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Ring preparations of canine coronary arteries were analyzed to determine the effects of adenosine on coronary constriction by polymorphonuclear leukocytes (PMN). The adhesion of PMNs to the vascular endothelium of canine coronary arteries and PMN-mediated vasoconstriction was inhibited by the activation of adrenergic A2a receptors with CGS-21680C receptor agonist. Furthermore, PMN-mediated vasoconstriction was restored by 3,7-dimethyl-1-propagrylxanthine which inhibited adenosine activity.

Tyrosine kinase acts as a messenger of neuronal cell death during the selective degeneration of hippocampal pyramid cells in transient forebrain ischemia models. Protein tyrosine phosphorylation of pp42 was detected after the nonlethal and lethal ischemia of the hippocampus and cerebral cortex. The ischemic hippocampal CA1 neurons also exhibited increased expression of phosphotyrosyl proteins indicating the anti-microtubule-associated protein kinase activity of pp42.

The effects of aging and gender on diurnal heart rate variability was investigated as measurements of R-R intervals during a 24-hr. period using a Holter electrocardiogram. Male subjects showed higher values for the low-frequency (LF) component of cardiac beta-adrenergic function than female subjects. There were no differences in the peak of parasympathetic function between the two sexes. There was a significant relationship between LF and age, suggesting that heart beat is affected by aging and gender.

The opening of adenosine triphosphate-sensitive potassium channels due to adenosine synergistically contributed to the infarct size-limiting effects of ectosolic 5'-nucleotidase. The infusion of glibenclamide in open-chest dogs reduced the infarct size-limiting effect of ischemic preconditioning due to the inhibition of ectosolic 5'-nucleotidase. This reaction indicated that extracellular adenosine production is dependent on the activity of ectosolic 5'-nucleotidase during ischemic preconditioning.

A rise in the ecto-5'-nucleotidase activity induces cardioprotection of ischemic preconditioning (IP). Deactivation of the ecto-5'-nucleotidase activity by an inhibitor weakens the infarct size-limiting effect of IP. Analysis of the coronary arteries of experimental dogs reveals that the infarct size-limiting effect of IP reduces with time. The ecto-5'-nucleotidase activity indirectly affects the infarct size.

Transient short duration ischemia reversibly influences the coronary pressure-flow activity due to decreased vascular relaxation. Myocardial contractile dysfunction attenuates the downward shift relationship of the coronary pressure-flow. The experimental setup to determine the influence of ischemia on coronary pressure and previous studies in the field are discussed.

Leukocyte common antigen-related protein (LRP) mRNA is abundant in rat kidney and relatively rich in collecting ducts. It appears to play some role in the physiological function of renal distal tubules, especially by inactivating the function of EGF in the collecting tubule transport system. It also has abundant distribution in inner medullary collecting ducts. This pattern of expression gives suggests that LRP might be involved in the specific renal tubule function, such as urinary concentration mechanism.

Mitochondrial misuse of oxygen in the brain during hypertension may result in mitochondrial injury and neuron degeneration, as shown by hypertensive rats. Mitochondrial thiobarbituric acid-reactive substance (TBARS) and manganese superoxide dismutase (MnSOD) concentration in hyper tensive target organs (heart, brain and kidney) of spontaneously hypertensive rats (SHR) is analysed. TBARS and MnSOD in brain increased noticeably in rats during maturation. Marked increase of lipid peroxidation is observed in SHR but no increase in MnSOD in the brain is noticed.

The influence exerted by 5minutes of ischemia on brain 5-lipoxygenase (5-LO) and leukotriene C4 (LTC4) is investigated during reperfusion. The gerbil model of transient forebrain ischemia is used in the investigation. The investigation reveals that during reperfusion the production of LTC4 is reduced by superoxide dismutase and oxygen radical scavengers.

Analysis of the influence of a selenoorganic compound, ebselen on infarct size in a canine coronary artery occlusion-reperfusion model shows that ebselen causes a decrease in myocardial-reperfusion injury and reduces the infarct size. The infarct size reduction by ebselen correlates to the decrease in myeloperoxidase activity in ischemic myocardium and rise in reduced glutathione levels. Ebselen treatment has no effect on the regional myocardium, reduced glutathione levels, the regional myocardial blood flow and hemodynamic parameters involved in the experimental studies.

A study of osmoregulation in cultured mesangial cells by neutral amino acids transported by system A reveals an approximately two-fold increase in the contents of all amino acids under hypertonic conditions than in isotonic cells. Na+-dependent 2-(methylamino)isobutyric acid (MeAIB) uptake measurement reveals the system A transport activity in hypertonic cells to be 3.8-folds the uptake in isotonic cells, reaching a maximum 16 hours after the change to hypertonic medium. An increase in the maximal velocity without any change in the Michaelis constant leads to the response to hypertonicity, which depends on RNA and protein synthesis. Decreasing the medium osmolality from hypertonic to isotonic restores MeAIB uptake to the isotonic level within 16 h, accompanied by a large transient efflux of L-proline within 10 min.

Experiments on the blood-perfused and cannulated left anterior descending coronary artery of dogs to determine the effects of 5-amino-4-imidazolecarboxamide (AICA) riboside reduces the myocardial ischemic injury to enhance metabolic and myocardial contractile dysfunctions following coronary microembolization. AICA riboside induces the release of adenosine and increases hyperemia and 5'-nucleotidase functions in the ischemic myocardium. Alpha, beta-methyleneadenosine 5'-diphosphate and 8-phenyltheophylline block the beneficial effects of AICA riboside.

Superfusion of Tyrode solution consisting of arachidonic acid and soybean lipoxygenase, and indo 1 into rat cardiac myocytes to analyze the direct influence of arachidonate lipoxygenation reveals that arachidonate lipoxygenation products induce overload of intracellular Ca2+ and impair the cardiac myocytes. Arachidonic acid and lipoxygenase collectively enhance twitch amplitude and intracellular Ca2+ to cause irreversible hypercontracture. Alpha-tocopherol and ascorbic acid reduce cellular impairment and intracellular Ca2+ increases.

Mitochondrial cytochrome aa3 redox states were determined along various regions of the hepatic lobule using reflectance microspectroscopyto determine the distribution of oxygen tension across the lobule. Results showthat cytochrome aa3 reduction state increase with distance from the periportal area. Since the degree of cytochrome reduction is inversely proportional to theoxygen tension, results suggest a tension gradient for oxygen across the hepatic lobule.