Experimental Renal Ischemia Research Articles

Treatment of acute focal cerebral ischemia with propranolol.

Propranolol's potential as a protective agent against tissue injury has been noted in experimental myocardial, renal and early acute focal cerebral ischemia. The purpose of the present investigation was to study further the effects of racemic (d,l) propranolol on blood-brain barrier permeability, morphological changes, cortical electrical activity, and regional cerebral blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult cats, anesthetized with nitrous oxide, underwent 6 hours of right middle cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion, both directly into the right carotid artery. Right Sylvian rCBF did not significantly differ in the treated and untreated groups. Carbon filling defects and vital dye (i.e., Evans blue and fluorescein) extravasation were less severe in the propranolol treated animals. Light microscopic findings demonstrated no difference in infarct size between the two groups. The findings suggest that at doses given, racemic propranolol does not exert a protective effect upon cerebral tissue subjected to 6 hours of incomplete ischemia.

Alterations in 203HG Isotopic Kinetics in Experimental Renal Ischemia: Correlation with Renal Hemodynamics and Metabolism

Alterations in 203HG Isotopic Kinetics in Experimental Renal Ischemia: Correlation with Renal Hemodynamics and Metabolism

Renal hemodynamics and metabolism in chronic experimental renal ischemia, with and without hypertension, and their alteration by ganglionic blocking agents

Renal hemodynamics and metabolism in chronic experimental renal ischemia, with and without hypertension, and their alteration by ganglionic blocking agents

Activity of some serum enzymes in experimental renal ischemia

Experiments were staged on cats to analyze the mechanism of hyperenzymemia in ischemic injury of the organ. A study was made of the effect produced by temporary arrest of renal circulation on the content of transaminase, aldolase, alkaline phosphtase and copper-oxidase in the arterial and venous (flowing from the kidney) blood. As established, hyperenzymemia following a 6-hour renal ischemia may be caused by the passing of enzymes into the blood from other organs, as well as by “washing out” of some enzymes from the ischemic kidney.

Production of a Sustained Neurogenic Hypertension of Renal Origin

Several methods have been devised for producing experimentally a renal ischemia hypertension. That of Goldblatt, Lynch, Hanzal and Summerville1 is most frequently used. These methods have all involved the use of a foreign material such as a clamp and have produced blood pressure changes that are not reversible without removing the foreign material or the involved kidney.It has therefore been difficult to apply these technics to experimental studies analysing the value of various methods of surgical treatment of hypertension in man. It has also been difficult to evaluate the possible importance of a primary nervous factor or a primary vascular disease factor in attempting to correlate experimental renal ischemia hypertension with essential hypertension in man.A technic has been devised to determine in dogs whether an over-activity of the renal vasoconstrictor splanchnic nerves can produce hypertension. The technic consists of sympathectomizing all of the animal except the origin and the distribution of the...