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Biomedical subjects

A Garay

Publications and source records attributed to A Garay.

5 recordsLinked to original sources
PubMed1995

Clinical and genetic studies of fatal familial insomnia.

We report a 42-year-old man who, for 8 months, had intermittent motor abnormalities and mild difficulty falling asleep. A diagnosis of fatal familial insomnia (FFI) became evident over the next 6 months when he developed progressive insomnia, myoclonus, sympathetic hyperactivity, and dementia. The amyloid or prion protein (PrP) genotype showed features typically seen in FFI, with a 178Asn mutation and a 129Met polymorphism. There was also a deletion of one octapeptide repeat, suggesting that the association of 178Asn mutation with the 129Met polymorphism is not due to "founder effect." Western immunoblot showed a trace of protease-resistant PrP in the thalamus--which had the most significant neuronal loss and gliosis--a moderate amount of PrP in the fronto-temporal area, and no detectable protein elsewhere in the brain. Endocrine studies showed that a circadian modulation of hormonal levels could be maintained despite a near-total absence of sleep. Administration of gamma-hydroxybutyrate induced a remarkable increase in slow-wave sleep.

Adult↗
PubMed1986

Critical evaluation of isometric indexes of relaxation in rat and cat papillary muscles and toad ventricular strips.

The effects of increasing calcium concentration and isoproterenol on myocardial relaxation were compared in cat and rat papillary muscles and toad ventricular strips. Isoproterenol effects were studied at equivalent positions of the calcium contractility response curve in the three species: at the plateau and at 25% and 50% of maximum. Calcium concentration was increased from the 25% point to the plateau of the calcium contractility curve for each species. Contractility was characterized by maximal velocity of tension development (+T). To study the relaxation phase, the following parameters were measured: maximal velocity of relaxation, (-T), the relationship between +T and -T (+T/-T), time to peak tension (TTP), time to half relaxation (t 1/2), relaxation time (Rt), total twitch duration (Tt) and the time constant of isometric tension decline from the time of -T (Tau). In rat muscles, t 1/2, Rt and Tt at all calcium levels, and Tau and +T/-T at the 50% and 100% of the calcium contractility curve, behaved as 'lusitropic': they significantly decreased with isoproterenol and not with calcium. Similar results were obtained in cat muscles except that at the 50% point of the calcium contractility curve, +T/-T was not significantly decreased. The behaviour of toad ventricle was different from that of mammalian heart: +T/-T and Tau appeared as lusitropic at all levels of the calcium curve, whereas only at the plateau some of the 'time' parameters were able to discriminate the isoproterenol lusitropic effect. These differences may reflect the strong dependence in amphibian heart of the time course of the action potential duration, not observed in mammalian ventricle.

Animals↗
PubMed1983

Negative inotropic effect of verapamil, nifedipine and prenylamine and its reversal by calcium or isoproterenol.

The type of antagonism between verapamil, nifedipine or prenylamine and calcium or isoproterenol on myocardial contractility, was investigated in cat papillary muscles. Dose response curves to calcium or to isoproterenol were performed in the absence and presence of a single dose of either verapamil, nifedipine or prenylamine. Non significantly different maximum values of tension (T) and maximal rate of rise of tension (+dT/dtmax) were obtained at the "plateau" of the dose responses curves to calcium in the absence and presence of the slow channel inhibitors. The (Ca2+)50, i.e. the calcium concentration necessary to obtain 50% of the maximal effect (T or +dT/dtmax), was significantly greater in the presence of the calcium channel blockers (Lineweaver-Burk method). The decrease in time to peak tension (TTP) associated with the negative inotropic effect of calcium channel blockers was also completely off-set by the addition of extra calcium. A Shild plot with a slope close to the unity confirmed simple competitive antagonism between calcium and nifedipine or prenylamine but not between calcium and verapamil. Isoproterenol was unable to completely overcome the negative inotropic effect of verapamil 10(-5) M and nifedipine 5 X 10(-7) M on T and +dT/dtmax. In addition, it enhanced the decrease in TTP produced by these two calcium entry blockers. The results do not support the view of a competitive antagonism between isoproterenol and verapamil or nifedipine on myocardial contractility. They also indicate that in restoring the decrease in myocardial contractility produced by calcium channel blockers, it is not the same to add extra calcium than isoproterenol.

Animals↗
PubMed1982

Decrease in time to peak tension produced by calcium blockers and isoproterenol. Its dependence on extracellular calcium.

The present experiments were designed to analyze the effect of verapamil, nifedipine and isoproterenol on myocardial contractility (+dT/dtmax) and time to peak tension (TTP) and its dependence on extracellular calcium concentration (Ca2+). The experiments were performed on cat papillary muscles from reserpinized cats. At (Ca2+) 1.34 mM the negative inotropic effect of cumulative doses of verapamil and nifedipine and the positive inotropic effect of isoproterenol occurred associated with a significant and dose-dependent decrease in TTP. The decrease in TTP produced by calcium blockers was completely reversed by the addition of calcium in a close parallelism with the recovery in myocardial contractility: At (Ca2+) 1.34 mM; verapamil 10(-6)M significantly decreased TTP from 299 +/- 14 msec to 250 +/- 11 msec. At (Ca2+) 15 mM values for TTP were 285 +/- 7 msec (control) and 291 +/- 5 msec (verapamil). Nifedipine 5 X 10(-7) M decreased TTP from 343 +/- 20 msec to 246 +/- 4 msec (Ca 1.34 mM). Values of TTP at calcium 15 mM were 296 +/- 6 msec (control) and 300 +/- 17 msec (nifedipine). On the contrary, the significant decrease in TTP produced by isoproterenol 10(-5)M at (Ca2+) 1.34 from 266 +/- 14 msec to 222 +/- 14 msec was still present at (Ca2+) 15 mM: 233 +/- 8 msec (control) and 220 +/- 8 msec (isoproterenol). The results suggest that the decrease in TTP produced by calcium blockers and isoproterenol is mediated by different mechanisms.

Animals↗