Effects of direct transfer from freshwater to seawater on respiratory and circulatory variables and acid-base status in rainbow trout

Summary The effects of increased ambient salinity (35 mg · ml^-1) were studied at 1, 6, and 24 h after direct transfer of rainbow trout from freshwater to seawater. Two series of experiments were carried out successively. The first series was designed to simultaneously study all the respiratory (except Hb affinity for O₂), circulatory, and acid-base variables in each fish. In this series, fish were fitted with catheters chronically inserted into the cardiac bulbus, the dorsal aorta, and the opercular and buccal cavities. In the second series, designed to study haemoglobin O₂ affinity, fish were fitted with only a dorsal aorta catheter. The ventilatory flow ( ) was markedly increased just after transfer (by 55% at 1 h), then more moderately (by 20% at 6 h and 32% at 24 h). The initial hyperventilation peak was associated with frequent couphing motions. These ventilatory changes resulted essentially from increase in ventilatory amplitude. Initially, standard oxygen consumption (MM}O₂) decreased slightly, the moderately increased (by 12% at 24 h), so that the oxygen convection requirement ( ) increased substantially. In spite of an increased ventilation, the partial pressure of oxygen in arterial blood (P _aO₂) decreased slightly at 1 h, prior to returning to control levels, while partial pressure of carbon dioxide in arterial blood (P _aCO₂) was not significantly decreased. Gill oxygen transfer factor decreased substantially at 1 h (by 35%) then more moderately (by 7% at 1 h and 12% at 24 h). These results suggest a decrease in gas diffusing capacity of the gills. As P _aCO₂ remained approximatively unchanged, the gradual decrease in arterial pH (pH_a) from 7.94 to 7.67 at 24 h must therefore be regarded as a metabolic acidosis. The strong ion difference decreased markedly because the concentration of plasma chloride increased more than that of sodium. Arterial O₂ content (C _aO₂) gradually decreased (by 38% at 24 h) simultaneously with the decrease in pH_a, while the ratio P _aO₂/C _aO₂ increased. In parallel, seawater exposure induced a marked decrease in affinity of haemoglobin for O₂, so that at 24 h, P₅₀ was increased by 26% above the value obtained in freshwater-adapted trout. The increase in could be ascribed initially (at 1 h) to the decrease of P _aO₂ and later to a stimulation of respiratory neurons resulting from the lowered medullary interstitial pH. The decrease in C _aO₂ could be interpreted mainly as a consequence of a decreased affinity of haemoglobin for O₂, likely to be due to the blood acidosis and a predictable increase in chloride concentration within erythrocytes. Cardiac output ( ) slightly decreased at 1 h, then progressively increased by 30% at 24 h. Branchial vascular resistance increased at 1 h by 28%, then decreased by 18% of the control value at 24 h. Systemic vascular resistance decreased markedly by 40% at 24 h. As heart rate (HR) remained significantly unchanged, the cardiac stroke volume initially decreased then increased in relation to the changes in . The increase of , allowing compensation for the effect of decreased C _aO₂ in tissue O₂ supply, was interpreted as a passive consequence of the decrease in total vascular resistance occurring during seawater exposure.Abbreviations a.u. arbitrary units - C _aO₂ arterial oxygen content - pH₅₀ arterial pH at P₅₀ - C _vO₂ venous oxygen content - Hb haemoglobin - HR heart rate - Hct hematocrit - n_Hill Hill coefficient - O₂ standard oxygen consumption - P _aCO₂ arterial partial pressure of carbon dioxide - P _aO₂ arterial partial pressure of oxygen - P _vO₂ oxygen partial pressure in mixed venous blood - P₅₀ oxygen tension at half saturation of haemoglobin - P _VA, P _DA blood pressure in ventral and dorsal aorta - pH_a arterial pH - PIO₂, PEO₂ oxygen partial pressure of inspired and expired water - PO₂ oxygen partial pressure - cardiac output - SEM standard error of mean - S.I.D. strong ion difference - SV cardiac stroke volume - TO₂ gill oxygen transfer factor - U oxygen extraction coefficient - VA ventilatory amplitude - VF ventilatory frequency - VR_G, VR_S branchial and systemic vascular resistances - ventilatory flow - ventilatory oxygen convection requirement     

Pulmonary arterial hypertension: an update

Pulmonary arterial hypertension (PAH), defined as group 1 of the World Heart Organisation (WHO) classification of pulmonary hypertension, is an uncommon disorder of the pulmonary vascular system. It is characterised by an increased pulmonary artery pressure, increased pulmonary vascular resistance and specific histological changes. It is a progressive disease finally resulting in right heart failure and premature death. Typical symptoms are dyspnoea at exercise, chest pain and syncope; furthermore clinical signs of right heart failure develop with disease progression. Echocardiography is the key investigation when pulmonary hypertension is suspected, but a reliable diagnosis of PAH and associated conditions requires an intense work-up including invasive measurement by right heart catheterisation. Treatment includes general measures and drugs targeting the pulmonary artery tone and vascular remodelling. This advanced medical therapy has significantly improved morbidity and mortality in patients with PAH in the last decade. Combinations of these drugs are indicated when treatment goals of disease stabilisation are not met. In patients refractory to medical therapy lung transplantation should be considered an option.     

Mean arterial pressure nonlinearity in an elastic circulatory system subjected to different hematocrits

The level of hematocrit (Hct) is known to affect mean arterial pressure (MAP) by influencing blood viscosity. In the healthy population, an increase in Hct (and corresponding increase in viscosity) tends to raise MAP. However, data from a clinical study of type 2 diabetic patients indicate that this relationship is not universal. Instead, individuals in the lower levels of Hct range display a decrease in MAP for a given rise in Hct. After reaching a minimum, this trend is reversed, so that further increases in Hct lead to increases in MAP. We hypothesize that this anomalous behavior occurs due to changes in the circulatory autoregulation mechanism. To substantiate this hypothesis, we develop a physically based mathematical model that incorporates autoregulation mechanisms. Our model replicates the anomalous U-shaped relationship between MAP and Hct found in diabetic patients in the same range of Hct variability.     

Pulmonary control systems in exercise: update

We examined recent ideas and findings concerned with the regulation of ventilation and gas transport in moderate and heavy exercise. The primary mediation of exercise hyperpnea remains unknown and highly controversial, but two unique approaches to the problem have advanced our understanding of this neurohumoral regulatory scheme. On the one hand, experimental separation of the pulmonary and systemic circulations was used to reveal a vagally mediated ventilatory response that is clearly attributable to CO2 flow to the lung. This mechanism seems to be most effective as a homeostatic regulator of ventilatory control near resting levels of metabolic rate. On the other hand, a descending neurogenic drive to hyperpnea from the locomotor regions of the central nervous system was also demonstrated experimentally. The importance of regulatory feedback by conventional chemoreceptors in determining the precision of the hyperpneic response was emphasized in explaining the wide spectrum of arterial acid-base regulation during exercise in humans and non-human species. Two commonly accepted homeostatic regulators believed to be operative during heavy exercise were questioned, i.e., the compensatory hyperventilatory response and the maintenance of arterial oxygenation. For example, the hyperventilatory response was shown not to require metabolic acidosis; hyperventilation was not always observed at high work rates despite an abundance of chemical stimuli; and arterial hypoxemia occurred at very high metabolic rates in a significant number of highly fit athletes. These data implied that the capabilities of some aspects of even the healthy pulmonary system may be approached-or even exceeded-during heavy exercise.     

Pressure diuresis mechanism in the control of renal function and arterial pressure

Precise knowledge of the interrelationships between arterial pressure and urinary excretion of sodium and water is crucial to understanding the long-term control of arterial pressure. Although increases in renal perfusion pressure have been known for more than 35 years to inhibit tubular reabsorption, the mechanism of this pressure diuresis response, the humoral or physical factors involved, and even the nephron segments in which the changes in tubular function occur remain relatively unknown. This review focuses on the experimental evidence that supports current hypotheses concerning the mechanism of pressure diuresis. Specifically, it examines the possibility that pressure diuresis is caused by a small increase in glomerular filtration rate, alterations in the humoral or physical factors regulating proximal tubular reabsorption, and/or inhibition of tubular reabsorption in deep nephrons secondary to changes in hemodynamics in juxtamedullary nephrons. The concept originally proposed that the kidney serves as the dominant long-term controller of arterial pressure is largely based on the assumptions that the pressure diuresis phenomenon exists and that it occurs via a nonadaptive mechanism. It has been proposed that hypertension can develop only if the relationship between arterial pressure and sodium excretion is shifted toward higher pressures. The remainder of this review examines recent evidence indicating that an abnormality in the pressure natriuresis relationship may be associated with the development of hypertension in humans and in the genetic rat models of the disease.     

Propranolol and the respiratory, circulatory, and ECG responses to high altitude

The role of the sympatho-adrenal system in the acute respiratory and cardiovascular responses to high altitude was studies in 20 volunteers during ascent to 6,000 m in a low pressure chamber, once without (control) and once with beta-adrenergic blockade. Special attention was paid to the hypoxia-induced ECG changes. Propranolol lowered the level of hypoxia-induced cardiovascular reactions, whereas it had no effect on hypoxic hyperventilation and alveolar gases. At altitude, ECG changes during myocardial depolarization occurred in both the propranolol and the control groups, probably due to the direct effects of hypoxia. During the repolarization phase, propranolol led to an almost complete abolition of S-T depression and to significant reduction of T wave flattening. The minor but still significant flattening of the T wave as well as the relative (to the heart rate) lengthening of Q-T is probably due to the direct effects of hypoxia. Propranolol abolishes or diminishes the signs of cardiac hypoxia by antagonizing the effects of catecholamine release and/or by reducing myocardial oxygen consumption, thus probable increasing the ability to withstand oxygen-want at altitude.     

Motor control: the importance of stiffness

An octopus brings food grasped by a tentacle to its mouth by bending the tentacle around a joint formed by stiffened distal and proximal tentacle muscles, and thus may use motor control strategies analogous to those in animals with articulated limbs.