Biomedical subjects

C E Lundgren

Publications and source records attributed to C E Lundgren.

At least 19 recordsLinked to original sources

PubMed1997

Cardiovascular changes during deep breath-hold dives in a pressure chamber.

Electrocardiogram, cardiac output, and blood lactate accumulation were recorded in three elite breath-hold divers diving to 40-55 m in a pressure chamber in thermoneutral (35 degrees C) or cool (25 degrees C) water. In two of the divers, invasive recordings of arterial blood pressure were also obtained during dives to 50 m in cool water. Bradycardia during the dives was more pronounced and developed more rapidly in the cool water, with heart rates dropping to 20-30 beats/min. Arrhythmias occurred, particularly during the dives in cool water, when they were often more frequent than sinus beats. Because of bradycardia, cardiac output decreased during the dives, especially in cool water (to <3 l/min in 2 of the divers). Arterial blood pressure increased dramatically, reaching values as high as 280/200 and 290/150 mmHg in the two divers, respectively. This hypertension was secondary to peripheral vasoconstriction, which also led to anaerobic metabolism, reflected in increased blood lactate concentration. The diving response of these divers resembles the one described for diving animals, although the presence of arrhythmias and large increases in blood pressure indicate a less perfect adaptation in humans.

Adult↗

PubMed1997

Diving decompression fails to activate complement.

The present study evaluated complement activation during decompression after air dives in a hyperbaric chamber. Intravascular bubbles were quantified by Doppler ultrasound scoring. Eighteen subjects completed 92 dives, of which 74 produced bubbles. Complement activation was assessed by plasma C3a des Arg and red-cell-bound C3d before and after each dive. These parameters of in vivo complement activation failed to show significant activation. In vitro complement activation susceptibility tests on pre-dive sera were performed to explore their association with in vivo complement activation and intravascular bubbles. Such tests failed to identify a distinct complement-sensitive group and did not correlate with in vivo complement activation during the dives and/or intravascular bubble appearance. Two subjects developed decompression sickness but were not different from the rest of the group regarding in vitro complement sensitivity or complement activation during dives.

Adult↗

PubMed1996

Maximal breath-holding time and immediate tissue CO2 storage capacity during head-out immersion in humans.

This study tested three possible mechanisms that could explain the prolonged breath-holds (BH) previously observed in humans during submersion in 35 degrees C (thermoneutral) water, including a reduced metabolism, a decreased CO2 sensitivity, and an increased CO2 storage capacity. During immersed BH (n = 13), maximal BH time was prolonged by 20.3% (P < 0.05), the rate of rise of end tidal partial pressure of carbon dioxide (PETCO2) was slower (P < 0.05) by 31% (compatible with increased CO2 storage capacity), but the breaking-point PETCO2 (CO2 sensitivity) and the rate of decrease of end tidal partial pressure of oxygen (metabolism) were unchanged. During air breathing (n = 5), immersion resulted in a significant decrease in tidal volume (11%), but did not affect O2 uptake, CO2 elimination (VCO2), or respiratory exchange ratio (R). During a 4-min CO2-rebreathing (n = 9), the slope of the hypercapnic ventilatory response curve (CO2 sensitivity index) was unchanged by immersion, but the significantly decreased VCO2, R, and rate of rise in PETCO2 during immersed rebreathing indicated an increase in the acute CO2 storage capacity (SC). The estimated SC (n = 9), based on an assumed cellular respiratory quotient of 0.8, were 0.52 (SEM 0.03) ml.kg-1.mmHg-1 for control and 0.66 (SEM 0.04) ml.kg-1.mmHg-1 for immersion. A proposed mechanism for the increased SC during immersed BH and during immersed rebreathing is that immersion accelerated CO2 redistribution in the body by increasing perfusion to some low-perfused, low-metabolism, and high-capacity tissues, such as resting skeletal muscle. The increased SC during immersion, however, did not correlate with the prolonged BH duration (n = 9, P > 0.05). The mechanism of the latter remains unclear.

Adult↗

PubMed1995

Dead space in the breathing apparatus; interaction with ventilation.

Dead space in breathing apparatus may cause increased ventilation and/or CO2 retention. Interactions between ventilation and dead space were tested in the breathing apparatus of three divers: a full face mask with an oro-nasal cup (AGA), a full face mask without an oro-nasal cup (EXO-26) but designed to minimize dead space, and one mouthpiece. Experiments were performed at three depths; 0, 30 and 45 m seawater (msw). The breathing gas was air except at 30 msw where it was 36 O2 in N2. Five certified SCUBA divers were exercised at three levels (0, 50 and 100 W). Ventilation and gas exchange were measured. The dead space in the AGA mask was not influenced by either depth or exercise (mean 0.201). The mean dead space of the EXO-26 was 0.341, but it increased with exercise (p < 0.001) and decreased with depth (p < 0.03). Since the dead space can vary with ventilation levels it is not sufficient to test breathing apparatus only at rest as is required by the US National Institute of Occupational Safety and Health. The mean ventilation with the EXO-26 was higher than with the AGA by 10% at 50 W (p < 0.05) and by 12% (p < 0.01) at 100 W. The same comparison for end-tidal CO2 showed mean increase by 0.30 kPa at the 100-W workload (P < 0.05); changes at other workloads were not statistically significant. Comparisons of the mean inspired PCO2 to the maximum values considered acceptable by various organizations showed that the mouthpiece was always acceptable, the AGA mask was marginally acceptable or better, while sometimes the EXO-26 was not acceptable.

Adult↗

PubMed1995

CO2 chemosensitivity during immersion in humans.

Hypercapnic ventilatory response was compared in 9 seated subjects during head-out immersion in 35 degrees C (thermoneutral) water and during non-immersion in 28 degrees C (thermoneutral) room air. Using Read's CO2-rebreathing technique, minute ventilation (VE) and end-tidal (ET) PCO2 were sampled continuously for 4-5 min with a spirometer and a mass spectrometer, while the subject rebreathed a 6 L gas mixture initially containing 7% CO2 and 93% O2 in a bag-in-box system. The slope of the hypercapnic ventilatory response curve, expressed as delta VE/delta PETCO2, ranged from 0.76 to 2.49 L/min/mmHg. Immersion affected neither the slope nor the position of the hypercapnic ventilatory response curve. The rate of rise of PETCO2 during immersed CO2-rebreathing was significantly reduced (4.47 +/- 0.19 [SE] mmHg/min), as compared to the control value (5.67 +/- 0.24). It was concluded that the CO2 chemosensitivity during immersion in humans did not change and that the capacity to store CO2 in tissue might have been increased.

Administration, Inhalation↗

PubMed1994

Ventilatory responses to hypercapnia and hypoxia in elite breath-hold divers.

It was recently hypothesized that elite breath-hold divers may display blunted ventilatory responses to hypoxia and/or hypercapnia (Ferretti et al., J. Appl. Physiol. 70: 794-802, 1991). To test this hypothesis, the following measurements were made on three elite breath-hold divers (members of the same family), and on 9 healthy untrained control subjects (C): (1) Steady-state pulmonary ventilation (VE) at rest in the supine posture while breathing room air or normoxic CO2-enriched mixtures. (2) Breath-by-breath VE changes (delta VE), with respect to baseline conditions, after 4 breaths of 100% O2, under the following conditions: normoxia (PIO2 = 146 Torr) at rest (NR); normoxic exercise (60 watt on a bicycle ergometer) (NE); hypoxia (PIO2 = 77 Torr) at rest (HR); hypoxic exercise (HE). The results were as follows: (1) In hypercapnic experiments VE (normalized per unit of body surface area) was significantly lower in the divers than in C (4.32 +/- 0.04 [mean +/- SD]L.min-1.m-2 vs. 5.31 +/- 0.62 at FICO2 = 1.5%; 5.21 +/- 0.17 vs. 7.72 +/- 1.39 at FICO2 = 3%; 8.86 +/- 0.76 vs. 13.14 +/- 2.27 at FICO2 = 5%), as well as than in subjects described by previous authors as being characterized by 'low CO2 sensitivity'. (2) The 100% O2-breathing maneuvers did not induce significant delta VE both in NR and in HR, whereas peak delta VE were -6.73 +/- 1.38 L.min-1 (divers) vs. -5.24 +/- 3.10 (C) in NE, and -17.39 +/- 4.92 (divers) vs. -17.52 +/- 6.32 (C) in HE (no significant differences). It is concluded that the divers, compared to C, had a blunted ventilatory response to hypercapnia, but not to hypoxia. The former may represent an adaptive or genetically inherited phenomenon.

Adaptation, Physiological↗

PubMed1993

Moderate hypercapnia: cardiovascular function and nitrogen elimination.

Elevated carbon dioxide concentrations frequently encountered in diving operations may have cardiovascular effects. If so, changes in nitrogen loading and elimination may be induced. To study this possibility, whole body nitrogen elimination rates were determined using a rebreathing apparatus and gas chromatographic measurement of N2 in expired gas in six subjects as they breathed mixtures of 3 and 5% CO2 with 21% O2 and a balance of Ar for 125 min. No significant differences were observed among mean N2 yields, which were 815 ml (95% confidence interval +/- 51 ml), 831 ml (+/- 38 ml), and 845 ml (+/- 57 ml) for 0, 3, and 5% CO2 mixtures, respectively. Simultaneous measurements of heart rate showed a significant increase while breathing 5% CO2 as compared to 3 and 0% CO2. The increases in heart rate were not accompanied by any significant change in cardiac output, mean arterial pressure, or tissue perfusion. We conclude that at these levels of hypercarbia, tissue perfusion is not influenced enough to cause any changes in whole-body N2 elimination.

Adult↗

PubMed1993

Alveolar gas exchange during simulated breath-hold diving to 20 m.

Alveolar gas exchange, as affected by changes in pulmonary blood flow, was studied in five subjects performing breath holds lasting 75 s at the surface and during compression to 20 m in a hyperbaric chamber. After reaching the maximal depth, VO2 started to increase, compared to control, reaching a maximum of 346 +/- 66 (SE) ml (STPD).min-1.m2 (body surface area) at 50 s, i.e., early in the ascent; it exceeded the 50-s surface breath-hold value by 214 +/- 9 ml.min-1.m2. During descent, CO2 was absorbed from the alveoli into the blood, initially at 140 +/- 24 ml.min-1.m2; during ascent CO2 was transferred back into the lungs. These changes reflected compression and expansion of lung air. The increase in VO2 during the dives, which are not steady states, may be explained by an increasing cardiac output at depth. An augmented cardiac output had earlier been observed under identical conditions and explained by a drop in transthoracic pressure, enhancing venous return. Upon surfacing, the PAO2 was about 20 mmHg lower than after surface breath holds, reflecting the effects of changes in cardiac output.

Adult↗

PubMed1993

Perfusion of the visual cortex during pressure breathing at different high-G stress profiles.

The effects of pressure breathing for G protection (PBG) on perfusion of the visual cortex were studied in a subject during various high-G stress profiles. Blood flow velocity was measured in the posterior cerebral artery using a transcranial Doppler (TCD) ultrasound instrument. The G profiles examined included gradual and rapid onset rates. Mean cerebral blood flow velocity (MCBFV) declined with increasing +Gz with G-suit protection alone. The MCBFV increased in direct proportion with increase in +Gz acceleration with PBG. The mediating mechanisms for the effects of PBG may include improved gaseous exchange, the diminished sympathicoadrenal discharges, and cardiopulmonary reflexes. A role for TCD in further research is indicated.

Adult↗

PubMed1992

Physiologically and subjectively acceptable breathing resistance in divers' breathing gear.

To determine acceptable levels of breathing resistance in divers' gear, 6 subjects were exposed to varying levels of breathing resistance under demanding and realistic conditions. The immersed air-breathing subjects exercised in the prone position at 60% of their maximum oxygen uptake for 25 min in a hyperbaric chamber at 1.45 and 6.8 atm abs (145 and 690 kPa, 4.5 and 57 msw, 15 and 190 fsw). The breathing resistance ranged from minimal to 8-12 cmH2O (0.8-1.2 kPa).liter-1.s at flow rates of 2-3 liter/s. The higher resistance levels interfered with the respiration in terms of end-tidal PCO2 and dyspnea scores. There were considerable individual differences, and changes in one parameter were typically not paralleled by changes in the other. None of maximal voluntary ventilation, forced expiratory volume, expiratory reserve volume, vital capacities, or oxygen uptake was influenced by resistance. We set the maximum allowable end-tidal PCO2 at 60 mmHg and maximum dyspnea score at 1.0 on a scale from 0 (none) to 3 (severe). Based on these criteria we concluded that the external work of breathing should not exceed 1.5-2.0 J/liter in the ventilation range 30 to 75 liter/min BTPS.

Adult↗

PubMed1991

Alveolar gas composition and exchange during deep breath-hold diving and dry breath holds in elite divers.

End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.

Adult↗

PubMed1991

In vitro activation of human complement by nitrogen bubbles.

Complement activation may be responsible for some of the symptoms of decompression sickness. In the present study, complement activation was studied by exposing human sera with or without red blood cells to nitrogen bubbles. Nitrogen bubbles activated human complement as measured by generation of the fluid-phase, complement-split product C5a des Arg. In addition, we found that complement activation continued after exposure to bubbles was stopped. This continued complement activation may explain the failure of recompression treatment in some patients. Complement activation induced by nitrogen bubbles in human sera was enhanced when red cells were present. Red cells may be able to provide a stable membrane surface on which complement activation by bubbles can occur more efficiently. Complement activation by nitrogen bubbles in serum also led to the binding of activated C3 to red cells. Quantitation of bystander red-cell-bound C3d may allow the assessment of complement activation occurring by nitrogen bubbles in individuals undergoing decompression.

Complement Activation↗

PubMed1990

CO2 retention with minimal symptoms but severe dysfunction during wet simulated dives to 6.8 atm abs.

During wet dives in a hyperbaric chamber to 6.8 atm abs (690 kPa), air breathing subjects were experimentally exposed to external breathing resistance. Two of them were, unbeknownst to themselves, severely incapacitated. In the first incident the subject had been exercising for 25 min (end-tidal PCO2 60-65 mmHg, 7.3-8.0 kPa) when the breathing resistance was rapidly increased from low to very high (requiring pressure swings of 80 cmH2O, 8 kPa, peak to peak). He functioned normally (end-tidal PCO2 72 mmHg, 9.6 kPa) for about 100 s but 20 s later he was confused and irrational. After being extracted from the water (end-tidal PCO2 above 90 mmHg, 12 kPa), he lost consciousness for about 60 s. In the second incident the subject was exercising and breathing against a high resistance (pressure swings of 50-55 cmH2O, 5.0-5.6 kPa). His end-tidal PCO2 was high (65-68 mmHg, 8.7-9.3 kPa) throughout the exercise period, and after 24 min he reported mild dyspnea. A few seconds later he became confused. In other experiments both subjects voluntarily terminated experiments when the breathing resistance became overwhelming. These 2 subjects generally had high end-tidal PCO2 levels, but 1 other subject with end-tidal PCO2 levels in the same range never experienced any problems. These incidents indicate that severe hypercapnia does not necessarily correlate with dyspnea and that severe disturbances in mental function due to hypercapnia can develop suddenly when high breathing resistance is encountered in diving.

Blood Gas Monitoring, Transcutaneous↗

PubMed1990

Absence of diuresis during a 7-day saturation dive at 2.5 ATA N2-O2.

Three male divers were studied for 2 days during each of the predive and postdive 1 ATA air control periods and for 7 days at 2.5 ATA (2.3 ATA N2 and 0.2 ATA O2). The chamber temperature was always maintained at a comfort level. Average urine flow remained at 1500 ml.day-1 during both predive and 2.5 ATA periods; urine osmolality also remained constant at around 700 mOSM/kg. On the other hand, daily excretion of Na increased significantly from 139 mEq during the predive period to 178 mEq at 2.5 ATA (P less than 0.05) but returned to the predive level during the postdive period. In contrast, daily K excretion decreased progressively with a significant decrease during the postdive period (P less than 0.05). Plasma osmolality, Na, and K remained unchanged, whereas a 6% reduction of total protein concentration at 2.5 ATA (P less than 0.05) was observed. A quantitatively similar decrease (8%) was observed for hematocrit during the 2.5 ATA period, which did not recover at postdive. These changes were accompanied by a significant increase in urinary excretion of antidiuretic hormone (P less than 0.05) and by decreases in both plasma renin and aldosterone (P less than 0.05) level and urinary excretion of aldosterone (P less than 0.05). Plasma atrial natriuretic factor remained unchanged throughout the entire dive period.

Adult↗

PubMed1988

Development of pulmonary vascular response to oxygen.

The ability of the pulmonary circulation of the fetal lamb to respond to a rise in oxygen tension was studied from 94 to 146 days of gestation. The unanesthetized ewe breathed room air at normal atmospheric pressure, followed by 100% oxygen at three atmospheres absolute pressure in a hyperbaric chamber. In eleven near-term lambs (132 to 146 days of gestation), fetal arterial oxygen tension (PaO2) increased from 25 +/- 1 to 55 +/- 6 Torr (mean +/- SE), which increased the proportion of right ventricular output distributed to the fetal lungs from 8 +/- 1 to 59 +/- 5%. In five very immature lambs (94 to 101 days of gestation), fetal PaO2 increased from 27 +/- 1 to 174 +/- 70 Torr, but the proportion of right ventricular output distributed to the lung did not change, 8 +/- 1 to 9 +/- 1%. In five of the near-term lambs, pulmonary blood flow was measured. It increased from 34 +/- 3 to 298 +/- 35 ml.kg fetal wt-1.min-1, an 8.8-fold increase. We conclude that the pulmonary circulation of the fetal lamb does not respond to an increase in oxygen tension before 101 days of gestation; however, near term an increase in oxygen tension alone can induce the entire increase in pulmonary blood flow that normally occurs after the onset of breathing at birth.

Animals↗

PubMed1988

Prostacyclin does not change during an oxygen induced increase in pulmonary blood flow in the fetal lamb.

The role of prostacyclin in mediating the increase in pulmonary blood flow caused by an increase in oxygen tension in the fetal lamb was investigated. Plasma concentrations of 6-keto-PGF1 alpha, the hydrolysis product of prostacyclin, were measured during an increase in pulmonary blood flow caused by a rise in oxygen tension in eight intrauterine fetal lambs. Fetal oxygen tension was increased by placing the pregnant ewes in a hyperbaric chamber and having them breathe 100% oxygen at three atmospheres absolute pressure. This increased fetal PaO2 from 27 +/- 3 to 60 +/- 6 torr (mean +/- S.E., p less than or equal to 0.0001) and increased the proportion of right ventricular output distributed to the fetal lungs from 6 +/- 2 to 45 +/- 7% (mean +/- S.E., p less than or equal to 0.001). However, the fetal plasma concentration of 6-keto-PGF1 alpha did not change, 186 +/- 26 to 208 +/- 40 pg/ml (mean +/- S.E.). Indomethacin decreased plasma concentrations of 6-keto-PGF1 alpha in each of three fetuses but did not decrease the proportion of right ventricular output distributed to their lungs. The increase in pulmonary blood flow caused by an increase in oxygen tension in the fetal lamb is not associated with an increase in plasma concentrations of 6-keto-PGF1 alpha. Prostacyclin does not appear to be involved in the increase in pulmonary blood flow caused by the increase in oxygen tension at birth.

Animals↗

PubMed1988

Breath-hold duration in man and the diving response induced by face immersion.

The objective of this study in 5 selected volunteer subjects was to see whether the circulatory diving response which is elicited by breath holding and by cold water on the face would affect the duration of maximal-effort breath holds. Compared to control measurements (breath holding during resting, breathing with 35 degrees C water on the face) breath holding with the face cooled by 20 degrees C water caused a 12% reduction of heart rate, 6% reduction of cardiac output, 33% reduction in [corrected] forearm blood flow, and 9% rise in mean arterial blood pressure, but there was no difference in breath-hold duration (control and experimental both 94 s). There were also no differences in time of appearance of the first involuntary respiratory efforts during breath holding, in alveolar gas exchange, or in breaking-point alveolar O2 and CO2 tensions. When the diving response was magnified by a brief bout of exercise so that there was a 19% [corrected] reduction in heart rate, 23% reduction in cardiac output, and 48% reduction in forearm blood flow, breath-hold duration was still unaffected by face cooling. Compared to intermittent immersions, continuous exposure of the face to cold water abolished the diving response, probably by a cold adaptation of facial thermal receptors. These results with cooling of the face only are consistent with our earlier finding that there was a negative correlation between the duration of a maximal-effort breath hold and the diving response during whole-body submersion in cold water.

Adult↗

PubMed1987

Simulated breath-hold diving to 20 meters: cardiac performance in humans.

Cardiac performance was assessed in six subjects breath-hold diving to 20 m in a hyperbaric chamber, while nonsubmersed or submersed in a thermoneutral environment. Cardiac index and systolic time intervals were obtained with impedance cardiography and intrathoracic pressure with an esophageal balloon. Breath holding at large lung volume (80% vital capacity) decreased cardiac index, probably by increasing intrathoracic pressure and thereby impeding venous return. During diving, cardiac index increased (compared with breath holding at the surface) by 35.1% in the nonsubmersed and by 29.5% in the submersed condition. This increase was attributed to a fall in intrathoracic pressure. Combination of the opposite effects of breath holding and diving to 20 m left cardiac performance unchanged during the dives (relative to the surface control). A larger intrathoracic blood redistribution probably explains a smaller reduction in intrathoracic pressure observed during submersed compared with nonsubmersed diving. Submersed breath-hold diving may entail a smaller risk of thoracic squeeze (lesser intrathoracic pressure drop) but a greater risk of overloading the central circulation (larger intrathoracic blood pooling) than simulated nonsubmersed diving.

Adult↗