Arterial O2 Tension Research Articles

Cardiopulmonary bypass in humans – jejunal mucosal perfusion increases in parallel with well‐maintained microvascular hematocrit

An imbalance between splanchnic oxygen supply and demand occurs during cardiopulmonary bypass (CPB) in man, which might disrupt the intestinal mucosal barrier function. The aim of the present study was to evaluate the effects of mild hypothermic CPB on intestinal mucosal perfusion in man undergoing cardiac surgery. Additionally we aimed to identify variables, which independently could predict changes of intestinal mucosal microcirculatory variables during CPB. Jejunal mucosal perfusion (JMP), jejunal mucosal hematocrit (JMHt), red blood cell (RBC) velocity and arteriolar vasomotion using endoluminal jejunal laser Doppler flow metry were studied in eight cardiac surgical patients before and during CPB at a temperature of 34 degrees C. Cardiopulmonary bypass and the accompanied hemodilution (25-30%) induced a 44% increase in JMP (P < 0.05) and a 42% increase in RBC velocity (P < 0.01), with no change in JMHt. The oscillation amplitude of JMP, at a fundamental frequency of 2.8 cycles min(-1), increased with 175% (P < 0.05) during CPB. Splanchnic oxygen extraction increased by 64% during CPB (P < 0.05). Stepwise multiple regression analysis identified systemic hematocrit, arterial O2 and CO2 tension and splanchnic oxygen extraction as independent predictors of RBC velocity during CPB (R2=0.63, P < 0.001). The oscillation amplitude of JMP was predicted by RBC velocity and splanchnic oxygen extraction (R2= 0.68, P <0.0001). The increase in RBC velocity and enhanced arteriolar vasomotion, as well as maintained jejunal mucosal hematocrit, are microcirculatory, compensatory mechanisms for the splanchic oxygen supply/demand mismatch seen during cardiopulmonary bypass in humans.

Effects of acepromazine on pulmonary gas exchange and circulation during sedation and dissociative anaesthesia in horses

ObjectiveTo study pulmonary gas exchange and cardiovascular responses to sedation achieved with romifidine and butorphanol (RB) alone, or combined with acepromazine, and during subsequent tiletamine–zolazepam anaesthesia in horses. AnimalsSix (four males and two females) healthy Standardbred trotters aged 3–12 years; mass 423–520 kg. Study designRandomized, cross-over, experimental study. Materials and methodsHorses were anaesthetized on two occasions (with a minimum interval of 1 week) with intravenous (IV) tiletamine–zolazepam (Z; 1.4 mg kg−1) after pre-anaesthetic medication with IV romifidine (R; 0.1 mg kg−1) and butorphanol (B; 25 μg kg−1 IV). At the first trial, horses were randomly allocated to receive (protocol ARBZ) or not to receive (protocol RBZ) acepromazine (A; 35 μg kg−1) intramuscularly (IM) 35 minutes before induction of anaesthesia. Each horse was placed in left lateral recumbency and, after tracheal intubation, allowed to breathe room air spontaneously. Respiratory and haemodynamic variables and ventilation–perfusion ( V˙A/Q˙; multiple inert gas elimination technique) ratios were determined in the conscious horse, after sedation and during anaesthesia. One- and two-way repeated-measures anova were used to identify within- and between-technique differences, respectively. ResultsDuring sedation with RB, arterial oxygen tension (PaO2) decreased compared to baseline and increased V˙A/Q˙ mismatch was evident; there was no O2 diffusion limitation or increase in intrapulmonary shunt fraction identified. With ARB, PaO2 and V˙A/Q˙ remained unaffected. During anaesthesia, intrapulmonary shunt occurred to the same extent in both protocols, and V˙A/Q˙ mismatching increased. This was less in the ARBZ group. Arterial O2 tension decreased in both protocols, but was lower at 25 and 35 minutes of anaesthesia in RBZ than in ARBZ. During sedation, heart rate (HR) and cardiac output ( Q˙t) were lower while arterial-mixed venous oxygen content differences and haemoglobin concentrations were higher in RBZ compared with ARBZ. Total systemic vascular resistance, mean systemic, and mean pulmonary arterial pressures were higher during anaesthesia with RBZ compared to ARBZ. Conclusions and clinical relevanceAcepromazine added to RB generally improved haemodynamic variables and arterial oxygenation during sedation and anaesthesia. Arterial oxygenation was impaired as a result of increased shunt and V˙A/Q˙ mismatch during anaesthesia, although acepromazine treatment reduced V˙A/Q˙ disturbances and falls in PaO2 to some extent. Haemodynamic variables were closer to baseline during sedation and anaesthesia when horses received acepromazine. Acepromazine may confer advantages in healthy normovolaemic horses.

Cerebral blood flow response to isocapnic hypoxia during slow-wave sleep and wakefulness

Nocturnal hypoxia is a major pathological factor associated with cardiorespiratory disease. During wakefulness, a decrease in arterial O2 tension results in a decrease in cerebral vascular tone and a consequent increase in cerebral blood flow; however, the cerebral vascular response to hypoxia during sleep is unknown. In the present study, we determined the cerebral vascular reactivity to isocapnic hypoxia during wakefulness and during stage 3/4 non-rapid eye movement (NREM) sleep. In 13 healthy individuals, left middle cerebral artery velocity (MCAV) was measured with the use of transcranial Doppler ultrasound as an index of cerebral blood flow. During wakefulness, in response to isocapnic hypoxia (arterial O2 saturation -10%), the mean (+/-SE) MCAV increased by 12.9 +/- 2.2% (P < 0.001); during NREM sleep, isocapnic hypoxia was associated with a -7.4 +/- 1.6% reduction in MCAV (P <0.001). Mean arterial blood pressure was unaffected by isocapnic hypoxia (P >0.05); R-R interval decreased similarly in response to isocapnic hypoxia during wakefulness (-21.9 +/- 10.4%; P <0.001) and sleep (-20.5 +/- 8.5%; P <0.001). The failure of the cerebral vasculature to react to hypoxia during sleep suggests a major state-dependent vulnerability associated with the control of the cerebral circulation and may contribute to the pathophysiologies of stroke and sleep apnea.

NaHCO(3) does not affect arterial O(2) tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds.

The objective of the present study was to examine the effects of preexercise NaHCO(3) administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO(3) (250 mg/kg i.v.), were carried out on 13 healthy, sound Thoroughbred horses in random order, 7 days apart. Blood-gas variables were examined at rest and during incremental exercise, leading to 120 s of galloping at 14 m/s on a 3.5% uphill grade, which elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. NaHCO(3) administration caused alkalosis and hemodilution in standing horses, but arterial O(2) tension and hemoglobin-O(2) saturation were unaffected. Thus NaHCO(3) administration caused a reduction in arterial O(2) content at rest, although the arterial-to-mixed venous blood O(2) content gradient was unaffected. During maximal exercise in both treatments, arterial hypoxemia, desaturation, hypercapnia, acidosis, hyperthermia, and hemoconcentration developed. Although the extent of exercise-induced arterial hypoxemia was similar, there was an attenuation of the desaturation of arterial hemoglobin in the NaHCO(3)-treated horses, which had higher arterial pH. Despite these observations, the arterial blood O(2) content of exercising horses was less in the NaHCO(3) experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O(2) content gradient was observed. It was concluded that preexercise NaHCO(3) administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.

Erythropoietin

This article summarizes recent advances in understanding the production and action of the hormone erythropoietin (Epo) with respect to high altitude physiology and sports medicine. Hypoxia is the main stimulus for Epo gene expression. An O2-labile protein (hypoxia-inducible factor 1, HIF-1) has been identified that is hydroxylated and degraded under normoxic conditions but active in hypoxia, where it enhances Epo gene transcription resulting in elevated hemoglobin levels and O2 capacity of the blood. The stimulation of Epo production at lowered arterial O2 tension can be maladaptive, if erythrocytosis develops such as seen in high altitude habitants. Within physiological limits the aerobic power increases in parallel with blood O2 capacity. Therefore, some elite athletes have misused recombinant human Epo (rhEpo), which is a beneficial anti-anemic drug in clinical practice. Indirect and direct methods to detect rhEpo doping have been recently developed.

Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise.

It is reported that preexercise hyperhydration caused arterial O(2) tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425-429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 +/- 1.8% increase in plasma volume was induced with NaCl (0.30-0.45 g/kg dissolved in 1,500 ml H(2)O) administered via a nasogastric tube, 285-290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant (P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O(2) content gradient.

Aerosolized salbutamol (albuterol) improves PaO2 in hypoxaemic anaesthetized horses – a prospective clinical trial in 81 horses

ObjectiveTo compare the arterial pH and blood gas values, heart rate and mean arterial blood pressure, in hypoxaemic anaesthetized horses, before and after treatment, with a salbutamol (albuterol) aerosol. Animal populationEighty-one client-owned horses weighing between 114 and 925 kg. Fifty-seven underwent emergency abdominal surgery and 24 were anaesthetized for elective procedures. Materials and methodsPre-anaesthetic medication included xylazine, detomidine, butorphanol and morphine, alone or in various combinations. Induction of anaesthesia was achieved with guaifenesin and ketamine, diazepam and ketamine, or guaifenesin and thiopental. The trachea of all animals was intubated and anaesthesia maintained with either halothane (33 horses) or isoflurane (48 horses) in oxygen. Heart rate and rhythm were monitored continuously. Arterial blood pressure was monitored directly, and arterial blood collected for pH and blood gas analyses. When arterial PaO2 fell below 9.3 kPa (70 mm Hg) and failed to respond to corrective measures including positive pressure ventilation and treatment of hypotension (mean arterial blood pressures <70 mm Hg), a salbutamol aerosol (2 μg kg−1) was delivered via the endotracheal tube. Twenty minutes later, a second arterial blood sample was analysed. ResultsThere were no significant differences in mean arterial blood pressure, heart rate, arterial pH, base excess and bicarbonate before and after treatment. Arterial O2 tension increased significantly from a mean ± SD of 8.3 ± 1.7 kPa (62.4 ± 13.1 mm Hg) before administration to 15.9 ± 9.8 kPa (119.4 ± 57.7 mm Hg) after treatment. There was a small but significant decrease in PaCO2 from 7.4 ± 1.5 kPa (55.2 ± 11.2 mm Hg) to 7.0 ± 1.3 kPa (52.9 ± 9.8 mm Hg) between sample times. No changes in heart rhythm were observed. A high percentage (approximately 70%) of animals sweated following treatment. ConclusionsSalbutamol administered at a dose of 2 μg kg−1 via the endotracheal tube of anaesthetized horses with PaO2 values less than 9.3 kPa (70 mm Hg) resulted in an almost two-fold increase in PaO2 values within 20 minutes of treatment. No changes in heart rate or mean arterial blood pressure were associated with the use of salbutamol in this study. The improvement in PaO2 may be a result of bronchodilatation and improved ventilation, increased perfusion secondary to an increase in cardiac output, or a combination of these two factors. Cardiac output and ventilation–perfusion distribution were not measured in this study; therefore, the reason for the increase in PaO2 values cannot be conclusively determined. Clinical relevanceAdministration of a salbutamol aerosol is a simple but effective technique that can be used to improve PaO2 values in hypoxaemic horses during inhalant anaesthesia with no apparent detrimental side effects.

Regional brain blood flow and cerebral hemispheric oxygen consumption during acute hypoxaemia in the llama fetus.

Unlike fetal animals of lowland species, the llama fetus does not increase its cerebral blood flow during an episode of acute hypoxaemia. This study tested the hypothesis that the fetal llama brain maintains cerebral hemispheric O2 consumption by increasing cerebral O2 extraction rather than decreasing cerebral oxygen utilisation during acute hypoxaemia. Six llama fetuses were surgically instrumented under general anaesthesia at 217 days of gestation (term ca 350 days) with vascular and amniotic catheters in order to carry out cardiorespiratory studies. Following a control period of 1 h, the llama fetuses underwent 3 x 20 min episodes of progressive hypoxaemia, induced by maternal inhalational hypoxia. During basal conditions and during each of the 20 min of hypoxaemia, fetal cerebral blood flow was measured with radioactive microspheres, cerebral oxygen extraction was calculated, and fetal cerebral hemispheric O2 consumption was determined by the modified Fick principle. During hypoxaemia, fetal arterial O2 tension and fetal pH decreased progressively from 24 +/- 1 to 20 +/- 1 Torr and from 7.36 +/- 0.01 to 7.33 +/- 0.01, respectively, during the first 20 min episode, to 16 +/- 1 Torr and 7.25 +/- 0.05 during the second 20 min episode and to 14 +/- 1 Torr and 7.21 +/- 0.04 during the final 20 min episode. Fetal arterial partial pressure of CO2 (P(a,CO2), 42 +/- 2 Torr) remained unaltered from baseline throughout the experiment. Fetal cerebral hemispheric blood flow and cerebral hemispheric oxygen extraction were unaltered from baseline during progressive hypoxaemia. In contrast, a progressive fall in fetal cerebral hemispheric oxygen consumption occurred during the hypoxaemic challenge. In conclusion, these data do not support the hypothesis that the fetal llama brain maintains cerebral hemispheric O2 consumption by increasing cerebral hemispheric O2 extraction. Rather, the data show that in the llama fetus, a reduction in cerebral hemispheric metabolism occurs during acute hypoxaemia.

Pleuropulmonary and cardiovascular consequences of thoracoscopy performed in healthy standing horses

Six healthy, awake, and pharmacologically restrained mature horses were studied in order to define the changes in cardiopulmonary function during and after exploratory thoracoscopy and to determine the presence of postoperative complications occurring 48 hours after thoracoscopy. In a randomised 3 x 3 latin square design with 2 replications, 18 procedures were performed: 6 right (RTH) and 6 left thoracoscopies (LTH) and 6 sham procedures (STH). Prior to each procedure a physical examination and a bronchoalveolar lavage fluid analysis were performed. During thoracoscopy and sham protocols, horses were sedated with a continual drip of detomidine HCl and data were collected at 6 time intervals: T1 (baseline), T2 (10 min detomidine administration), T3 (first 15 min pneumothorax), T4 (5 min recovery from pneumothorax), T5 (second 15 min pneumothorax), and T6 (10 min recovery from the second pneumothorax and detomidine). An endoscopic thoracic examination was conducted during the 2 pneumothorax periods. An identical protocol was followed for sham procedures without surgery or pneumothorax. Data were analysed by ANOVA with time and surgical procedure as main factors. Physical examinations, thoracic radiography and ultrasound, CBC and bronchoalveolar lavage fluid analysis were performed 48 h after thoracoscopy. Heart rate, respiratory rate, and cardiac output decreased following detomidine administration. There was a trend for cardiac output to be lower during thoracoscopy. Mild systemic hypertension was associated with thoracoscopy although there was no effect on pulmonary arterial pressure. Total and pulmonary vascular resistances were increased following detomidine administration. Thoracoscopy caused a further increase in systemic and pulmonary vascular resistances especially during the second pneumothorax. Arterial O2 tension decreased following detomidine administration and was further decreased during the second pneumothorax period. PaO2 values were lower when thoracoscopy was performed on the left rather than the right hemithorax. No significant complications were found during the 48 h follow-up evaluation. A subclinical postoperative pneumothorax occurred in 2 horses, one of which had sustained a lung laceration by the trocar. Thoracoscopy performed in healthy, awake, and pharmacologically restrained horses did not have detrimental cardiopulmonary effects and did not cause postoperative complications within the first 48 h period.

Arterial blood gas tensions during exercise in neonatal lambs.

At the onset of exercise, adult animals increase ventilation to match or exceed the metabolic requirement. This error-free regulation of arterial blood gas tensions may be attributable to 'adaptive feed-forward control'--respiratory control based on experience gained in infancy. This hypothesis predicts that neonates exhibit hypercapnia at the onset of exercise. To test this prediction, seven lambs were exercised on a treadmill at 0.8 m/sec at the ages of 2-5 days, and again at 9-12 days. Arterial blood samples were drawn pre-exercise and at 0.5, 1, 2, 5, 7 and 10 min of exercise. Seven adult sheep were similarly tested for comparison. The lambs had significantly higher arterial CO2 tensions (PaCO2) and lower arterial O2 tensions (PaO2) than adult sheep both at rest and during exercise. Nonetheless, the lambs maintained PaCO2 at or below the resting level throughout exercise. PaO2 rose significantly during exercise in the sheep and lambs. The results do not support the hypothesis since hypercapnia was not observed in the exercising neonatal lambs.

The effects of increasing concentrations of desflurane on systemic oxygenation during one-lung ventilation in pigs.

During one-lung ventilation (OLV), hypoxic pulmonary vasoconstriction reduces venous admixture and attenuates the decrease in arterial O2 tension by diverting blood from the nonventilated to the ventilated lung. In vitro, increasing concentrations of desflurane depresses hypoxic pulmonary vasoconstriction in a dose-dependent manner. Accordingly, we investigated the effects of increasing concentrations of desflurane on oxygenation during OLV in vivo. Thirteen pigs (25-30 kg) were anesthetized (induction: propofol 2-3 mg/kg IV; maintenance: N2O/O2 50%/50%, desflurane 3%, propofol 50 microg x kg(-1) min(-1), and vecuronium 0.2 mg x kg(-1) x h(-1) IV), orotracheally intubated, and mechanically ventilated. After placement of femoral arterial and thermodilution pulmonary artery catheters, a leftsided, 28F, double-lumen tube was placed via tracheotomy. After double-lumen tube placement, N2O and desflurane were discontinued, propofol was increased to 200 microg x kg(-1) x min(-1), and the fraction of inspired oxygen was adjusted at 0.8. Anesthesia was then continued in random order with desflurane 5%, 10%, or 15% end-tidal concentrations while propofol was discontinued. Whereas mixed venous PO2, mean arterial pressure, cardiac output, and shunt fraction decreased in a dose-dependent manner, PaO2 remained unchanged with increasing concentrations of desflurane during OLV. These findings indicate that, in vivo, increasing concentrations of desflurane do not necessarily worsen oxygenation during OLV. Oxygenation during one-lung ventilation depends on reflex vasoconstriction in the nonventilated lung. In vitro, desflurane inhibits this reflex dose-dependently. Our results indicate that, in vivo, this does not necessarily translate to dose-dependent decreases in oxygenation during one-lung ventilation.

Microvascular responses to hemodilution with Hb vesicles as red blood cell substitutes: influence of O2 affinity.

Phospholipid vesicles encapsulating purified hemoglobin (HbV) were developed to provide O2-carrying capacity to plasma expanders. Microvascular perfusion was determined for HbV with different O2 affinity (P50 = 9, 16, and 30 mmHg) prepared by coencapsulating pyridoxal 5'-phosphate (PLP) at the molar ratios of [PLP]/[Hb] = 0, 0.5, and 3, respectively (cf. hamster blood, P50: 28 mmHg), and suspended in 8 g/dl human serum albumin (HSA). Eighty percent of the red blood cell (RBC) mass of conscious Syrian golden hamsters fitted with dorsal skinfold windows was substituted with either of the HbV-HSA suspensions, washed hamster RBC suspended in HSA (RBC-HSA), and HSA alone. All three HbV-HSA groups and RBC-HSA groups showed stable blood pressure and heart rate, which could not be sustained with HSA alone. Only the HbV (P50 = 9)-HSA group showed an increase in arterial O2 tension (89.8 +/- 14.7 mmHg, baseline 58.4 +/- 4.0 mmHg) because of hyperventilation, and microvascular perfusion was decreased, indicating that facilitated O2 unloading of HbV by decreasing the O2 affinity (increasing P50) with PLP as an allosteric effector is important. Microvascular perfusion and microvascular and interstitial O2 tensions in the HbV (P50 = 16 and 30)-HSA groups were significantly higher than those in the HSA group. The O2 release rate from the HbV was 18-32 s-1 vs. 4.4 s-1 for RBC. Functional capillary density was improved from 17 to 41% on average by decreasing P50 from 30 to 16 mmHg, which appears to be an optimal value for the P50 in this system.

Arterial O2 content and tension in regulation of cardiac output and leg blood flow during exercise in humans.

A universal O2 sensor presumes that compensation for impaired O2 delivery is triggered by low O2 tension, but in humans, comparisons of compensatory responses to altered arterial O2 content (CaO2) or tension (PaO2) have not been reported. To directly compare cardiac output (QTOT) and leg blood flow (LBF) responses to a range of CaO2 and PaO2, seven healthy young men were studied during two-legged knee extension exercise with control hemoglobin concentration ([Hb] = 144.4 +/- 4 g/l) and at least 1 wk later after isovolemic hemodilution ([Hb] = 115 +/- 2 g/l). On each study day, subjects exercised twice at 30 W and on to voluntary exhaustion with an FIO2 of 0.21 or 0.11. The interventions resulted in two conditions with matched CaO2 but markedly different PaO2 (hypoxia and anemia) and two conditions with matched PaO2 and different CaO2 (hypoxia and anemia + hypoxia). PaO2 varied from 46 +/- 3 Torr in hypoxia to 95 +/- 3 Torr (range 37 to >100) in anemia (P < 0.001), yet LBF at exercise was nearly identical. However, as CaO2 dropped from 190 +/- 5 ml/l in control to 132 +/- 2 ml/l in anemia + hypoxia (P < 0.001), QTOT and LBF at 30 W rose to 12.8 +/- 0.8 and 7.2 +/- 0.3 l/min, respectively, values 23 and 47% above control (P < 0.01). Thus regulation of QTOT, LBF, and arterial O2 delivery to contracting intact human skeletal muscle is dependent for signaling primarily on CaO2, not PaO2. This finding suggests that factors related to CaO2 or [Hb] may play an important role in the regulation of blood flow during exercise in humans.

Surfactant nebulization versus instillation during high frequency ventilation in surfactant-deficient rabbits.

Surfactant nebulization improves lung function at low alveolar doses of surfactant. However, efficiency of nebulization is low, and lung deposition seems to depend on lung aeration. High frequency ventilation (HFV) has been shown to improve lung aeration. We hypothesize that the combination of HFV and surfactant nebulization may benefit lung deposition of surfactant and consequently, lung function. The aim of this study was to compare the effect of surfactant nebulization versus instillation during HFV on lung function, surfactant distribution, and cerebral blood flow. Therefore, severe respiratory failure was induced by lung lavages in 18 rabbits. HFV was applied: frequency = 8 Hz, mean airway pressure = 12 cm H2O, amplitude = 100%, fraction of inspired O2 = 1.0. Technetium-99m-labeled surfactant (Alveofact, 100 mg/kg of BW) was nebulized or instilled (n = 6 each). Six other rabbits did not receive surfactant (control, HFV only). We found that after instillation partial arterial O2 tension increased from 7.0 kPa (95% confidence interval, 6.3-8.0 kPa) to 34 kPa (16-51 kPa), and during nebulization from 7.0 kPa (6.0-9.0 kPa) to 46 kPa (27-58 kPa). Partial arterial CO2 tension decreased after instillation from 6.1 kPa (5.3-7.1 kPa) to 4.8 kPa (3.9-5.6 kPa), and during nebulization, after an initial rise, it decreased from 6.3 kPa (5.3-7.4 kPa) to 4.9 kPa (4.4-5.6 kPa). Both treatments resulted in nonuniform distribution. Surfactant deposition after nebulization was 9.8%. Instillation resulted in a drop of mean arterial blood pressure of 17% (8-31%), and an even more pronounced drop in cerebral blood flow of 39% (18-57%). Nebulization did not affect blood pressure. Cerebral blood flow decreased with a maximum of 27% (10-37%). We conclude that surfactant nebulization during HFV improves lung function in rabbits with severe respiratory failure, without improving distribution, but with less effects on blood pressure and cerebral blood flow, when compared with surfactant instillation.

Clinical assessment of gas exchange in mature horses.

There are limited methods of assessing pulmonary function in horses at rest. We developed clinical techniques to measure gas exchange efficiency in horses and evaluated 3 groups of horses that were 1) asymptomatic based on auscultation with rebreathing, transtracheal aspirate cytology, and thoracic radiographs (n = 6), 2) asymptomatic at rest but symptomatic with rebreathing (n = 11) and 3) symptomatic at rest (n = 9). Blood samples were obtained from the transverse facial artery and jugular vein. Maximal end-tidal CO2 tension (PETCO2) was measured by an infrared capnograph through a facemask. Alveolar O2 tension, dead space fraction (V(D)/V(T)), and physiological shunt fraction (Q(S)/Q(T)) were calculated using standard formulae. Arterial O2 tension in Group 1 horses (mean +/-s.d.103+/-3 mmHg) was significantly higher than in Group 2 or Group 3 horses. Q(S)/Q(T) in Group 1 horses (0.37+/-0.98%) was significantly lower than in Group 2 and Group 3 horses. Mean +/-s.d.V(D)/V(T) in Group 1 horses (-18.2+/-3.1) was significantly lower than Group 3 horses but not Group 2 horses.

Cardio-vascular and ventilatory effects of prostaglandin E 2 in the European eel Anguilla anguilla

Prostaglandin E2 (PGE2) injection caused an initial decrease in heart rate (HR) (55%), cardiac output (QC) (55%), ventral (VAP, 40%) and dorsal (DAP, 60%) aortic pressures, associated with a marked gill vasoconstriction (100%) and a systemic vasodilation (30%) while cardiac stroke volume (CSV) remained unchanged. It was followed by a progressive recovery of HR, DAP, and vascular resistances to control values while VAP, QC, and CSV significantly increased (20%, 40%, and 40%, respectively). Bradycardia was abolished either by atropine treatment or bilateral section of the cardiac vagus, suggesting that bradycardia could be the consequence of a vagal mechanism triggered by a central action of PGE2. The increase in QC is due to the increase in CSV, which suggests a positive inotropic action of PGE2. Infusion with PGE2 (10−9 to 10−5 mol · l−1) did not cause any significant effect on the branchial vasculature in vitro, but when the preparation was pre-treated with adrenaline (10−8 mol · l−4), a dose-related vasoconstrictory response to PGE2 (10−9 to 10−5 mol · l−1) occurred. A significant rise (25%) in gill vascular resistance was observed in vivo after treatment with the β-blocker propranolol (2.0 mg · kg−1), suggesting the existence of a vasodilatory β-adrenergic control of the branchial vasculature. PGE2 caused an apnea followed by a simultaneous tachypnea (50%) and decrease in ventilatory amplitude (40%). The resulting decrease in ventilatory water flow (Qw) was accompanied by a fall in arterial O2 tension (Pa O2). Under steady Qw in curarized eels, an initial fall in Pa O2 was still observed during the PGE2-induced gill vasoconstriction. It is concluded that PGE2 could play a role in the regulation of gas exchanges and blood circulation in particular environmental conditions which require an impairment of gill respiration and a redistribution of blood to the benefit of the systemic vascular bed.

Effects of carbon dioxide insufflation combined with changes in body position on blood gas and acid-base status in anesthetized llamas (Llama glama).

To study the combined effects of intra-abdominal CO2 insufflation with changes in body position during laparoscopy in xylazine-ketamine-halothane anesthetized llamas. Prospective, controlled study. Nine castrated, male llamas weighing 114 +/- 23 kg, 3 to 13 years old. Three llamas (preliminary study [PS] group) were used to study the effect of right, lateral, dorsal, and left lateral recumbency on gas exchange and acid-base status. The other six (experimental study [ES] group) were used to study the combined effects of changes in body position and CO2 insufflation to an intraabdominal pressure of 10 to 12 mm Hg. Heart rate, respiratory rate, and indirect arterial blood pressures (systolic [SAP], mean [MAP], and diastolic [DAP]) were recorded every 5 minutes during anesthesia. Arterial blood gases (PaO2 and PaCO2) and acid-base status (pHa and HCO3-) were measured immediately after induction of anesthesia and before each change of position. In the PS group, significant decreases in SAP, MAP and PaCO2 and increases in PaO2 and pHa were observed when the llamas were turned from right lateral to dorsal recumbency. Values for HCO3- were lower than the postinduction values, but they remained unaffected by the changes in position. In the ES group, values for MAP were significantly lower when the llamas were placed in dorsal and left lateral recumbency than those observed during right lateral recumbency. Arterial O2 tension during right lateral recumbency was lower but returned to preinsufflation values when the llamas were placed in the dorsal position. All llamas recovered uneventfully within 30 minutes after termination of anesthesia. Insufflation of CO2 and changing body position induce minor and transient changes in cardiovascular and respiratory function. Laparoscopy with mild intra-abdominal CO2 insufflation (10 to 12 mm Hg) can be used safely in spontaneously breathing llamas anesthetized with xylazine, ketamine, and halothane.

A comparison of the response to induced exercise in red- and white-blooded Antarctic fishes

The physiological responses to forced exercise were studied in yellowbelly and marbled rockcod (Notothenia coriiceps and N. rossii), and the haemoglobinless icefish (Chaenocephalus aceratus), from blood samples obtained via indwelling catheters. The maximal exertion tolerable by N. coriiceps was 3–5 min, although N. rossii was not fully exhausted by this effort, and it proved difficult to elicit sustained maximal activity in C. aceratus. Arterial O2 tension reflected the relative degree of exhaustion, showing a significant fall in the case of N. coriiceps, little change in N. rossii, and even a rise in C. aceratus as a result of hyperventilation. Such changes in the red-blooded species were not caused by altered O2 carrying capacity, as there was no change in haematocrit. In Notothenia spp. the decrease in arterial pH was better correlated with a rise in arterial CO2 tension than with blood lactate concentration, which is reflected in a modest net metabolic acid load. In contrast, the icefish showed an attenuated hypercapnia and a more pronounced lactacidosis, but an insignificant net metabolic acid load. Disturbance in ionoregulation following exercise was limited to an elevated [Cl−] in Notothenia, while circulating catecholamine levels remained unusually low in all specimens. The response to stress appears to reflect lifestyle and/or endemic speciation, rather than specific adaptations to the stenothermal environment.

Pulmonary function measurements during repeated environmental challenge of horses with recurrent airway obstruction (heaves)

Abstract Objectives To evaluate the degree of reproducibility in clinical variables, blood gas measurements, and lung function variables, and the changes in these variables caused by exposure to moldy hay in naturally sensitized and control horses. Procedure The magnitude of variation in arterial blood gas and pulmonary function measurements were evaluated in a model of naturally acquired heaves. Horses with heaves and similarly aged control horses were studied prior to moldy hay challenge and again after the horses with heaves manifested clinical signs of airway obstruction. This cycle of testing was repeated 3 times to determine the variation of the before and after challenge measurements. Variables evaluated for repeatability included: clinical score; arterial O2 and CO2 tensions; pulmonary function variables, such as breathing rate (f), tidal volumes, and flow rates; lung resistance (Rl); dynamic compliance; and work of breathing (Wb). Results Before challenge, significant differences observed between control horses and horses with heaves included clinical score, expiratory flow rate at near-end expiration, Rl, and Wb. After exposure to moldy hay, variables measured in control horses were largely unchanged. However, in the afflicted horses, significant changes were observed for clinical score, arterial O2 and CO2 tensions, breathing rate, peak tidal inspiratory and expiratory flow rates, dynamic compliance, Rl, and Wb, compared with prechallenge values and with control horses' postchallenge values. Analysis of the data revealed few statistically significant differences between repeats of challenges. Conclusion Horses afflicted with heaves manifest airway obstruction that can be measured in repeatable fashion. (Am J Vet Res 1996;57:1214-1219)

Effects of freshwater to seawater transfer on osmoregulation, acid-base balance and respiration in river migrating whitefish (Coregonus lavaretus)

Osmoregulation, acid-base balance and respiratory parameters were investigated in whitefish following transfer from freshwater to salt water. Whitefish acclimated successfully to 25 ppt brackish water but died after direct transfer to 32 ppt sea water. Transfer to brackish water induced rapid (<6 h) and permanent increases in plasma [Na+], [Cl−], total [Ca] and [Mg]. The extracellular hyperosmolality effected a transient (<3 days) muscle tissue dehydration and red blood cell shrinkage. Exposure to brackish water decreased both the arterial O2 tension and whole body O2 uptake. The extracellular acid-base status changed from an initial respiratory acidosis at 1 h towards a pronounced metabolic acidosis at 48 h of brackish water exposure. Red cell pHi decreased in parallel with extracellular pHe, but the in vivo ΔpHi/ΔpHe was only 0.26, suggesting some selective protection of red cell pHi. Plasma cortisol concentration and gill Na+, K+-ATPase activity increased after exposure to high ambient salinity, reflecting the induction of hypo-osmoregulatory mechanisms. The physiological changes in whitefish are discussed in relation to salinity-induced effects in other salmonid fishes.