Artificial reproduction of magnetic fields produced by a natural geomagnetic storm increases systolic blood pressure in rats.

The incidence of geomagnetic storms may be associated with changes in circulatory physiology. The way in which the natural variations of the geomagnetic field due to solar activity affects the blood pressure are poorly understood and require further study in controlled experimental designs in animal models. In the present study, we tested whether the systolic arterial pressure (AP) in adult rats is affected by simulated magnetic fields resembling the natural changes of a geomagnetic storm. We exposed adult rats to a linear magnetic profile that simulates the average changes associated to some well-known geomagnetic storm phases: the sudden commencement and principal phase. Magnetic stimulus was provided by a coil inductor and regulated by a microcontroller. The experiments were conducted in the electromagnetically isolated environment of a semi-anechoic chamber. After exposure, AP was determined with a non-invasive method through the pulse on the rat's tail. Animals were used as their own control. Our results indicate that there was no statistically significant effect in AP when the artificial profile was applied, neither in the sudden commencement nor in the principal phases. However, during the experimental period, a natural geomagnetic storm occurred, and we did observe statistically significant AP increase during the sudden commencement phase. Furthermore, when this storm phase was artificially replicated with a non-linear profile, we noticed a 7 to 9 % increase of the rats' AP in relation to a reference value. We suggested that the changes in the geomagnetic field associated with a geomagnetic storm in its first day could produce a measurable and reproducible physiological response in AP.

[Development of a canine model of chronic progressive right ventricular hypertension]. / Desarrollo de un modelo canino de hipertensión ventricular derecha crónica progresiva.

INTRODUCTION: Several animal models of right ventricle hypertension (RVH) have been produced through pulmonary artery banding with linen, tygon or teflon. Nevertheless few devices attempting a progressive, step by step graduated chronic development of RVH have been reported. The present study describes the results in our animal model of chronic RVH. MATERIAL AND METHODS: We designed a software programmed to obtain hemodynamic data and installed a small occlusive hydraulic device (OHD) at the pulmonary artery trunk producing a raise in the right ventricular systolic pressure (RVSP); this pressure can be modified externally through the OHD. We studied 12 healthy mongrel dogs (18 to 28 kg of weight) in the course of 6 months. Hemodynamic measurements were performed at different RVSP at two months intervals; (Baseline, 40 mmHg and 60 mmHg). RESULTS: The software was useful to analyze several hemodynamic variables at each RVSP. At 60 mmHg, the end diastolic pressure of the right ventricle (RVEDP) increased from 4.2 +/- 0.4 mmHg to 13.2 +/- 1.1 mmHg, p < 0.000, accompanied with a fall in cardiac output adjusted to the dogs weight from 0.16 +/- 0.03 L/min/kg to 0.09 +/- 0.01 L/min/kg, p > 0.000. Also an increase of the end diastolic pressure of the left ventricle (LVEDP) from 7.4 +/- 0.8 mmHg to 16.3 +/- 2.8 mmHg, p < 0.000, was observed. RVSP was maintained in chronic condition and the intraclass correlation coefficient was 0.83, P < 0.005. CONCLUSIONS: Right ventricular chronic hypertension is created. The device is useful and reliable to maintain chronic increments of RVSP. The software permits a versatile analysis.

[A system for non-invasive measurement of arterial pulse velocity in different vascular territories]. / Sistema para la medición no invasiva de la velocidad del pulso arterial en diferentes territorios vasculares.

Blood pulse wave velocity (PWV) is a known index of arterial rigidity and its measurement has proved its usefulness in the study of some cardiovascular pathologies. In this study we describe the design and implementation of a system for noninvasive PWV determination in the aorto-braqui-humero-radial (A-->h), aorto-ileo-femoro-pedial (A-->f) and aorto-carotid (A-->c) regions. This system was examined with 36 normotensives (NT) and 34 hypertensives (HT) patients with (LVH, n = 20) and without (WLVH, n = 14) left ventricular hypertrofy. The equipment consist of a personal computer with an analog to digital converter and hardware and software items adapted to take simultaneously the electrocardiogram (ECG), two photopletismographic pulses and one oscilometric pulse. The Q-pP interval (time between a Q ECG wave and distal blood pulse) and the distance to the register sites are taken into account to calculate the beginning of cardiac prexpulsive period (time zero of pulse trip) which allow the determination of the PWV (in meters/second) from the aortic root to the distal point of the via. PWV was significant higher (p < 0.001) in HT vs. NT (A-->h: 9.3 +/- 2.6 vs. 7.2 +/- 0.8, A-->c: 9.5 +/- 2.8 vs. 6.0 +/- 1.9 and A-->f: 9.5 +/- 1.8 vs. 7.2 +/- 0.9) in each evaluated arterial region. Same thing occurred in cases with LVH vs. WLVH (A-->h: 10.5 +/- 1.6 vs. 8.0 +/- 1.9, A-->c: 10.2 +/- 1.9 vs. 8.0 +/- 1.9 and A-->f: 10.5 +/- 2.0 vs. 8.6 +/- 1.2) (p < 0.025). This is consistent with the relationship more pressure [symbol: see text] more rigidity and with other reports. This method may have clinical application.