Circulatory and Metabolic Effects of Oxygen in Myocardial Infarction

The circulatory and metabolic effects of inhalation of oxygen in high concentration were investigated in 50 patients with acute myocardial infarction. The heart rate, arterial blood pressure, cardiac out-put, blood gas tensions, pH, and lactate and pyruvate levels were measured. In general, oxygen inhalation produced a fall in cardiac output and stroke volume and a rise in blood pressure and systemic vascular resistance. In a small number of patients with very low cardiac out-puts there was a rise in output. A substantial rise in arterial oxygen tension was obtained even in patients with low initial values. The raised arterial blood lactate levels which were frequently present were reduced after oxygen. The therapeutic implications of these effects are discussed.     

Respiratory Insufficiency in Acute Myocardial Infarction

Arterial blood gases and pH were assessed in 115 patients who had suffered a myocardial infarction, with or without complicating cardiogenic shock or cardiac standstill. In 11 of the 78 uncomplicated cases and in 16 of the 37 complicated cases, the arterial O₂ tension was much lower than would be expected on the basis of a three-fold drop in cardiac output, indicating considerable right to left shunting. The death rate in the patients with uncomplicated myocardial infarction was 32% and that of the complicated cases 65%. In both groups it was greatest when the arterial pH was low, indicating that correction of the acidosis is essential. In many instances administration of 100% oxygen is inadequate to restore the oxygen tension to normal levels, and controlled ventilation may be necessary to maintain adequate alveolar ventilation. The findings indicate the necessity for repeated assessment of the arterial blood gas tensions and pH in any patient who has suffered a myocardial infarction. If the management of such patients is designed to provide adequate oxygenation, to maintain adequate alveolar ventilation and to correct the acid-base disturbances, the patient may be tided over the stage of “cardiac pump failure”.     

Lung compliance, plasma electrolyte levels and acid-base balance are affected by scorpion envenomation in anesthetized rats under mechanical ventilation

To determine the effects of Tityus serrulatus scorpion toxin on lung compliance and resistance, ionic equilibrium and acid-base balance over time in anesthetized and mechanically ventilated rats, we measured air flow, tracheal and esophageal pressure. Lung volume was obtained by electronic integration of airflow signal. Arterial blood samples were collected through a catheter at baseline (before) and 5, 15, 30 and 60 min after scorpion toxin injection for arterial blood gases, bicarbonate, and alkali reserve levels as well as for, sodium, potassium, magnesium, glucose, lactate, hematocrit, and osmolality analysis. Injection of the gamma fraction of the T. serrulatus scorpion venom in rats under mechanical ventilatory support leads to a continuous decrease in lung compliance secondary to pulmonary edema, but no change in airway resistance. The changes in arterial blood gases characterizing metabolic acidosis were accompanied by an increase in arterial lactate and glucose values, suggesting a scorpion toxin-induced lactic acidosis, in association with poor tissue perfusion (hypotension and low cardiac output). Moreover, scorpion toxin injection resulted in hyperosmolality, hyperkalemia, hypermagnesemia and an increase in hematocrit. The experiments have shown a clinically relevant animal model to study severe scorpion envenoming and may help to better understand the scorpion envenoming syndrome.     

Acid-base, plasma lactate and glucose changes in the rabbit following administration of Gaboon viper (Bitis gabonica) venom

The acid-base and metabolic effects of Bitis gabonica venom administered intravenously to the anaesthetised rabbit were studied. Doubling doses of venom from 0.125 mg/kg to 1.0 mg/kg were used. Venom caused progressive and significant increases in plasma glucose and plasma lactate levels although oxygen consumption only became significantly lower after the fourth dose. Standard base excess (SBE) became significantly more negative after the third dose of venom and the fall in pH became significant at the same point. The results indicate that venom induces a metabolic acidosis in the rabbit and because the acidosis occurs in the absence of any fall in arterial PO2, it cannot be considered a consequence of impaired pulmonary ventilation. The reduction in oxygen uptake is likely to occur at a cellular level with a shift from aerobic to anaerobic metabolism hence the increase in plasma lactate levels. However, the magnitude of the acidosis is unlikely to be the principal cause of death under experimental conditions.     

Systemic responses to prolonged hemorrhagic hypotension

Studies are needed to provide a rigorous examination of the relevance of monitored variables during prolonged hemorrhagic hypotension (HH). This study was designed to investigate the parameters that describe biochemical and O2 transport patterns in animals subjected to HH. Systemic parameters that could differentiate survivors from nonsurvivors were identified. An aortic flow probe was implanted in rats (n = 21) for continuous measurement of cardiac output. Experiments were performed 6-9 days after surgery. Rats were bled to a mean arterial pressure of 40 mmHg and kept at that level using Ringer-lactate solution. Arterial and venous blood pressures, gases, acid-base status, glucose, lactate, electrolytes, hemoglobin, O2 saturation, heart and respiratory rates, total peripheral resistance, and O2 delivery and consumption were measured before hemorrhage, soon after 40 mmHg was reached, and 0.5, 1, 2, 3, and 4 h later. Fifty-three percent of rats survived > or =3 h (survivors); others were considered nonsurvivors. Nonsurvivors showed a significantly greater degree of metabolic acidosis than survivors. Arterial PO2, respiratory rate, O2 saturation, O2 content, glucose, and pH were significantly higher in survivors. The rate of Ringer-lactate infusion, arterial K+, and PCO2 were lower in survivors. Arterial K+ and respiratory rate were the only parameters significantly different between survivors and nonsurvivors at all time points during HH. Arterial levels of K+ showed the clearest distinction between survivors and nonsurvivors and may explain the sudden death experienced by animals during HH. The data suggest that early respiratory and metabolic compensations are essential for survival of prolonged HH.     

Effect of methylene blue on cardiac output response to exercise in dogs

To determine whether the increase in cardiac output during mild to moderate exercise is related to an increase in the tissue redox potential, we compared the responses of cardiac output, total body oxygen consumption, and arterial blood lactate-to-pyruvate ratio (a measure of NADH/NAD) to treadmill exercise between dogs treated with normal saline and those treated with a hydrogen acceptor, new methylene blue. Normal saline was infused into the left atrium in the first group of dogs at a rate of 0.38 ml/min throughout the treadmill exercise (2.5 mph and 5.0 mph on a 6% incline, each for 20 min). In the second group, methylene blue was administered as a loading dose (4 mg/kg) before exercise, followed by a continuous infusion (0.15 mg X kg-1 X min-1) throughout exercise. A similar infusion of methylene blue was given to a third group of dogs without exercise; it reduced the arterial lactate-to-pyruvate ratio from 6.70 +/- 0.35 to 4.12 +/- 0.27 but had no or little effects on cardiac output, heart rate, arterial pressure, and left ventricular dP/dt and (dP/dt)/P. Treadmill exercise doubled cardiac output and increased total body O2 consumption three- to fourfold in the first two groups but increased arterial blood lactate-to-pyruvate ratio only in group 1 (6.0 +/- 0.54 to 9.97 +/- 0.91). The relationship between cardiac output and total body O2 consumption was unaffected by the simultaneous administration of methylene blue during exercise. Groups 1 and 2 also did not differ in their heart rate, left ventricular dP/dt and (dP/dt)/P, and plasma catecholamine responses to exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of dichloroacetate on hemodynamic responses to dynamic exercise in dogs.

To determine whether lactic acid production contributes significantly to the cardiac responses to muscular dynamic exercise, we administered intravenous sodium dichloroacetate (32 mumol.kg-1.min-1), a pyruvate dehydrogenase activator that facilitates lactate metabolism via the tricarboxylic cycle, in 12 dogs during two graded levels of treadmill exercise. Similar exercise was carried out in nine normal dogs receiving equimolar doses of NaCl. In the latter group, arterial lactate increased progressively from 0.80 +/- 0.11 (SE) mmol/l at rest to 2.13 +/- 0.28 mmol/l by the end of exercise. In contrast, arterial lactate did not change significantly (0.98 +/- 0.12 to 0.95 +/- 0.11 mmol/l) during exercise in dogs receiving dichloroacetate infusion. Dichloroacetate infusion also reduced the increases in plasma norepinephrine, heart rate, and left ventricular contractile indexes that occurred during exercise, suggesting that the sympathetic cardiac stimulation occurring during exercise may be related to the production of lactic acid. However, dichloroacetate affected neither the net increase in cardiac output nor the relationship between total body oxygen consumption and cardiac output that occurred during exercise. Thus we conclude that lactic acid production is not essential to the increase in cardiac output that occurs during mild-to-moderate exercise.     

Assessment of cardiac output as a predictor of metabolic rate in rainbow trout

When water temperature was increased from 12 to 27°C at a rate of 2°C h⁻¹, oxygen consumption of rainbow trout Oncorhynchus mykiss was correlated strongly with both heart rate and blood oxygen extraction but the relationship with cardiac output was variable and weak. On the other hand, when water temperature was decreased from 21 to 12°C at a rate of 0·5°C h⁻¹, oxygen consumption was correlated with both heart rate and cardiac output but not with blood oxygen extraction. When fish were forced to swim increasingly faster, heart rate, cardiac output and blood oxygen extraction all correlated positively with oxygen consumption. For both cardiac output and heart rate, the slope of the regression line with oxygen consumption was elevated significantly more when the fish were forced to swim at increasingly higher swimming speeds than when water temperature was increased or decreased. The variation of the regression lines between cardiac output and oxygen consumption indicated that cardiac output presents few advantages over heart rate as a predictor of metabolic rate.     

Pulmonary and circulatory changes in conscious sheep exposed to 100% O2 at 1 ATA

We have measured the effects of normobaric hyperoxia on arterial and mixed venous gas tensions, cardiac output, heart rate, right atrial, pulmonary, and aortic pressures in 12 conscious chronically instrumented sheep. Regional blood flow to brain, heart, kidney, intestines, and respiratory muscles was assessed in five sheep by injecting 15-micrometers microspheres labeled with gamma-emitting isotopes. Survival time ranged from 60 to 120 h (mean = 80 h). All variables except arterial O2 partial pressure (PaO2) and mixed venous O2 partial pressure remained at base-line level during the first 40 h of exposure, after which PaO2 decreased gradually but remained above 200 Torr at death. After this there was a progressive uncompensated respiratory acidosis with terminal arterial CO2 partial pressure values exceeding 90 Torr. There was a considerable rise in the brain blood flow, whereas flow to the other organs either remained unchanged or increased in proportion to cardiac output. Our experiments also showed that systemic hyperoxic vasoconstriction did not occur, and any local changes were not of sufficient magnitude to affect perfusion.     

Plasma glucose, insulin and free fatty acids in infants with congenital heart disease.

The effect of congestive cardiac failure, hypoxia and hypoglycaemia on glucose tolerance and insulin secretion were studied in selected groups of infants with congenital heart disease. Fasting blood glucose level was significantly decreased in patients with congestive heart failure and in cyanotic infants without congestive heart failure. In the former it seemed to be correlated with the degree of malnutrition, while in cyanotic infants it was independent of the nutritional state. Plasma insulin levels were reduced in infants, with congestive cardiac failure, although their glucose tolerance test and free fatty acid concentrations were normal. It is suggested that the decreased plasma insulin concentration was a consequence of adaptation to reduced requirements. Glucose tolerance and insulin secretion were not affected by hypoxia or hypoglycaemia.     

Anesthetic effects on liver and muscle glycogen concentrations: rest and postexercise

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.     

Influence of Bohr-Haldane effect on steady-state gas exchange

The influence of the Bohr-Haldane effect (BH) on steady-state gas exchange has previously been described by its effect of gas transfer from the blood when arterial and venous blood gas tensions were held constant. This report quantifies by computer analysis the effects of BH when either or both arterial and venous blood gas tensions are subject to change. When mixed venous blood gas composition is held constant, elimination of BH from a single lung unit typically reduces CO2 output by 6.5% and O2 uptake by 0.5%. Similar effects occur in a two-compartment lung model whether alveolar ventilation-perfusion (VA/Q) mismatch occurs in a parallel or series ventilatory arrangement. When arterial blood gas composition is held constant, elimination of BH increases systemic venous CO2 partial pressure, but O2 partial pressure is hardly affected in the absence of metabolic acidosis. When both mixed venous and arterial blood gas tensions vary and gas exchange is stressed by VA/Q inequality, altitude, anemia, or exercise, elimination of BH predominantly affects mixed venous rather than arterial blood gas tensions. it is concluded that BH may act primarily to reduce tissue acidosis.     

Acidaemia reduces cardiac output and left ventricular contractility in conscious lambs

We studied the effects of HCI-induced metabolic acidaemia on cardiac output, contractile function, myocardial blood flow, and myocardial oxygen consumption in nine unanaesthetized newborn lambs. Through a left thoracotomy, catheters were placed in the aorta, left atrium and coronary sinus. A pressure transducer was placed in the left ventricle. Three to four days after surgery, we measured cardiac output, dP/dt, left ventricular end diastolic and aortic mean blood pressures, heart rate, aortic and coronary sinus blood oxygen contents, and left ventricular myocardial blood flow during a control period, during metabolic acidaemia, and after the aortic pH was restored to normal. We calculated systemic vascular resistance, myocardial oxygen consumption and left ventricular work. Acidaemia was associated with reduction in cardiac output, maximal dP/dt, and aortic mean blood pressure. Left ventricular end diastolic pressure and systemic vascular resistance increased, and heart rate did not change significantly. The reduction in myocardial blood flow and oxygen consumption was accompanied by fall in cardiac work. Cardiac output returned to control levels after the pH had been normalized but maximal dP/dt was incompletely restored. Myocardial blood flow and oxygen consumption increased beyond control levels. This study demonstrates that HCI-induced metabolic acidaemia in conscious newborn lambs is associated with a reduction in cardiac output which could have been mediated by the reduction in contractile function and/or the increase in systemic vascular resistance. The decreases in myocardial blood flow and oxygen consumption appear to reflect diminished cardiac work. The restoration of a normal cardiac output after normalization of the pH appears to have resulted from the increases in heart rate and left ventricular filling pressures in conjunction with an incomplete restoration of contractile function.     

Oxygen Transport in Acute Pulmonary Oedema and in Acute Exacerbations of Chronic Bronchitis

When breathing air, the average arterial oxygen tension in eight patients with acute pulmonary oedema was significantly higher than in eight other patients suffering from an acute exacerbation of chronic bronchitis, but the mixed venous oxygen tension was very similar in both groups. This largely arose from the smaller arteriovenous difference of oxygen content in the bronchitic cases, presumably due to their higher cardiac output, associated with raised arterial CO₂ tensions. Oxygen therapy (60-90% for pulmonary oedema, 30% for the bronchitics) raised the mixed venous oxygen tensions to a similar level in both groups. We suggest that the major need for oxygen therapy lies in patients who maintain their oxygen consumption but show a reduction in mixed venous tension when breathing air. Although partial correction of arterial hypoxaemia is adequate in chronic bronchitis—in which the cardiac output is maintained—high concentrations of oxygen are necessary in pulmonary oedema, in which the cardiac output is low.     

Haematological, blood gas and acid-base effects of central histamine-induced reversal of critical haemorrhagic hypotension in rats.

In a rat model of volume-controlled irreversible haemorrhagic shock, which results in a severe metabolic acidosis and the death of all control animals within 30 min., intracerebroventricular injection of histamine (100 nmol) produces a prompt and long-lasting increase in mean arterial pressure and heart rate, with a 100% survival of 2 h after treatment. Histamine action is accompanied by a decrease in haematocrit value, haemoglobin concentration, erythrocyte and platelet count, and an increase in residual blood volume at the end of the experiment (2 h). Cardiovascular effects are also associated with a long-lasting rise in respiratory rate and biphasic blood acid-base changes - initial increase of metabolic acidosis with the decrease in arterial and venous pH, bicarbonate concentration and base excess, followed by almost a complete recovery of blood gas and acid-base parameters to the pre-bleeding values, with normalisation of arterial and venous pH, Pco2 bicarbonate concentration and base excess at the end of experiment. It can be concluded that in the late phase of central histamine-induced reversal of haemorrhagic hypotension there is almost a complete restoration of blood gas and acid-base status due to circulatory and respiratory compensations, while accompanying haematological changes are the result of the haemodilution and the increase in residual blood volume.     

Reference cardiopulmonary values in normal dogs

The purpose of this project was to collate canine cardiopulmonary measurements from published and unpublished studies in our laboratory in 97 instrumented, unsedated, normovolemic dogs. Body weight; arterial and mixed-venous pH and blood gases; mean arterial, pulmonary arterial, pulmonary artery occlusion, and central venous blood pressures; cardiac output; heart rate; hemoglobin; and core temperature were measured. Body surface area; bicarbonate concentration; base deficit; cardiac index; stroke volume index, systemic and pulmonary vascular resistance indices; left and right cardiac work indices; alveolar partial pressure of oxygen (pO2) ; alveolar-arterial pO2 gradient (A-apO2); arterial, mixed-venous, and pulmonary capillary oxygen content; oxygen delivery; oxygen consumption; oxygen extraction; venous admixture; arterial and mixed-venous blood CO2 contents; and CO2 production were calculated. In the 97 normal, resting dogs, mean arterial and mixed-venous pH were 7.38 and 7.36, respectively; partial pressure of carbon dioxide (pCO2), 40.2 and 44.1 mm Hg, respectively; base-deficit, -2.1 and -1.9 mEq/liter, respectively; pO2, 99.5 and 49.3 mm Hg, respectively; oxygen content, 17.8 and 14.2 ml/dl, respectively; A-a pO2 was 6.3 mm Hg; and venous admixture was 3.6%. The mean arterial blood pressure (ABPm), mean pulmonary arterial blood pressure (PAPm), pulmonary artery occlusion pressure (PAOP) were 103, 14, and 5.5 mm Hg, respectively; heart rate was 87 beats/min; cardiac index (CI) was 4.42 liters/min/m2; systemic and pulmonary vascular resistances were 1931 and 194 dynes.sec.cm-5, respectively; oxygen delivery, consumption and extraction were 790 and 164 ml/min/m2 and 20.5%, respectively. This study represents a collation of cardiopulmonary values obtained from a large number of dogs (97) from a single laboratory using the same measurement techniques.     

Tissue carbon dioxide tension: a putative specific indicator of ischemia in porcine latissimus dorsi flaps

Free flap surgical procedures are technically challenging, and anastomosis failure may lead to arterial or venous occlusion and flap necrosis. To improve myocutaneous flap survival rates, more reliable methods to detect ischemia are needed. On the basis of theoretical considerations, carbon dioxide tension, reflecting intracellular acidosis, may be suitable indicators of early ischemia. It was hypothesized that tissue carbon dioxide tension increased rapidly when metabolism became anaerobic and would be correlated with acute venoarterial differences in lactate levels, potassium levels, and acid-base parameters. Because metabolic disturbances have been observed to be less pronounced in flaps with venous occlusion, it was hypothesized that tissue carbon dioxide tension and venoarterial differences in lactate and potassium levels and acid-base parameters would increase less during venous occlusion than during arterial occlusion. In 14 pigs, latissimus dorsi myocutaneous flaps were surgically isolated, exposed to acute ischemia for 150 minutes with complete arterial occlusion (seven subjects) or venous occlusion (seven subjects), and reperfused for 30 minutes. After arterial occlusion, pedicle blood flow decreased immediately to less than 10 percent of baseline flow. Blood flow decreased more slowly after venous occlusion but within 3 minutes reached almost the same low levels as observed during arterial occlusion. Venous oxygen saturation decreased from approximately 70 percent to approximately 20 percent, whereas oxygen uptake was almost arrested. Tissue carbon dioxide tension increased to two times baseline values in both groups (p < 0.01). The venoarterial differences in carbon dioxide tension, pH, base excess, glucose levels, lactate levels, and potassium levels increased significantly (p < 0.01). Tissue carbon dioxide tension measured during the occlusion period were closely correlated with venoarterial differences in pH, base excess, glucose levels, lactate levels, and potassium levels (median r2, 0.67 to 0.92). After termination of arterial or venous occlusion, more pronounced hyperemia was observed in the arterial occlusion group than in the venous occlusion group (p < 0.05). Oxygen uptake (p < 0.05) and venoarterial differences in lactate and potassium levels (p < 0.05) were significantly more pronounced in the arterial occlusion group. In the venous occlusion group, with less pronounced hyperemia, venoarterial differences in acid-base parameters remained significantly different from baseline values before occlusion (p < 0.01). The data indicate that tissue carbon dioxide tension can be used to detect anaerobic metabolism, caused by arterial or venous occlusion, in myocutaneous flaps. The correlations between carbon dioxide tension and venoarterial differences in acid-base parameters were excellent. Because carbon dioxide tension can be measured continuously in real time, such measurements are more likely to represent a clinically useful parameter than are venoarterial differences.     

A comparison of blood gases and acid-base measurements in arterial, arterialized venous, and venous blood during short-term maximal exercise

The purpose of this study was to determine the relationship between blood gases and acid-base measurements in arterial, arterialized venous, and venous blood measured simultaneously during short-term maximal exercise. Ten well-trained male cyclists performed a graded maximal exercise test on a cycle ergometer to determine the power output corresponding to their peak oxygen consumption (test I), and a short-term maximal test on a cycle ergometer at peak power output (test II). During test II arterial, arterialized venous and venous blood were sampled simultaneously for determination of partial pressures of oxygen and carbon dioxide, pH, bicarbonate (HCO3-), base excess (BE), and lactate (La). Samples were taken at rest, the end of 1 min of exercise (1 ME), at the end of exercise (EE), and at 2 min of recovery (REC). During test II, subjects maintained a peak power output of 370.6 (62.1) W [mean (SD)] for 4.5, SD 1.6 min. Except at rest venous and arterialized venous measurements tended to be the same at all sampling intervals, but differed significantly from measurements in arterial blood (P less than 0.05). BE was the only variable that rendered consistently significant correlations between arterial and arterialized venous blood at each sampling interval. The pooled correlation coefficient between arterial and arterialized venous BE was r = 0.83 [regression equation: BEa = (0.84 BEav)-0.51]. Arterial La was significantly higher than venous La at 1 ME (2.8, 0.7 vs 0.8, 0.3 mmol.l-1) and higher than both venous and arterialized venous La at EE.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increases in coronary vein CO2 during cardiac resuscitation

We investigated the aortic, mixed venous, and great cardiac vein acid-base changes in eight domestic pigs during cardiac arrest produced by ventricular fibrillation and during cardiopulmonary resuscitation (CPR). The great cardiac vein PCO2 increased from a control value of 52 +/- 2 to 132 +/- 28 (SD) Torr during CPR, whereas the arterial PCO2 was unchanged (39 +/- 4 vs. 38 +/- 4). The coronary venoarterial PCO2 gradient, therefore, increased remarkably from 13 +/- 2 to 94 +/- 29 Torr. The simultaneously measured great cardiac vein lactate concentrations increased from 0.24 +/- 0.06 to 7.3 +/- 2.34 mmol/l. Much more moderate increases in the lactate content of aortic blood from 0.64 +/- 0.25 to 2.56 +/- 0.27 mmol/l were observed. Increases in great cardiac vein PCO2 and lactate were highly correlated during CPR (r = 0.91). After successful CPR, the coronary venoarterial PCO2 gradient returned to normal levels within 2 min after restoration of spontaneous circulation. Lactate content was rapidly reduced and lactate extraction was reestablished within 30 min after CPR. These studies demonstrate marked but reversible acidosis predominantly as the result of myocardial CO2 production during CPR.     

Statistical relations of some blood parameters along recovery from imposed stress in dogfish

Selected blood parameters (arterial pH, O2 and CO2 tensions, oxygen content, bicarbonate and lactate concentrations, haematocrit, haemoglobin, red blood cell count, mean corpuscular haemoglobin, mean corpuscular volume and mean corpuscular haemoglobin concentration), oxygen consumption and ventilatory frequency were measured 0, 3 and 24 hours after cannulation of the dorsal aorta of 22 dogfish. Correlations were calculated between all pairs of variables along the post-operational recovery period. Results are discussed in terms of the integrated dynamics of the recovery process subsequent to handling, anaesthesia and surgery stress. It is suggested that erythrocyte swelling plays an important role in maintaining tissue oxygen supply during recovery from operational procedures.