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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilator substances act either directly on vascular smooth muscle (e.g., adenosine) or indirectly (e.g., acetylcholine) on endothelial cells that respond by releasing an unknown powerful, short-lived relaxing factor. To determine whether chronic hypertension or hypercholesterolemia or both would alter the release of the endothelium-derived relaxing factor, experiments were performed in hypertensive rabbits (5-week cellophane wrap perinephritis; mean blood pressure, 134.7 mm Hg) and normotensive rabbits (mean blood pressure, 80 mm Hg) with a Doppler flow transducer and perivascular balloon implanted on the lower abdominal aorta. Rabbits were fed either 1% cholesterol or control diet for 4 weeks before the experiment. On the day of the experiment, resting hindlimb vascular resistance was greatest in hypertensive rabbits fed 1% cholesterol diet, followed (in descending order) by hypertensive rabbits, normotensive rabbits fed 1% cholesterol diet, and normotensive rabbits. Pharmacological autonomic reflex blockade was induced, and steady state intravenous infusion curves to acetylcholine, serotonin, and adenosine were constructed. Sensitivity (location of effective dose, 50%) to the three vasodilator agents was altered less than twofold from the values in normotensive rabbits for any treatment group. The maximum vasodilator response to acetylcholine, but not to adenosine or serotonin, infusion was reduced significantly in the treated rabbits compared with that in normal rabbits. Reactive hyperemic responses to 5 to 80 seconds of ischemia were not significantly different among the treatment groups. These results indicate that hypertension with or without hypercholesterolemia does not greatly alter the responsiveness of the hindlimb resistance vasculature to these three vasodilator agents or to ischemia.
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PMID:Effects of hypertension and hypercholesterolemia on vasodilatation in the rabbit. 369 79

Page kidney is the name ascribed to a rare syndrome of hyperreninemic hypertension caused by unilateral compressive perinephritis. Blood or fluid that accumulates in the perinephric subcapsular space compresses the renal parenchyma leading to ischemia. This syndrome is analogous to the description of cellophane-induced perinephritis by Page in 1939. Page kidney typically presents in healthy young men after blunt trauma to the flank or abdomen, although cases have been noted after medical or surgical interventions. We report a case of a Page kidney in a young man with hepatitis B virus-associated polyarteritis nodosa. The patient presented with severe hypertension, hypokalemia, hyperreninemia, and radiographic evidence of a unilateral subcapsular hematoma. Perinephric hemorrhage developed because of necrotizing vascular inflammation and spontaneous or traumatic vascular rupture. In patients who present with new-onset hypertension and hypokalemia with a history of trauma or coexisting vasculitis, the presence of a Page kidney should be considered.
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PMID:Hyperreninemic hypertension secondary to a subcapsular perinephric hematoma in a patient with polyarteritis nodosa. 974 Jan 70