions of PNA+Tempol on liver injury and inflammation induced by hepatic ischemia and reperfusion (I/R) were examined. Rats were subjected to 1 h ischemia followed by 24 h reperfusion in the absence (I/R) or presence of PNA+Tempol (25%; 15 mL/kg, i.v.) (I/R+PNA+Tempol) or human serum albumin (23%; 13.5 mL/kg, i.v.) (I/R+HSA). Test solutions were administered prior to and for 2 h during reperfusion. Sham-operated rats underwent surgery with neither ischemia nor infusion. I/R+PNA+Tempol rats had significantly less liver injury and inflammation than I/R rats. I/R+PNA+Tempol livers exhibited focal lesions whereas I/R livers exhibited global necrosis. Likewise, plasma ALT activity was significantly lower in I/R+PNA+Tempol rats. PNA+Tempol reduced I/R-induced neutrophil accumulation and intercellular adhesion molecule-1 (ICAM-1) expression. HSA did not alter I/R-induced liver injury or inflammation. Sham-operated rats exhibited normal liver morphology and no inflammation. Attenuation of I/R liver injury by PNA+Tempol may be mediated by its effect on inflammation, the major contributor to I/R injury. Reduction of inflammation by PNA+Tempol is most likely due to the antioxidative nature of the nitroxides.
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PMID:Polynitroxyl albumin plus tempol attenuates liver injury and inflammation after hepatic ischemia and reperfusion. 1119 30

Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl, TPL), a low molecular weight stable nitroxyl radical (nitroxide), has been demonstrated in many in vitro and in vivo models to have protective effects against oxidative stress. The beneficial effect of TPL, however, is limited because of its short life-time in tissues. We have previously shown that polynitroxylated macromolecules such as polynitroxyl-human serum albumin (PNA) enable maintaining a sustained concentration of TPL for longer periods in tissues. PNA itself has previously been shown to inhibit ischemia-reperfusion (I/R) injury in the gut and to potentiate the activity of TPL. The aim of the present study was (i) to select an optimum formulation of PNA + TPL for therapeutic applications using in vivo EPR spectroscopy and (ii) to evaluate the efficacy of the PNA + TPL formulation in preventing I/R injury to heart, in an in vivo rat model. Rats were subjected to 45 min occlusion of the left anterior descending (LAD) coronary artery followed by 120 min reperfusion. PNA (100 mg/ml) + TPL (10 mg/ml), human serum albumin (HSA, 100 mg/ml) + TPL (10 mg/ml), or saline were injected 5 min before ischemia (3 ml/kg BW, i.v.) and 5 min before reperfusion (3 ml/kg BW, i.v.), followed by a 4 ml/kg BW infusion over 2 h reperfusion. Myocardial risk and infarct regions were then estimated. The results showed that the infarct volume, expressed as a percentage of the risk region, in the group treated with PNA + TPL was 39.7 +/- 3.1%, which was significantly smaller than for the saline (51.3 +/- 3.5%) or HSA + TPL (48.4 +/- 1.4%) groups. The results demonstrate that the PNA + TPL combination is very effective in reducing myocardial ischemia-reperfusion injury.
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PMID:Polynitroxyl-albumin (PNA) enhances myocardial infarction therapeutic effect of tempol in rat hearts subjected to regional ischemia-reperfusion. 1193 97

Epinephrine is known to be rapidly oxidized during sepsis. Ischemia and acidosis, which often accompany sepsis, are associated with the release of weakly bound cupric ions from plasma proteins. We investigated whether copper promotes oxidation of epinephrine at both physiological and acidic pH and whether D-Asp-D-Ala-D-His-D-Lys (D-DAHK), a human albumin (HSA) N-terminus synthetic peptide with a high affinity for cupric ions, attenuates this oxidation. Epinephrine alone [100 microM] or with CuCl(2) [10 microM], and with CuCl(2) [10 microM] and D-DAHK [20 microM] at pH 7.4, 7.0, 6.5, and 6.0 were incubated for 1h at 37 degrees C. Epinephrine oxidation was measured by the spectrophotometric quantification of its oxidation product, adrenochrome. We found that adrenochrome increased, suggesting copper-induced oxidation of epinephrine. At pH 7.4, 7.0, 6.5, and 6.0, adrenochrome increased by 47%, 53%, 24%, and 6% above baseline, respectively. D-DAHK attenuated the copper-induced oxidation of epinephrine to baseline levels. These in vitro results indicate that copper-induced epinephrine oxidation is greatest at the physiological pH 7.4 as well as in severe acidosis, pH 7.0, and that D-DAHK completely inhibits this oxidation.
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PMID:Copper-induced oxidation of epinephrine: protective effect of D-DAHK, a synthetic analogue of the high affinity copper binding site of human albumin. 1272 20

Nitric oxide (NO) supplementation may modify myocardial oxygen consumption and vascular function after ischemia. We investigated the effects of the NO donor, S-nitroso human serum albumin (S-NO-HSA), on cardiac oxygen metabolism during controlled reperfusion on normothermic cardiopulmonary bypass after severe myocardial ischemia. Pigs randomly received either S-NO-HSA or human serum albumin prior to and throughout global myocardial ischemia. Myocardial oxygen utilization is impaired at the onset of reperfusion, which is not amenable to S-NO-HSA. However, NO supplementation during ongoing supply dependency of oxygen consumption eventually leads to greater myocardial oxygen delivery and consumption. In conjunction with a better washout of lactate, this indicates an improved capillary perfusion in the S-NO-HSA group during reperfusion, which results in a better contractile function post bypass.
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PMID:S-nitroso human serum albumin improves oxygen metabolism during reperfusion after severe myocardial ischemia. 1533 16


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