Calibration of a TLD-100 powder dosimetric system to verify the absorbed dose to water imparted by 137Cs sources in low dose rate brachytherapy at the oncology unit in the Hospital General de Mexico.

A thermoluminescence dosimetry (TLD) system was characterised at SSDL-ININ to verify the air-kerma strength (S(K)) and dose-to-water (D(W)) values for (137)Cs sources used in low dose rate (LDR) brachytherapy treatments at the Hospital General de Mexico (HGM). It consists of a Harshaw 3500 reader and a set of TLD-100 powder capsules. The samples of TLD-100 powder were calibrated in terms of D(W) vs. nC or nC mg(-1), and their dose response curves were corrected for supralinearity. The D(W) was calculated using the AAPM TG-43 formalism using S(K) for a CDCSM4 (137)Cs reference source. The S(K) value was obtained by using a NE 2611 chamber, and with two well chambers. The angular anisotropy factor was measured with the NE 2611 chamber for this source. The HGM irradiated TLD-100 powder capsules to a reference dose D(W) of 2 Gy with their (137)Cs sources. The percent deviations between the imparted and reference doses were 1.2% < or = Delta < or = 6.5%, which are consistent with the combined uncertainties: 5.6% < or = u(c) < or = 9.8% for D(W).

The effects of milrinone (Win 47203) on the coronary blood flow and oxygen consumption of the dog heart-lung preparation.

Milrinone is a new bipyridine-positive inotropic agent that is closely related to amrinone. In the nonfailing heart, coronary blood flow was increased and coronary bed resistance was decreased by milrinone, most probably by a direct action of milrinone on the coronary vasculature. Oxygen consumption was increased at the lower workloads. In the failing heart milrinone (0.1 to 0.5 mg/L of blood) increased cardiac output and coronary blood flow and reduced coronary vascular resistance. With the 0.1 mg dose oxygen consumption was reduced, especially at the high workloads, and was not significantly changed at the low work levels. With higher doses of milrinone oxygen consumption of the heart was not changed significantly while external work was increased. These data show that milrinone can increase the work of the heart with a decrease or no significant change in oxygen consumption of the isolated failing heart. The use of this drug in heart failure accompanied by restricted blood flow may thus be indicated.

[Effects of amrinone, a new non-digitalic positive inotropic agent, on the efficiency and coronary circulation of the heart]. / Effectos del amrinone, un nuevo agente inotrópico positivo no digitálico, sobre la eficiencia y el flujo coronario del corazón.

It has been reported recently that 5-amino-34,4'-bipyridine-6(1H)-one is a new positive inotropic agent that appears to offer significant advantages over the cardiac glycosides. The effects of this agent were studied in a modified heart-lung preparation which allows the measurement of coronary flow and oxygen consumption in addition to a controlled study of cardiac contractility. In two models of cardiac insufficiency the administration of 5 mg amrinone caused a marked increase in cardiac output and a considerable decrease in left atrial pressure with complete reversal of the failure. In addition, the drug produces a 78% increase in coronary flow. Amrinone produces in these preparations a proportionally larger increase in cardiac output than in oxygen consumption, thus this agent increases cardiac efficiency. These results suggest that this new compound could be very useful in the treatment of cardiac insufficiency in congestive heart failure.

Site of cellular uncoupling in injured cardiac tissue in the dog.

We injured false tendons of the dog heart and examined the intercalated disks (ID) to locate the site of cardiac cell uncoupling. We put the preparations at two calcium concentrations: Ca++-free solution (no healing) and [Ca++] = 5.4 mM ('healing-over'). They were studied immediately, and 1 h, after the injury. We examined the diffusion of Procion yellow from the cut end and measured the relative area of nexus. After the 'healing-over' we found that the ID linking damaged and undamaged cells were the barrier to the diffusion of the dye, and that these ID underwent an exponential decrease in the nexal area (time constant 1.5 h). On the other hand, the next ID (i.e. the other extremity of the same cells) kept the nexal area they had in the unhealed condition. These facts indicate that the true uncoupling site is the ID that separate damaged from undamaged cells.

[Mechanism of the antiarrhythmic effect of inorganic phosphates in digitalis poisoning]. / Mecanismo del efecto antiarrítmico de los fosfatos inorgánicos en la intoxicación digitálica.

THe synergistic effects between calcium and the therapeutic and toxic actions of the cardiac glycosides have suggested that a way of treating digitalis intoxication could be through a decrease in free plasma calcium. In 1966, Burckhardt and La-Due published a study based on the inverse relationship that exists between plasma phosphates and calcium. It was shown then that potassium phosphate had a pronounced antiarrhythmic effect on digitalis induced arrhythmias. The use of potassium phosphate for this study prevented the analysis of the role of the phosphates in these effects, since the actions of potassium in digitalis toxicity precluded any conclusion. The purpose of the present paper is to study the effect of phosphates on digitalis intoxication and its possible mechanism of action. The results obtained demonstrated: 1) Phosphates have a marked antiarrhythmic effect in digitalis induced arrhythmias. 2) This effect is due to a decrease in free plasma calcium. 3) The lowering of this calcium pool occurs in the blood and is not mediated by hormonal or renal mechanisms. 4) The ions that disappear from the free calcium pool do not precipitate. 5) The use of phosphates could be useful in the treatment of some clinical cases of advanced digitalis intoxication.

[Mechanism of the decrease in free plasma calcium produced by the administration of inorganic phosphates]. / Mecanismo de la disminución de calcio libre plasmático producida por la administración de fosfatos inorgánicos.

The preceding paper (published in the issue) demonstrated that the administration of sodium phosphates exerted a marked antiarrhythmic effect on several models of digitalis intoxication; this action being due to a decrease in the free calcium fraction. THe purpose of the present paper is to analyze the effects that several concentrations of phosphates have on the different calcium fractions and determine the fate of the ions that are disappearing from the calcium pool. This study was done using two models of digitalis intoxication, one in the intact dog and the other in the heart-lung preparation and two protocols in which the experiments were carried out using blood in vitro. The results show: 1) the administration of phosphates into the intact dog produces a small decrease in the total calcium content of plasma and blood. 2) the increase in phosphate concentration runs parallel to an important decrease in free calcium. 3) In the heart-lung preparation, phosphate administration markedly decreases free calcium but does not lower total calcium in plasma or blood. 4) An increase in phosphate concentration of plasma in in vitro conditions does not alter total calcium and decreases free calcium in a linear relationship with the levels of phosphates. 5) A fraction of the phosphates added to the plasma and the ions that are disappearing from the free calcium pool are binding to a plasmatic macromolecule (most probably a protein) which prevents them from precipitating.