Effect of hyperthermia on the cardio- and hemodynamics and acid-base balance of the blood in dogs

The effect of severe hyperthermia on the circulatory function was studied in dogs. Arterial pressure was maintained at the normal level, cardiac output increased at the core temperature of about 40 degrees C. An abrupt fall of the arterial pressure and cardiac output was observed at the rectal temperature of about 41 degrees C. The results suggest that a decrease in the cardiac output during severe hyperthermia is due to the fall of the central venous pressure and to the increase of the vascular compliance.     

Arterial blood gases and acid-base status of dogs during graded dynamic exercise

The objective of this study was to determine whether arterial PCO2 (PaCO2) decreases or remains unchanged from resting levels during mild to moderate steady-state exercise in the dog. To accomplish this, O2 consumption (VO2) arterial blood gases and acid-base status, arterial lactate concentration ([LA-]a), and rectal temperature (Tr) were measured in 27 chronically instrumented dogs at rest, during different levels of submaximal exercise, and during maximal exercise on a motor-driven treadmill. During mild exercise [35% of maximal O2 consumption (VO2 max)], PaCO2 decreased 5.3 +/- 0.4 Torr and resulted in a respiratory alkalosis (delta pHa = +0.029 +/- 0.005). Arterial PO2 (PaO2) increased 5.9 +/- 1.5 Torr and Tr increased 0.5 +/- 0.1 degree C. As the exercise levels progressed from mild to moderate exercise (64% of VO2 max) the magnitude of the hypocapnia and the resultant respiratory alkalosis remained unchanged as PaCO2 remained 5.9 +/- 0.7 Torr below and delta pHa remained 0.029 +/- 0.008 above resting values. When the exercise work rate was increased to elicit VO2 max (96 +/- 2 ml X kg-1 X min-1) the amount of hypocapnia again remained unchanged from submaximal exercise levels and PaCO2 remained 6.0 +/- 0.6 Torr below resting values; however, this response occurred despite continued increases in Tr (delta Tr = 1.7 +/- 0.1 degree C), significant increases in [LA-]a (delta [LA-]a = 2.5 +/- 0.4), and a resultant metabolic acidosis (delta pHa = -0.031 +/- 0.011). The dog, like other nonhuman vertebrates, responded to mild and moderate steady-state exercise with a significant hyperventilation and respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Breathing-valve encumbrance and arterial blood gas and acid-base status in exercise in man

It has been suggested that the mouth-piece-breathing valve assemblies commonly used in laboratory investigations of ventilatory control may influence regulation of arterial blood gas and acid-base status during exercise. To examine this hypothesis, 10 healthy males each underwent two incremental cycle-ergometer tests (15 W min-1) to the limit of tolerance: one was conducted free of breathing apparatus; the other utilized a mouth-piece (with noseclip) connected to a low-resistance turbine volume sensor. The order was randomly assigned and tests were separated by a 2 h recovery. Blood sampled from an indwelling brachial artery catheter at rest and every 30 W during exercise was analyzed for PCO2, PO2, pH and HCO-3. Maximum power was not different between the two tests. Furthermore, no systematic effect of the assembly could be discerned on PaCO2, PaO2 or pHa over the entire range of power. We therefore conclude that although ventilation and its pattern may be affected by laboratory breathing apparatus, such encumbrance (if of low resistance and dead space) does not influence blood gas and acid-base regulation during exercise.     

Effects of acid-base status on acute hypoxic pulmonary vasoconstriction and gas exchange.

To investigate the relationship between hypoxic pulmonary vasoconstriction and respiratory and metabolic acidosis and respiratory alkalosis, the pulmonary gas exchange and pulmonary hemodynamic responses were measured in anesthetized, paralyzed, and mechanically ventilated dogs in two sets of experiments (series A, n = 6; series B, n = 10). The animals were treated with acute hypoxia, CO2 inhalation, hyperventilation, and dinitrophenol in various combinations. Multiple regression analysis indicated that mean pulmonary arterial pressure (Ppa) was significantly correlated with end-tidal PO2, mixed venous PO2, and the mean pulmonary capillary pH (average of arterial and mixed venous pH) as independent variables [series A: r = +0.999, standard error of estimate (SEE) = 0.4 mmHg; series B: r = +0.98, SEE = 1.4 mmHg]. Similar analyses of mean values published by other authors from an acute study on humans with exercise at sea level and simulated altitudes of 10,000 and 15,000 ft also indicated a good relationship (n = 14, r = +0.98, SEE = 2.1 mmHg). The mean data (n = 19) obtained in Operation Everest II at various exercise loads and simulated altitudes gave a correlation of r = +0.87, SEE = 6.1 mmHg. These empirical analyses suggest that variations in the rise of Ppa with hypoxia can be accounted for in vivo by the superimposed acid-base status. Furthermore, ventilation-perfusion inhomogeneity, as estimated in the dogs from end-tidal and arterial O2 and CO2 differences and assuming no true shunt or diffusion impairment, was highly correlated with Ppa and mean pulmonary capillary pH (r = +0.999 in series A, r = +0.77 in series B). The human data from the above studies also showed significant correlations between Ppa and directly measured ventilation-perfusion (standard deviation of perfusion obtained from inert gas measurements). These observations indicate that the beneficial effects of hyperventilation during hypoxia may be related to the marked alkalosis that serves to reduce Ppa and improve pulmonary gas exchange efficiency.     

External respiration and gas metabolism in orthostatic syncopes

Cardiorespiratory reactions to tilt tests were compared in 80 healthy male subjects with an adequate orthostatic tolerance and in 19 subjects who fainted during tilting. They showed significant differences in the gas exchange, hemodynamics, and external respiration. Variations in the heart rate, pulmonary ventilation and the alveolar CO2 tension were most demonstrative. The findings, particularly the lack of the expected decrease o= oxygen consumption in the presyncopal state contribute to the concepts of the pathogenesis of the orthostatic collapse.     

Pulmonary gas exchange in panting dogs

Pulmonary gas exchange during panting was studied in seven conscious dogs (32 kg mean body wt) provided with a chronic tracheostomy and an exteriorized carotid artery loop. The animals were acutely exposed to moderately elevated ambient temperature (27.5 degrees C, 65% relative humidity) for 2 h. O2 and CO2 in the tracheostomy tube were continuously monitored by mass spectrometry using a special sample-hold phase-locked sampling technique. PO2 and PCO2 were determined in blood samples obtained from the carotid artery. During the exposure to heat, central body temperature remained unchanged (38.6 +/- 0.6 degrees C) while all animals rapidly switched to steady shallow panting at frequencies close to the resonant frequency of the respiratory system. During panting, the following values were measured (means +/- SD): breathing frequency, 313 +/- 19 breaths/min; tidal volume, 167 +/- 21 ml; total ventilation, 52 +/- 9 l/min; effective alveolar ventilation, 5.5 +/- 1.3 l/min; PaO2, 106.2 +/- 5.9 Torr; PaCO2, 27.2 +/- 3.9 Torr; end-tidal-arterial PO2 difference [(PE' - Pa)O2], 26.0 +/- 5.3 Torr; and arterial-end-tidal PCO2 difference, [(Pa - PE')CO2], 14.9 +/- 2.5 Torr. On the basis of the classical ideal alveolar air approach, parallel dead-space ventilation accounted for 54% of alveolar ventilation and 66% of the (PE' - Pa)O2 difference. But the steepness of the CO2 and O2 expirogram plotted against expired volume suggested a contribution of series in homogeneity due to incomplete gas mixing.     

Arterial blood gas tensions and acid-base status of Wistar rats during thiopental and halothane anesthesia.

Arterial blood gas tensions and acid-base status of spontaneously-breathing, unanesthetized Wister rats were compared with values obtained during 4 hr of thiopental and 6 hr of halothane (1%) anesthesia. During thiopental anesthesia, marked respiratory depression occurred (PaCO-2:57.0 plus or minus 10.0 MM Hg, PaO-2:70.4 plus or minus 11.2 MM Hg). Thirty-six percent of the rats died. During inhalation of room air and 1% halothane, PaO-2 decreased also, whereas PaO-2 did not change. Twenty-seven percent of the original number of rats died. Lowered arterial oxygen tension may have caused death; no rats died during inhalation of oxygen and 1% halothane. This technic insured sufficient analgesia for surgical procedures without marked alterations of the acid base status and is recommended for long-term anesthesia of small laboratory animals like rats.     

Measurement of respiratory gas exchange during artificial respiration

This paper reports a new system for the continuous measurements of respiratory gas exchange in ventilated subjects. It involves mixing some of the inspired gas with all of the expired gas and withdrawing the mixture at a constant rate through a dry gas meter that measures the flow. The inspired gas and expired gas mixtures are sampled and O2 and CO2 concentrations measured with a paramagnetic gas analyzer and a capnograph, respectively, to an accuracy of 0.01%. Evidence is presented to confirm the necessary stability and sensitivity of these instruments. It is possible to use the system with high inspired O2 concentrations, with ventilators where there is incomplete separation of inspired and expired gas, and in the presence of intermittent mandatory ventilation, positive end-expiratory pressure, and continuous airway pressure. The system was compared with the N2-dilution method and with the collection of expired gas in a Douglas bag in dog experiments and with patients in the intensive therapy unit. Excellent correlation between these methods was found in all circumstances.     

Gas exchange and blood circulation status in dogs following replacement of acute blood loss by perfluoro compound emulsions

Blood circulation and gas exchange were examined after replacement of blood loss (50 ml/kg bw) in dogs by a preparation containing perfluorocompound (PFC) emulsion (20 v. %) and protein-salt solution (PSS) consisting of isotonic solution of electrolytes and donor's albumin, the final concentration of the latter in the preparation being equal to 5%. Animals with analogous blood loss replaced by PSS alone served as control. Infusion of the preparation under study led to a steady recovery of the main parameters of the hemodynamics disordered as a result of blood loss. Its infusion to experimental animals was followed by a noticeable increase in oxygen blood capacity, provoked a more considerable elevation of pO2 in arterial and venous blood as compared to control. Compensation with PFS emulsion for homeostatic changes that occurred in dogs after blood loss involved a more active oxygen utilization, whereas in controls, a more considerable increase of cardiac output. The study drug is offered as base for a blood substitute-oxygen carrier.     

A review of 126 Caesarean sections by blood gas and the acid-base status of newborn calves

Blood gas and acid-base status was determined in 126 Caesarean-derived calves. The newborn calves were assigned by venous blood pH value at birth to three groups as follows: Group 1 (normal): pH above 7.2; Group 2 (slight acidosis): pH 7.2 to 7.0; and Group 3 (severe acidosis): pH below 7.0. Following Caesarean section births 80 (63.5%) calves had normal acid-base values, while 30 (23.8%) had a slight acidosis, and 16 (12.7%) had severe acidosis. The degree of hypoxia was similar in each group. Six calves (37.5%) in Group 3 died within 48 h of birth. The blood gas and acid-base status of Caesarean-derived. calves was not significantly influenced by any examined parameters with the exception of sex in Groups 1 and 2. The occurrence of meconium-stained calves was 9.1% (n = 11), and only two calves were slightly or severely acidotic immediately after birth.     

Diurnal rhythm of acid-base equilibrium and blood gas composition

Diurnal fluctuations of acid-alkaline balance and blood gas composition were studied in March on 20 healthy males aged 20-26. Using cosinor analysis, mesors, amplitudes and acrophases were revealed. Calculated acrophases (in h and min) are as follows: pH--16 h 05 min, standard hydrogen carbonate--18 h 45 min, actual hydrogen carbonate--22 h 55 min, buffer bases--19 h 03 min, pCO2--2 h 47 min, pO2--4 h 39 min, HbO2--8 h 07 min, hemoglobin--14 h 16 min. All the values studied during diurnal cycle correlated, forming certain circadian rhythms.