Search PubMed⌕ Search

Biomedical subjects

A O Brubakk

Publications and source records attributed to A O Brubakk.

At least 19 recordsLinked to original sources

Effect of a short-acting NO donor on bubble formation from a saturation dive in pigs.

It has previously been reported that a nitric oxide (NO) donor reduces bubble formation from an air dive and that blocking NO production increases bubble formation. The present study was initiated to see whether a short-acting NO donor (glycerol trinitrate, 5 mg/ml; Nycomed Pharma) given immediately before start of decompression would affect the amount of vascular bubbles during and after decompression from a saturation dive in pigs. A total of 14 pigs (Sus scrofa domestica of the strain Norsk landsvin) were randomly divided into an experimental (n = 7) and a control group (n = 7). The pigs were anesthetized with ketamine and alpha-chloralose and compressed in a hyperbaric chamber to 500 kPa (40 m of seawater) in 2 min, and they had 3-h bottom time while breathing nitrox (35 kPa O(2)). The pigs were all decompressed to the surface (100 kPa) at a rate of 200 kPa/h. During decompression, the inspired Po(2) of the breathing gas was kept at 100 kPa. Thirty minutes before decompression, the experimental group received a short-acting NO donor intravenously, while the control group were given equal amounts of saline. The average number of bubbles seen during the observation period decreased from 0.2 to 0.02 bubbles/cm(2) (P < 0.0001) in the experimental group compared with the controls. The present study gives further support to the role of NO in preventing vascular bubble formation after decompression.

Animals↗

A single air dive reduces arterial endothelial function in man.

During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 +/- 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min(-1) with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 +/- 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 +/- 0.7 to 4.8 +/- 0.8 mm (mean +/- s.d.) and a significant reduction of FMD from 9.2 +/- 6.9 to 5.0 +/- 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 +/- 0.3 mm to 4.7 +/- 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 +/- 0.4 mm and 7.7 +/- 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.

Adult↗

Diving-induced venous gas emboli do not increase pulmonary artery pressure.

Venous gas emboli are frequently observed in divers even if proper decompression procedures are followed. This study was initiated to determine if pulmonary artery pressure increases in asymptomatic divers, which could increase the risk of arterial embolization due to passage of venous gas emboli from the right to the left side of the heart. Recordings of venous gas emboli and estimation of pulmonary artery pressure by non-invasive transthoracic echocardiography were applied in 10 recreational scuba diving volunteers before and 20, 40, 60, and 80 min after simulated dives to 18 m (80 min bottom time) in a hyperbaric chamber. The ratio between pulmonary artery acceleration time and right ventricular ejection time was used as an estimate of pulmonary artery pressure. None of investigated divers had signs of decompression sickness. Despite the post-dive presence of the venous gas emboli, measured in the region of the pulmonary valve annulus (mean=1.71 bubbles.cm-2, 40 min after dive), the ratio between pulmonary artery acceleration time and right ventricular ejection time did not decrease, but actually increased (from 0.43+/-0.06 to 0.49+/-0.06, 40 min after dive; p<0.05), suggesting a decrease in pulmonary artery pressure after the dive. We conclude that diving-induced venous gas bubbles do not cause significant changes in the central circulation which could increase the risk of arterial embolization.

Adult↗

A randomized, double blind study of the prophylactic effect of hyperbaric oxygen therapy on migraine.

In a double blind, placebo-controlled study to assess the prophylactic effect of hyperbaric oxygen therapy on migraine, 40 patients were randomly assigned to a treatment group receiving three sessions of hyperbaric oxygen, or a control group receiving three hyperbaric air treatments. The patients were instructed to keep a standardized migraine diary for eight weeks before and after the treatment. Thirty-four patients completed the study. Our primary measure of efficacy was the difference between pre- and post-treatment hours of headache per week. The results show a nonsignificant reduction in hours of headache for the hyperbaric oxygen group compared to the control group. Levels of endothelin-1 in venous blood before and after treatment did not reveal any difference between the hyperbaric oxygen and control groups. We conclude that the tested protocol does not show a significant prophylactic effect on migraine and does not influence the level of endothelin-1 in venous blood.

Adult↗

Decompression profile and bubble formation after dives with surface decompression: experimental support for a dual phase model of decompression.

The present study was initiated in order to determine the effect of decompression profiles on bubble formation following surface decompression using oxygen. Following an air dive to 496 kPa (130 fsw) for 90 minutes, three different profiles were tested in the pig; a USN staged decompression profile, a profile using linear continuous decompression with the same total decompression time as the USN profile (ABI) and a linear profile with half the total decompression time compared to the the first two (ABII). The subsequent surface decompression at 220 kPa lasted 68 minutes for all three schedules. The study demonstrated that, following final decompression, the two linear profiles produced the lowest amount of vascular gas, with the fastest profile producing significantly less bubbles in the Pulmonary artery than the other two. Similar results were obtained in the jugular vein. The results are in qualitative agreement with model simulation using the Reduced Gradient Bubble Model (RGBM), demonstrating that the controlling tissues are reduced from those with a half time of 40 minutes using the USN procedure to 5 minutes using the fastest linear profile.

Animals↗

Evaluation of cerebral gas retention and oedema formation in decompressed rats by using a simple gravimetric method.

OBJECTIVE: The objective of the study is twofold: first, to develop a specific gravity method for distinguishing between bubbles and oedema following decompression, and, second, to evaluate the extent to which the change in specific gravity is due to retained gas in cerebral tissue. METHODS: A brombenzene/kerosene gradient column was used to measure changes in brain specific gravity at 100 and 300 kPa, respectively. This study was performed on 23 rats. Non-exposed rats constituted the control group A (n=6). The exposed animals were divided into two groups according to the number of bubbles they developed upon decompression; group B (bubble grade 0-2, n=9) and group C (bubble grade 3-5, n=8). RESULTS: Cerebral gas retention was determined by increasing the pressure on the gradient column from 100 to 300kPa. Median specific gravity of the brain at 300kPa bar was significantly higher compared to 100 kPa for the decompressed groups B (p= 0.018) and C (p=0.012), thus implying gas retention. The cerebral gas volume was significantly higher for rats with a high bubble score compared to rats with a low bubble score (p=0.043). However, the major contribution to the change in specific gravity was due to oedema formation. CONCLUSION: The brombenzene/kerosene gradient column was found to be a sensitive method for distinguishing between gas retention and oedema formation in decompressed animals. There was a higher gas retention in rats with a high bubble score compared to rats with a low bubble score. The major contribution to the change in specific gravity in decompressed animals is due to oedema formation.

Animals↗

The effect of air bubbles on rabbit blood brain barrier.

Several investigators have claimed that the blood brain barrier (BBB) may be broken by circulating bubbles, resulting in brain tissue edema. The aim of this study was to examine the effect of air bubbles on the permeability of BBB. Three groups of 6 rabbits were infused an isoosmotic solution of NaCl w/macrodex and 1% Tween. The solution was saturated with air bubbles and infused at rates of 50-100 ml hr(-1), a total of 1.6, 3.3, or 6.6 ml in each group, respectively. Two groups, each consisting of 6 rabbits, served as controls; one was infused by a degassed isoosmotic NaCl solution and one was sham-operated. All animals were left for 30 min before they were sacrificed. Specific gravity of brain tissue samples was determined using a brombenzene/kerosene gradient column, where a decrease in specific gravity indicates local brain edema. Specific gravity was significantly lower for left (P = 0.037) and right (P = 0.012) hemisphere white matter and left (P = 0.0015) and right (P = 0.002) hemisphere gray matter for the bubble-infused animals compared to the sham-operated ones. Infusion of degassed NaCl solution alone affected white left (P= 0.011) and right (P= 0.013), but not gray matter of both hemispheres. We speculate that insufficient degassing of the fluid may cause the effect of NaCl solution on the BBB of the white matter, indicating that the vessels of the white matter are more sensitive to gas bubbles than gray matter. Increasing the number of infused bubbles had no further impact on the development of cerebral edema, indicating that a threshold value was reached already at the lowest concentration of bubbles.

Air↗

Microdialysis in cisterna magna during cerebral air embolism in swine.

Arterial gas embolism may occur as a consequence of lung rupture, decompression sickness, following operative procedures or as accidental infusion of gas during various diagnostic procedures. It can lead to severe morbidity or even death. Microdialysis is a technique that has been extensively used for evaluating localized changes in the brain. The microdialysis probe is only capable of measuring changes in the immediate adjacent tissue. In arterial gas embolism the changes are multifocal. Thus a probe located in the cerebral cortex will not detect the total amount of damage. We used microdialysis in the cisterna magna of 9 anaesthetized pigs to study the diffuse injury following arterial gas embolism. After injection of 5.0 mL of air in the internal carotid artery, we found a significantly increased lactate-pyruvate ratio in the cerebrospinal fluid, lasting for 2 hours. This indicates anaerobic metabolism. Mean levels of glycerol were significantly increased, indicating membrane disruption. Glutamate levels were also elevated, although not significantly. The injection of air affected carotid flow. Flow in the carotid artery of the side of injection decreased significantly, but returned to baseline in 1 hour. Flow in the contralateral carotid was increased, but not significantly. We conclude that massive air embolism causes ischemia and reduced blood flow in the brain that can be detected in the cisterna magna.

Animals↗

Aerobic endurance training reduces bubble formation and increases survival in rats exposed to hyperbaric pressure.

1. The formation of bubbles is the basis for injury to divers after decompression, a condition known as decompression illness. In the present study we investigated the effect of endurance training in the rat on decompression-induced bubble formation. 2. A total of 52 adult female Sprague-Dawley rats (300-370 g) were randomly assigned to one of two experimental groups: training or sedentary control. Trained rats exercised on a treadmill for 1.5 h per day for 1 day, or for 2 or 6 weeks (5 days per week) at exercise intervals that alternated between 8 min at 85-90% of maximal oxygen uptake (VO2,max) and 2 min at 50-60% of VO2,max. Rats were compressed (simulated dive) in a decompression chamber in pairs, one sedentary and one trained, at a rate of 200 kPa x min(-1) to a pressure of 700 kPa, and maintained for 45 min breathing air. At the end of the exposure period, rats were decompressed linearly to the 'surface' (100 kPa) at a rate of 50 kPa x min(-1). Immediately after reaching the 'surface' (100 kPa) the animals were anaesthetized and the right ventricle was insonated using Doppler ultrasound. 3. Intensity-controlled interval training significantly increased VO2,max by 12 and 60% after 2 and 6 weeks, respectively. At 6 weeks, left and right ventricular weights were 14 and 17 % higher, respectively, in trained compared to control rats. No effect of training was observed on skeletal muscle weight. Bubble formation was significantly reduced in trained rats after both 2 and 6 weeks. However, the same effect was seen after a single bout of aerobic exercise lasting 1.5 h on the day prior to decompression. All of the rats that exercised for 1.5 h and 2 weeks, and most of those that trained for 6 weeks, survived the protocol, whereas most sedentary rats died within 60 min post-decompression. 4. This study shows that aerobic exercise protects rats from severe decompression and death. This may be a result of less bubbling in the trained animals. The data showed that the increase in aerobic capacity per se was not the main mechanism, but rather an acute effect that was most notable 20 h after a single, or the last, exercise bout, with less effect after 48 h.

Animals↗

[Iatrogenic gas embolism].

BACKGROUND: Gas embolism may occur as a consequence of lung injury, decompression sickness, surgery or as accidental infusion of gas during various diagnostic procedures. Iatrogenic gas embolism is often not recognised, but can lead to severe morbidity or even death. MATERIAL AND METHODS: We present a case of iatrogenic paradoxical air embolism caused by a defect in a central venous catheter. A review of the literature is given. RESULTS: The patient recovered gradually, but suffered significant neurological deficits. INTERPRETATION: Gas embolism must be considered as a differential diagnosis when a patient presents with unexplained neurological symptoms. Prompt treatment using oxygen at increased pressures (hyperbaric oxygen treatment) may be lifesaving and prevent serious sequelae.

Adult↗

Arterial air embolism after venous air infusion in newborn piglets.

UNLABELLED: In the newborn period, decreased right atrial pressure results in functional closure of the foramen ovale (FO). The objective of this study was to investigate whether air bubbles infused in the vena cava will pass through the FO into the arterial circulation in a newborn animal. Since air tends to rise to the highest point in a fluid, the study also investigated whether the animal's position could influence arterialization of air. Twelve 1-3-d-old piglets were anaesthetized and mechanically ventilated, and had catheters placed in the vena cava for infusion of air, in the aorta for blood gas and blood pressure measurements, and in the pulmonary artery for pressure measurements. After stabilization, 0.05 ml kg(-1) per minute of air was infused for 25 min followed by a 3 h observation period. Six piglets were placed in the left, and six in the right lateral recumbent position. Air bubbles in the left atrium or ventricle was monitored by echocardiography. Ultrasound Doppler probes were placed on both carotid arteries for detection of air embolism. Gas bubbles were detected in the left ventricle within 45 s of air infusion in 11 of 12 piglets. Eight piglets had air bubbles in the carotid arteries. Mean pulmonary arterial pressure (PAP) increased significantly after 1 min of air infusion, whereas mean systemic arterial pressure remained unchanged. When arterial air embolism occurred, PAP had not increased significantly. The time to reach maximum PAP with the animals in the left recumbent position was significantly shorter than in the right. CONCLUSION: This study shows that venous gas bubbles enter the arterial circulation through the FO in newborn piglets and that body position may influence the haemodynamic effect of these bubbles.

Air↗

Comparison of three different ultrasonic methods for quantification of intravascular gas bubbles.

For evaluating different decompression schedules, the use of ultrasound is common. Systems based on the Doppler principle have mostly been used. However, ultrasonic scanners producing images where the bubbles are easily detected, may be an alternative, because analysis of the signals is simpler than when using Doppler methods. In this study, three methods of bubble detection were used following a series of air dives. The divers were investigated using a "blind" Doppler system where only auditory signals were used for positioning the probe. They were also studied using ultrasonic images and finally an "image-assisted" Doppler method was used, where the sample volume of the Doppler system was positioned using the images. Both Doppler systems were pulsed Doppler systems. The agreement between the methods was determined using weighted kappa statistics. The results show that, at rest, the agreement between the images and the blind Doppler method was very good, and between the two Doppler methods and the images and the image-assisted method the agreement was good. Generally, the agreement is better at higher bubble grades. After movement, the agreement was not good. We conclude that grades from the different methods can be directly compared at rest.

Decompression Sickness↗

Lack of effect of anti-C5a monoclonal antibody on endothelial injury by gas bubbles in the rabbit after decompression.

Previous studies have shown that gas bubbles activate the complement system in vitro, generating C5a. The effect of anti-C5a monoclonal antibody 4B1C11 in preventing endothelial damage caused by decompression in the pulmonary artery of the rabbit was examined. The endothelial response was measured using tension measurements in the blood vessel wall. The mean bubble count for all rabbits (n = 24) was 4.2+/-3.1 bubbles x cm(-2), and ranged from 0 to 15 bubbles x cm(-2). Animals with many bubbles showed significantly more vascular damage than those with fewer bubbles. Anti-C5a monoclonal antibody could not prevent endothelial damage than that occurred after exposure to this level of gas bubbles. The maximum number of gas bubbles present is important for the endothelial damage. We speculate that the endothelial damage observed was mainly mechanical. A possible beneficial effect of anti-C5a antibody can thus be masked at a high degree of bubble generation. This study, together with a previous paper, demonstrates that gas bubbles cause endothelial damage from decompression both in the pig and in the rabbit.

Acetylcholine↗

Man in extreme environments.

Humans have demonstrated the ability to live and work in many adverse environments. Many examples demonstrate that our understanding of humans ability to adapt to extreme environments is limited, but it is reasonable to assume that the main problems in space exploration will be psychological and social. It is argued that polar expeditions of an earlier age are a better model for space exploration than confinement studies or Antarctic overwintering. Some aspects of the reason for the success of these expeditions are discussed and the lessons that can be used are pointed out.

Adaptation, Physiological↗

Endothelial damage by bubbles in the pulmonary artery of the pig.

A method for measuring endothelial damage caused by decompression was developed for vessels with a large radius. Segments of the pulmonary artery from pigs (8-12 wk old) were tested for endothelium damage using a system for recording changes in the tension in the vessel wall. Substance P (SP) was used as an endothelial-dependent dilation agonist. A significant decrease was found in the total response (Tmax) for SP as a result of endothelium damage, and the reduction in response was related to the number of bubbles. Furthermore, the sensitivity of the vessels to the agonist was significantly reduced after exposure to bubbles. Staining the endothelium with silver nitrate and light microscopy confirmed mechanical endothelium damage.

Animals↗

Effect of anti-C5a antibody on blood-lung and blood-brain barrier in rabbits after decompression.

The complement activation product C5a may be an important mediator of tissue injury after decompression stress. This study investigated whether the administration of anti-C5a antibody may reduce changes after decompression in the lung and in the brain. Two groups of rabbits were used; one receiving anti-C5a monoclonal antibody (n = 7) and the other receiving a sham antibody as control (n = 7) before pressure exposure. Five rabbits (4 in the anti-C5a group and 1 in the control group) died during the 2-h observation period postdive due to massive bubbling. Polymorphonuclear leukocyte (PMN) infiltration of lung tissue and pulmonary edema was observed, but this accumulation was unaffected by anti-C5a pretreatment. However, a significant positive correlation was observed between PMN accumulation and survival time postdive. Brain-specific gravity was lower for the group treated with anti-C5a antibody compared to the control group. Further, it was lower for those rabbits that died early compared to the ones that survived the 2-h period. This study was unable to prove a protective effect on the blood-brain and blood-lung barrier by injecting anti-C5a antibody. A possible beneficial effect of anti-C5a antibody may be masked by the mechanical damage caused by the gas bubbles.

Animals↗

Effect of oxygen tension and rate of pressure reduction during decompression on central gas bubbles.

Reduction in ascent speed and an increase in the O2 tension in the inspired air have been used to reduce the risk for decompression sickness. It has previously been reported that decompression speed and O2 partial pressure are linearly related for human decompressions from saturation hyperbaric exposures. The constant of proportionality K (K = rate/partial pressure of inspired O2) indicates the incidence of decompression sickness. The present study investigated the relationship among decompression rate, partial pressure of inspired O2, and the number of central gas bubbles after a 3-h dive to 500 kPa while breathing nitrox with an O2 content of 35 kPa. We used transesophageal ultrasonic scanning to determine the number of bubbles in the pulmonary artery of pigs. The results show that, for a given level of decompression stress, decompression rate and O2 tension in the inspired air can be traded off against each other by using pulmonary artery bubbles as an end point. The results also seem to confirm that decompressions that have a high K value are more stressful.

Animals↗