Biomedical subjects

J Rho

Publications and source records attributed to J Rho.

22 records · Page 2Linked to original sources

PubMed1989

Norepinephrine overflow in perfused mesenteric arteries of spontaneously hypertensive rats.

We examined the overflow of endogenous norepinephrine with electrical stimulation, the associated pressor response, and rate of initial neuronal uptake of [3H]norepinephrine in perfused mesenteric arteries of 7- and 13-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The tissues of two rats, a spontaneously hypertensive and a WKY control rat, were simultaneously processed and subjected to the same electrical stimulation. Both absolute and fractional overflow of endogenous norepinephrine during periarterial nerve stimulation (5 and 10 Hz for 1 minute) in the tissue of 7-week-old SHR was significantly greater whereas overflow of 13-week-old SHR was equivalent as compared with that of the age-matched WKY rats. The tissue content of norepinephrine was 20-25% higher in SHR of both ages. There was significantly enhanced [3H]norepinephrine uptake in the tissues of young SHR, but no difference was observed in the older SHR. The pressor response to periarterial nerve stimulation was significantly enhanced in 7-week-old SHR and much more so at the older age as compared with the WKY control rats. Exogenous norepinephrine dose-response curves in the tissues of 7-week-old SHR exhibited a parallel leftward shift, characteristic of a change in sensitivity, whereas that of 13-week-old SHR showed a much steeper slope as compared with the respective WKY control rats. This finding suggests that in addition to smooth muscle supersensitivity, structural alterations had occurred in vasculature of 13-week-old SHR. These data indicate that in SHR both the exocytotic release of norepinephrine and the responsiveness of the vascular smooth muscle cells are enhanced in the developmental stage of hypertension whereas smooth muscle supersensitivity to norepinephrine and nonspecific structural alterations primarily contribute to the maintenance of hypertension at 13 weeks of age.

Animals↗

PubMed1983

Plasma clonidine levels in hypertension.

Ten patients with essential hypertension were treated orally with clonidine, and the dose was titrated until the diastolic pressure fell below 90 mm Hg or at least 10 mm Hg below baseline, or until a maximum dose of clonidine of 1.2 mg/day was reached. After at least 2 wk on a constant dose of clonidine, the patients were hospitalized and blood pressure and plasma clonidine concentrations were measured by a highly specific and sensitive gas chromatographic, electron-capture method (sensitivity as low as 0.1 ng clonidine/ml). There was good correlation between daily clonidine dose and plasma clonidine concentration. The average blood pressure reduction during 12 hr after clonidine correlated poorly with steady-state plasma levels of clonidine, but when the individual maximum decrease in mean blood pressure was paired with the corresponding peak plasma concentration of clonidine, the correlation was strong.

Adult↗

PubMed1977

The specific interaction between LSD and serotonin-binding protein.

In this report, we describe the chemical interaction between lysergic acid (LSD) and serotonin-binding protein (SBP) by a three-dimensional spectroscopic technique. This instrument records simultaneously the activation and fluorescence spectra, and plots fluorescence intensity level by a series of isointensity contours. Free LSD exhibits maximum fluorescence at 435 nm with excitation maximum at 330 nm. While SBP-bound LSD shifted its fluoresence and excitation maximum to 465 nm and 375 nm respectively. These results suggest that the drug-protein interaction caused an extensive delocalization of the molecular orbital electrons and thereby lengthen the electronic conjugation of the drug molecule. Such shift was not observed when LSD was incubated with bovine serum albumin under the same condition. This technique is sensitive and requires a small volume of samples. It permits us to determine both free and bound drug in the same sample and provides us specific information about the drug and protein interaction.

Animals↗

PubMedDate not supplied

Age-dependent fatigue behaviour of human cortical bone.

Despite a general understanding that bone quality contributes to skeletal fragility, very little information exits on the age-dependent fatigue behavior of human bone. In this study four-point bending fatigue tests were conducted on aging bone in conjunction with the analysis of stiffness loss and preliminary investigation of nanoindentation based measurements of local tissue stiffness and histological evaluation of resultant tensile and compressive damage to identify the damage mechanism responsible for the increase in age-related bone fragility. The results obtained show that there is an exponential decrease in fatigue life with age, and old bone exhibits different modulus degradation profiles than young bone. In addition, this study provides preliminary evidence indicating that during fatigue loading, younger bone formed diffuse damage, lost local tissue stiffness on the tensile side. Older bone, in contrast, formed linear microcracks lost local tissue stiffness on the compressive side. Thus, the propensity of aging human bone to form more linear microcracks than diffuse damage may be a significant contributor to bone quality, and age related fragility in bone.

Age Factors↗