Changes in cardiac and respiratory function, and in blood carbon dioxide pressure and pH, in cats exposed to oxygen under high pressure

Abstract

Earlier experiments on rats (Taylor, 1958) showed that on exposure to pure oxygen under a pressure of 6 atmospheres, slowing of the heart and of respiration took place much earlier when the rats were anaesthetized with chloralose than when barbiturate was the anaesthetic. There was evidence, too, that such slowing was accompanied by a fall in pH of the arterial blood, but there was no evidence of a rise in C02 pressure before the onset of cardiac or respiratory failure.These experiments suffered from the disadvantages that the rats underwent a fairly rapid and considerable fall in body temperature, that the size and frequency of blood samples were strictly limited and that only arterial blood was sampled. It was desirable therefore to repeat and extend the work on larger animals such as cats. METHODSYoung cats of both sexes (av. wt. 1-50 kg) were used in all experiments and were anaesthetized by an intraperitoneal injection of either an aqueous solution of 1 % chloralose and 10% urethane (1 ml./100 g body wt.) or with pentobarbitone sodium B.P. (Veterinary Nembutal; Abbott Laboratories Ltd.; 50 mg/100 g body wt.).Any such procedures as vagotomy and section of sinus nerves were then carried out before heparin dissolved in 0-9 % NaCl solution (5000 i.u./ml.) was injected intravenously (0.5 ml./kg body wt.). The femoral arteries were then cannulated with polythene tubing, as was the right atrium via the right jugular vein, the animal was placed in the pressure chamber, and the appropriate connexions made to recording and sampling apparatus. The method of compression was as has already been described (Taylor, 1956).Heart rate, mean arterial blood pressure, respiration, body temperature and blood pH were recorded as described by Taylor (1958). In the first seven experiments the recorded pH was that of the femoral arterial blood; thereafter, it was that of the mixed venous blood drawn from the right atrium.Blood samples were collected and analysed for total COs and 02. The CO2 pressure was calculated as in the earlier experiments, using the form of the Henderson-Hasselbalch equation and the tables given by Severinghaus, Stupfel & Bradley (1956a, b). A series of both arterial and right atrial samples could be collected in any experiment, but in any one experiment the pH could be recorded, and thus the CO2 presure calculated, for one type of sample only. A rapid flow of blood through the chamber containing the glass electrode permitted the pH to be recorded at a blood temperature not significantly different from

Bifurcation of the respiratory response to lung inflation in anesthetized dogs

“…With urethane and α-chloralose anesthesia, lung inflation began earlier in expiration than with pentobarbital anesthesia. This result supports the concept that respiratory reflexes are less depressed during urethane and α-chloralose than pentobarbital anesthesia (Taylor, 1960). Vagotomy abolished TE prolongation to lung inflation which consequently eliminated bifurcation of TE responses.…”

Ventilation in intact and glossopharyngeal nerve sectioned anaesthetized rats exposed to oxygen at high pressure.

“…We found in IX-sectioned rats that f decreased rather than increased during o.h.p. at 6 and 8 atm absolute whereas Taylor (1960) reported no obvious difference between the f response of carotid sinus nerve-sectioned and intact cats at 6 atm absolute. The differences between our data and those of earlier workers may be species dependent or may reflect the more accurate estimation of respiratory variables which is possible today.…”

“…However, arterial and mixed venous PCO2 actually decreased in anaesthetized rats and cats exposed to o.h.p. at 6 atm absolute; the PCO2 increased only when severe respiratory failure followed the initial hyperventilation (Taylor, 1958(Taylor, , 1960Drysdale & Taylor, 1964, 1965. Furthermore, doses of Tris buffer sufficient to cause a considerable metabolic alkalosis in anaesthetized cats did not reduce hyperventilation at 6 atm absolute of o.h.p.…”

“…above 3-5 atm absolute mammals exhibit an initial, slowly increasing hyperventilation which is followed by an irregular and then a slow deep dyspneic pattern of breathing until the onset of respiratory failure (Bean, 1945;Taylor, 1958Taylor, , 1960Clark & Lambertsen, 1971). The initial P. A. CRAGG, D. B. DRYSDALE AND J. H. HAMILTON increase in ventilation (VE) is largely due to an increase in tidal volume (VT); frequency of breathing (f ) either increases slightly, stays the same or decreases.…”

“…and pulmonary poisoning contribute to the eventual death. Anaesthetics, in particular barbiturates, prevent the convulsions, retard the development of pulmonary damage and prolong the survival time without modifying the progressive changes in breathing (Taylor, 1958(Taylor, , 1960Clark & Larbertsen, 1971).…”