The Elbe flood in August 2002--occurrence of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans (PCDD/F) and dioxin-like PCB in suspended particulate matter (SPM), sediment and fish.

As a result of extreme precipitation in August 2002 major flooding occurred in the catchment area of the rivers Elbe, Vltava (Moldau) and Mulde. Pollutants from industrial sites and from municipal sewage treatment works (STW) entered the Elbe and led to a serious pollution problem in the river. PCDD/F concentrations (in pg WHO-TEQ/g dw) in SPM ranged from 7-150, in sediments from 3-140; the "safe sediment value" of 20 was exceeded in 46% of the samples. 24 eels showed a wide concentration variation for these contaminants. The WHO-PCDD/F+PCB-TEQ values lay in the range from 11-56 pg/g ww, whereby the WHO-PCB-TEQ values were several times higher than the WHO-PCDD/F-TEQ values. The maximum permitted value of 4 pg WHO-PCDD/F/g ww (EU Directive No. 2375/2001) was reached or exceeded in 54% of the individuals. A statistical analysis using data from SPM and sediment samples showed that in the Czech river section the flooding activated a contamination source in the vicinity of the Spolana works. The influence of the tributary Mulde could be clearly demonstrated. Only a major clean-up of the contaminated sites in Bitterfeld can lead to a mid to long term improvement in respect of PCDD/F and dioxin-like PCB input into the Elbe.

Evaluation of cold face test bradycardia by means of spectral analysis.

The cold face test (CFT) is a non-invasive challenge maneuver of the autonomic nervous system which activates the peripheral sympathetic and the cardiac parasympathetic nervous system and induces peripheral vasoconstriction and bradycardia. The physiology of CFT-induced bradycardia is still controversial. The heart rate decrease might result from a direct central up-regulation of cardiovagal activity or might be a secondary effect of baroreceptor activation or of changes of respiration. The purpose of this study was to analyze the origin of CFT-induced bradycardia. To evaluate the influence of respiration on bradycardia during CFT, we studied cardiac responses in 10 healthy volunteers during CFT (0-1 degrees C cold compresses for 60 s) with three different respiratory patterns: one with spontaneous and two with paced respiration (6 and 15 cycles/minute). We continuously monitored heart rate (HR), blood pressure (BP) and respiration and determined heart rate variability by assessment of coefficient of variation (CV), standard deviation (SD) and the root mean square of successive differences (RMSSD) of HR as well as low (LF) and high (HF) frequency spectra power of HR and BP. When coherence was above 0.5, we calculated the transfer function gain between HR and respiration in the HF band, as an index of respiratory sinus arrhythmia, and between HR and BP in the LF band, as an index of baroreflex sensitivity. HR decreased and BP increased significantly during the three types of CFT. The decrease of HR and the increase of BP, of time and frequency domain parameters did not differ between the three breathing patterns. Respiration, and HF and LF power of respiration did not change during CFT. The gain of the HF-transfer function between HR and respiration and the LF-transfer function gain between HR and BP increased significantly during CFT, but the increase did not differ between the three breathing patterns. The increase of the gain of both transfer functions is most likely due to an increase of vagal traffic and together with the unchanged respiratory pattern suggests that CFT-induced bradycardia is not due to baroreflex or respiratory influences, but seems to result from central vagal activation.

Sympathetic and parasympathetic pupillary dysfunction in familial dysautonomia.

Objective assessment of autonomic dysfunction in familial dysautonomia (FD) is largely based on the analysis of cardiovascular responses to challenge maneuvers such as orthostatic stress. Infrared pupillometry (IPM) provides an additional reliable method for cranial autonomic evaluation and has the advantage of requiring minimal cooperation.This study was performed to determine whether IPM contributes to the assessment of autonomic function in FD patients. In 14 FD patients and 14 healthy controls, we studied absolute and relative light reflex amplitude, pupillary constriction velocity (v(constr)), pupillary diameter, early and late pupillary re-dilatation velocity (v(dil 1), v(dil 2)) after dark adaptation. Prior to IPM, all patients had an ophthamological examination to evaluate refraction and corneal integrity. In comparison to controls, patients had a significant reduction of the parameters reflecting parasympathetic pupillary function (absolute light reflex amplitude 1.34 +/- 0.21 vs. l.86 +/- 0.14 mm, relative light reflex amplitude 22.74 +/- 7.11% vs. 30.76 +/- 3.57%, v(constr) 3.75 +/- 1.09 vs. 5.80 +/- 0.59 mm/s) and of the parameters reflecting sympathetic pupillary function (diameter 5.69 +/- 0.66 vs. 6.35 +/- 0.60 mm, v(dil 1) 1.29 +/- 0.23 vs. 1.95 +/- 0.23 mm/s, v(dil 2) 0.64 +/- 0.13 vs. 0.72 +/- 0.l2 mm/s; Mann-Whitney U-test: p<0.05). The non-invasive technique of IPM demonstrates dysfunction not only of the cranial parasympathetic, but also of the cranial sympathetic nervous system and, thus, further characterizes autonomic dysfunction in FD.

Hemispheric influence on autonomic modulation and baroreflex sensitivity.

Several studies suggest hemispheric lateralization of autonomic cardiovascular control. There is controversy regarding which hemisphere dominates sympathetic or parasympathetic activity. Hemispheric influences on baroreflex sensitivity (BRS) have not yet been evaluated. To determine hemispheric autonomic control in epilepsy patients, we assessed cardiovascular and baroreflex modulation before and during hemispheric inactivation. For 15 patients with drug-refractory epilepsy, we analyzed autonomic heart rate (HR) and blood pressure (BP) modulation and BRS before and during left and right intracarotid amobarbital procedure (IAP). After Blackman-Tukey spectral analysis, we calculated the low-frequency (LF: 0.04-0.15 Hz) and high-frequency (HF: 0.15-0.5 Hz) power of HR and BP as well as BRS as the LF transfer function gain between BP and HR. Right hemispheric inactivation induced a significant decrease of BP and an increase of HF power of HR and BP (p < 0.05). Left inactivation increased HR, BP, and LF power of both signals and decreased BRS by nearly 30% (p < 0.05). The results confirm previous IAP studies showing sympathetic lateralization in the right hemisphere and, moreover, demonstrate parasympathetic predominance and up-regulation of BRS in the left hemisphere. In epilepsy patients, unilateral electrical activity might derange autonomic balance between both hemispheres and contribute to cardiovascular dysregulation and sudden fatalities.

[Kidney function and arterial acid-base status during continuous stimulation of the carotid chemoreceptors in vagotomized cats]. / Nierenfunktion und arterieller Säure-Basen-Status bei anhaltender Reizung der Karotis-Chemorezeptoren an vagotomierten Katzen

In spontaneously breathing, chloralose narcotized and bilaterally vagotomized cats under mannite saline diuresis, the isolated carotid sinus were perfused for 1 hr with arterial and then for 1 hr with venous blood, and subsequently again with arterial blood for 1 hr. Either measure d or calculated were the parameters of arterial acid-base status, the arterial systemic bl-od pressure, the p-aminohippuric acid (PAH), inulin (IN), and osmolar clearance, the filtration fraction, the tubular reabsorption of oxmotically free water, the urinary time volume, and fractional excretions of the kidneys. Stimulation of the carotic chemoreceptors increased respiration, slightly enhanced the CPAH, and caused a minor fall of CIN with little altered filtration fraction. The renal resistance increased. The absolute and fractional excretions of urine, sodium, potassium, and of osmotically active particles rose significantly. Tubular reabsorption of osmotically free water showed a singificant increase. Urinary osmolarity remained constant in general. The changes of water and electrolyte excretion did not correlate with those of renal hemodynamics. The results argue against natriuresis being caused on chemoreceptor stimulation by increased filtrate volume of the whole kidney, or by decreased osmolarity of the renal medulla. The results are discussed with regard to the renal function in arterial oxygen deficiency.

[The function of innervated kidneys during stimulation of the carotid chemoreceptors under constant renal perfusion pressure]. / Die Funktion der innervierten Nieren während der Reizung der Karotis-Chemorezeptoren bei konstantem renalem Perfusionsdruck

The carotid chemoreceptors of narcotized, vagotomized and spontaneously breathing hydropenic cats in hypertonic mannite diuresis were stimulated by perfusion with venous blood penic cats in hypertonic mannite diuresis were stimulated by perfusion with venous blood for 70 min. Elevation of blood pressure at the innervated kidneys was prevented by an automatically controlled balloon located within the aorta. Stimulation of the chemoreceptors intensified respiration and raised the arterial systemic pressure. With the renal arteries at constant pressure, the effective renal plasma flow and the glomerular filtration rate significantly declined. The filtration fraction remained unchanged. The absolute urinary and sodium excretion did not change significantly, whereas the fractional time-volume, fractional sodium excretion, and the fractional osmotic excretion significantly increased. The fractional tubular reabsorption of osmotically free water was significantly enhanced. These reactions subsided during subsequent perfusion of the glomerula carotici with arterial blood. The results suggest that tubular sodium reabsorption is inhibited by stimulation of the carotid chemoreceptors, although re-adjustment of renal perfusion and filtrate volume cannot be excluded.