Cytochrome oxidase activity from the retina can be enhanced or depressed by free radical-mediated reactions both in positive and negative aspect. The greatest effect was exerted by ischemia/reperfusion, which significantly increased the fluorescent products of lipid peroxidation (358 %, P<0.01) and inhibited the enzyme activity (14 %, P<0.001). After hyperoxia the fluorescent products slightly increased (192 %, P< 0.05) as well as the enzyme activity (133 %, P<0.05). Hypoxia had no effect on any of these parameters. Specific changes in the composition of fluorophores after ischemia/reperfusion were revealed in the fluorescence spectra. The fact that increased lipid peroxidation after hyperoxia and after ischemia/reperfusion does not produce the same effect upon cytochrome oxidase activity might be explained by changes in the kinetic behavior of cytochrome oxidase. In the control enzyme preparation, two binding sites for cytochrome c were observed. One was of the low-affinity (Km=60 mM) and the other of the high-affinity (Km=1.12 mM). After in vitro-initiated lipid peroxidation, the low-affinity binding site was lost and the activity measured under "optimum" conditions at a single cytochrome concentration was higher than in the controls. This implies that oxidative damage to cytochrome oxidase in vivo can be site-specific and its extent should be estimated by performing detailed kinetic analysis as otherwise the results might be misleading., A. Šišková, J. Wilhelm., and Obsahuje bibliografii
The Frank orthogonal corrected ECG and its first derivation were recorded in 27 healthy volunteers (women aged 19-22 years) during normal ventilation at rest (control group), after voluntary hyperventilation lasting 75 seconds, and during hypoxic-hypercapnic ventilation (through the enlarged dead space) lasting 5 min. The projections of the magnitude and direction of the positive and negative QRS derivation maxima into the horizontal, frontal, left sagittal planes and their spatial distribution were constructed. The magnitude of the positive and negative QRS derivation maxima was significantly decreased during hypoxic-hypercapnic ventilation. A significant alteration in the direction only arose at the positive maximum during hypoxic-hypercapnic ventilation in the frontal plane. The intrinsicoid deflection was not significantly altered. The normal values of the maxima of the first QRS derivation in young healthy women are given. It is supposed that the decrease in amplitude of the maxima of the first QRS derivation is caused by slowed propagation of the depolarization wave under hypoxic- hypercapnic conditions and alteration of the direction of the positive maximum is caused by a greater participation of the right ventricle at the origin of the resulting QRS vector.
a1_Vascular resistance in the mammalian pulmonary circulation is affected by many endogenous agents that influence vascular smooth muscle, right ventricular myocardium, endothelial function, collagen and elastin deposition, and fluid balance. When the balance of these agents is disturbed, e.g. by airway hypoxia from high altitude or pulmonary obstructive disorders, pulmonary hypertension ensues, as characterized by elevated pulmonary artery pressure (PPA). Among neuropeptides with local pulmonary artery pressor effects are endothelin-1 (ET-1), angiotensin II (AII), and substance P, and among mitigating peptides are calcitonin gene-related peptide (CGRP), adrenomedullin (ADM), atrial natriuretic peptide (ANP), vasoactive intestinal peptide (VIP) and ET-3. Moreover, somatostatin28 (SOM28) exacerbates, whereas SOM14 decreases PPA in hypoxic rats, with lowering and increasing of lung CGRP levels, respectively. Pressure can also be modulated by increasing or decreasing plasma volume (VIP and ANP, respectively), or by induction or suppression of vascular tissue remodeling (ET-1 and CGRP, respectively). Peptide bioavailability and potency can be regulated through hypoxic up- and down- regulation of synthesis or release, activation by converting enzymes (ACE for AII and ECE for ET-1), inactivation by neutral endopeptidase and proteases, or by interaction with nitric oxide (NO). Moreover, altered receptor density and affinity can account for changed peptide efficacy. For example, upregulation of ETA receptors and ET-1 synthesis occurs in the hypoxic lung concomitantly with reduced CGRP release. Also, receptor activity modifying protein 2 (RAMP2) has been shown to confer ADM affinity to the pulmonary calcitonin-receptor-like receptor (CRLR). We recently detected the mRNA encoding for RAMP2, CRLR, and the CGRP receptor RDC-1 in rat lung., a2_The search for an effective, lung selective treatment of pulmonary hypertension will likely benefit from exploring the imbalance and restoring the balance between these native modulators of intrapulmonary pressure. For example, blocking of the ET-1 receptor ETA and vasodilation by supplemental CGRP delivered i. v. or via airway gene transfer, have proven to be useful experimentally., I. M. Keith., and Obsahuje bibliografii
The influence of some pulmonary ventilation alterations (the normal ventilation at rest = control), the hyperventilation (HV) lasting 75 s, the hypoxic-hypercapnic ventilation (HXV) lasting 3 and 6 min) on the instantaneous QRS vectors was investigated in 42 young healthy women (19-24 years old). The magnitude and the direction of instantaneous QRS vectors in the 10th to the 70th ms and in QRS max were constructed from the Frank lead ECG. The significant alterations of the direction (angle) were found in the 30th ms and QRS max at HXV and in the 60th ms at HV. A significant decrease in the magnitude of instantaneous vectors was found in the 10th to 50th ms after 6 min of HXV, in the 30th to 50th ms at 3 min of HXV, in the 40th to 50th ms at HV. These alterations were the most marked in the horizontal plane. We suggest that the alterations of the instantaneous QRS vectors were caused by the influence of the autonomic nervous system or humoral agents, but not by heart position, Brody’s effect or lung hyperinflation.