Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that coronary ischemia increases extravascular lung water. To determine whether pulmonary microvascular permeability is increased by coronary ischemia, we measured pulmonary hemodynamics, lung lymph flow (QL), and lymph-to-plasma protein concentration ratio (L/P) in 12 sheep with chronic lung lymph fistulas. Studies were done in 3 groups: in group 1 (n = 7) a marginal branch of the left circumflex artery (Lcx) was occluded, in group 2 (n = 5) left atrial pressure (Pla) was mechanically raised by 10 mmHg, and in group 3 (n = 5) Lcx was occluded and Pla was raised by 10 mmHg. In group 1, coronary occlusion increased QL (4.6 +/- 0.4 to 8.3 +/- 2.6 ml/h) without changes in L/P. In group 2, elevated Pla increased QL (5.1 +/- 1.2 to 10.1 +/- 3.0 ml/h) with decreases in L/P (0.71 +/- 0.02 to 0.61 +/- 0.02). In group 3, coronary occlusion with elevated Pla caused a further increase in QL (5.0 +/- 1.5 to 16.9 +/- 4.6 ml/h) without significant decreases in L/P (0.71 +/- 0.01 to 0.65 +/- 0.06). Lung lymph concentrations of 6-keto-prostaglandin F1 alpha (a degradation product of prostacyclin) increased transiently after coronary occlusion. These results indicate that coronary occlusion can increase transcapillary protein transport in lungs of conscious sheep and simultaneously increase prostacyclin production in the lung.
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PMID:Effects of coronary ischemia on lung fluid balance in conscious sheep. 317 Apr 13

Increased extravascular lung water has been reported following periods of myocardial ischemia. To determine whether increased pulmonary microvascular permeability was produced by ischemia, total protein lymph-to-plasma concentration ratios (CL/CP) were obtained at mechanically increased left atrial pressures (Pla) before and after ligation of the left anterior descending coronary artery in dogs. Pulmonary and systemic vascular pressures and cardiac output were monitored and lymph flow was measured from an afferent tracheobronchial lymphatic. Osmotic reflection coefficients (sigma) for total protein were estimated using CL/CP = 1-sigma at high filtration rates, and permeability-surface area (PSf) products were fit to the data. The postischemic lung lymph data best fit average values of sigma = 0.68 and PSf = 0.073 ml X min-1 X 100 g-1 wet weight. There were no significant differences in lymph protein or water clearances between the pre- and postischemic increased Pla states or for myocardial ischemia compared with control values for the experimental preparation. Levels of 6-ketoprostaglandin F1 alpha, a degradation product of prostacyclin, increased by 10- to 14-fold above preischemic values in pulmonary lymph, and there was a significant increase in pulmonary vascular resistance during ischemia. Extravascular lung water was not increased above that attributed to the increased Pla alone. These data indicate no significant increase in pulmonary microvascular permeability to plasma proteins during myocardial ischemia.
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PMID:Failure of myocardial ischemia to increase pulmonary microvascular permeability in dogs. 654 45

We observed temporal changes in NACP (precursor protein of non-Abeta component of Alzheimer's disease amyloid), a presynaptic protein a.k. a. alpha-synuclein, in the hippocampus after 5 min ischemia. Intense NACP immunoreactivity was seen transiently around cerebral blood vessels in the CA1 subfield on day 4, and NACP-positive unusual tubal and chain-like structures developed on month 6. We suggest that the changes in NACP may play an important role in the ischemic pathogenesis.
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PMID:Changes in presynaptic protein NACP/alpha-synuclein in an ischemic gerbil hippocampus. 955 70

The beta-adrenergic pathway may have a role in the pathophysiology of ischemic syndromes characterised by reversible left ventricular dysfunction, such as myocardial stunning and other clinical conditions of unstable angina or coronary spasms, or chronic reversible left ventricular dysfunction, which might be a consequence of repeated events of short-term ischemia ("repetitive stunning"). A partial-to-total occlusion of the left anterior descending coronary artery in pigs was used to induce short periods of ischemia (total ischemic time 12 +/- 2 min). Hypokinesis and dyskinesis of the myocardium were considered signs of myocardial dysfunction. We found a maintained function of the beta-adrenergic signalling system. Density and affinity of beta-adrenergic receptors were not different in stunned and non-ischemic regions, nor were cyclic AMP and cyclic GMP intracellular contents and ratio, nor well as the ratio of stimulatory/inhibitory G protein a subunits. Our findings are in agreement with a maintained beta-adrenergic signalling system in the pathophysiology of chronic reversible left ventricular dysfunction.
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PMID:Beta-adrenergic receptors and intracellular signalling pathway in stunned and non-ischemic regions of pig myocardium. 1151 95

Neonatal rat hearts are more tolerant to ischemia compared to adult rat hearts. We hypothesized that opioid receptors and mitochondrial potassium channels are involved in the elevated ischemia tolerance of neonatal rats. Newborn rats were treated by an intraperitoneal injection with sodium chloride (placebo, Pla; n = 7), naloxone (Nal; n = 8), or K+ (ATP) channel blocker 5-hydroxydecanoate (HD; n = 8), or were left untreated (sham; n = 8). Thirty minutes after injection, the rats were sacrificed and hearts were arrested cardioplegically and fixed with aldehyde fixative 90 min after global ischemia at room temperature. For control, newborn rat hearts were fixed immediately after sacrifice. Ventricular tissue blocks were prepared for electron microscopy. Mitochondrial (volume-weighted mean volume of mitochondria) and cardiomyocyte volume (cellular edema index, CEI) were estimated to quantify the ischemic injury. Compared to control myocardium, CEI was increased by 244% +/- 39% in sham, 173% +/- 28% in Nal, 142% +/- 25% in HD, and 101% +/- 24% in Pla (P < 0.05 between groups). Volume-weighted mean volume of mitochondria was increased by 514% +/- 235% in sham, 341% +/- 110% in Nal, 458% +/- 149% in HD, and 175% +/- 70% in Pla. Differences between Pla and other groups were significant (P < 0.01 for all). No significant difference was observed between the other groups. Thus, ischemic injury was smallest with placebo, indicating a mechanism similar to preconditioning induced by the intraperitoneal injection. This response was attenuated by blockade of opioid receptors and mitochondrial potassium channels, suggesting their involvement in the elevated ischemia tolerance of newborn rat hearts.
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PMID:Myocardial ischemia tolerance in the newborn rat involving opioid receptors and mitochondrial K+ channels. 1645 73

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