Repeated normoxic hyperbaric exposures induce haemodynamic and myocardial changes in rats

Stuhr, Linda Elin Birkhaug; Bergø, G. W.; S, Skei; Mæhle, Bjørn Ove; Tyssebotn, I

doi:10.1007/bf00235098

Cited by 4 publications

(9 citation statements)

References 21 publications

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“…The blood¯ow to the CNS accounted for 4% of the c in both groups. The correlation between +dP/dt and LVP, as well as between SBP and LVP, were in the same range as found previously (Stuhr et al 1993(Stuhr et al , 1994. The cardiac O 2 calculated using SV or +dP/dt (HuÈ tter et al 1985) was also similar to previously reported values (r 2 = 0.93±0.97).…”

Section: Control Condition In Airsupporting

confidence: 87%

“…The eect is independent of the previous hypercapnia. Thus, the increased contractile state induced by the HBO remains for a considerably longer time than the exposure itself, which agrees with ®ndings obtained after repeated exposure to normoxic (Stuhr et al 1993) and other hyperoxic pressures (Bergù and Tyssebotn 1992b), where the contractility was found to be elevated for more than 24 h.…”

Section: Kpa Ambient Pressuresupporting

confidence: 86%

“…Similar matching changes were observed in both groups, although the P a CO 2 increased only in the rats of group 2. The raised SBP cannot be associated with HBO alone, as suggested by Torbati (1987), since a similar rise has been found to occur in normoxic hyperbaric environments (Aanderud et al 1985;Hordnes and Tyssebotn 1985;Stuhr et al 1993;Bergù and Tyssebotn 1995c). On the other hand, f c was only reduced in the hyperoxic atmosphere and may be caused by a direct O 2 eect on the chemoreceptors.…”

Section: Kpa Ambient Pressurementioning

confidence: 65%

“…This indicates that changes in these parameters last longer than the hyperbaric exposure itself. This phenomenon is also observed after normoxic hyperbaric exposures (Stuhr et al 1993). The TPR returned to control levels while the resistance in the coronary arteries dropped, resulting in an increased myocardial blood¯ow.…”

Section: Kpa Ambient Pressurementioning

confidence: 83%

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Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

Bergø¹,

Tyssebotn²

1999

Eur J Appl Physiol

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It is commonly believed that during hyperbaric oxygen (HBO) treatment, in spite of the vasoconstriction induced by the increased O2 content in the breathing gas, the elevated carrying capacity of O2 in the arterial blood results in augmented O2 delivery to tissues. The experiments described here tested the hypothesis that HBO treatment would be more efficient in delivering O2 to poorly perfused tissues if the vasoconstriction induced by elevated O2 could be abolished or attenuated by adding CO2 to the breathing gas. Organ blood flow (QOBF), systemic hemodynamics, and arterial blood gases were measured before, during and after exposure to either 300 kPa O2 (group 1) or 300 kPa O2 with 2 kPa CO2 (group 2), in awake, instrumented rats. During the HBO exposure the respiratory frequency (fb) fell (4 breaths x min(-1) x 100 kPa O2(-1)), with no changes in arterial CO2 tension (PaCO2), but when CO2 was added, fb and PaCO2 increased. The left ventricular pressure (LVP) and the systolic arterial pressure (SBP) increased. The maximum velocity of LVP (+dP/dt) rose linearly with LVP whether CO2 was added or not (r2 = 0.72 and 0.75 respectively). Similarly, the cardiac output (Qc) and heart rate (fc) fell, while the stroke volume (SV) was unaltered, independent of PaCO2. There was a general vasoconstriction in most organs in both groups, with the exception of the central nervous system (CNS), eyes, and respiratory muscles. HBO reduced the blood flow to the CNS by 30%, but this vasoconstriction was diminished or eliminated when CO2 was added. In group 2, the blood flow to the CNS rose linearly with increased PaCO2 and decreased pH. After decompression fc and SBP stayed high, while Qc returned to control values by reducing the SV; CNS blood flow remained markedly elevated in group 2, while in group 1, it returned to control levels. We conclude that the changes in fc, Qc, LVP, dP/dt, SBP and most QOBF values induced by HBO were not changed by hypercapnia. Blood flow to the CNS decreased during HBO treatment at a constant PaCO2. Hypercapnia prevented this decline. Elevated PaCO2 augmented O2 delivery to the CNS and eyes, but increased the susceptibility to O2 poisoning. A prolonged suppression of O2 supply to the CNS occurred during the HBO exposure and in air following the decompression in the absence of CO2. This suppression was offset by the addition of CO2 to the breathing gas.

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Section: Control Condition In Airsupporting

confidence: 87%

Section: Kpa Ambient Pressuresupporting

confidence: 86%

Section: Kpa Ambient Pressurementioning

confidence: 65%

Section: Kpa Ambient Pressurementioning

confidence: 83%

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Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

Bergø¹,

Tyssebotn²

1999

Eur J Appl Physiol

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“…The development of myocardial hypertrophy is a fundamental mechanism by which the heart hypertrophy (LVH) in professional divers [2], and in rats after 40 repeated exposures to 5 bar normoxic He-N 2 [3]. The mechanism behind such a development is unclear.…”

Section: Introductionmentioning

confidence: 99%

Effects of SCH 42495, a neutral endopeptidase inhibitor, on cardiac function and mass in rats after repeated hyperbaric exposures

Stuhr

2000

Scandinavian Journal of Clinical and Laboratory Investigation

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The aim of the present study was to investigate the effects of inhibition of neutral endopeptidase on left ventricular hypertrophy (LVH), myocardial necrosis and haemodynamic changes, previously shown in rats after repeated hyperbaric exposures to 5 bar, by using the novel neutral endopeptidase inhibitor SCH 42495. Ten test rats underwent chamber dives daily for 40 consecutive days, and 10 control rats were exposed in the same chamber for an equivalent period of time, but in air at 1 bar. The rats received SCH 42495 orally (30 mg/kg twice a day) for 40 days. After 40 days, the body mass was identical in the two groups. Test rats and control rats had equal heart mass (both totally and left ventricular myocardium, including the ventricular septum/100 g), thus indicating that long-term treatment with SCH 42495 inhibits hyperbarically induced LVH. The left ventricular pressure (LVP) and the maximal velocity of LVP increase and decrease (+/- dP/dt) were similar in the test rats compared to the control rats at 1 bar. Previously, we found a higher LVP and dP/dt in non-treated test rats in otherwise identical experiments. This indicates that SCH 42495 "normalizes" the cardiac function of test rats after repeated hyperbaric exposures. The systolic arterial pressure, heart rate (HR) and respiratory frequency (RF) were similar in the two groups throughout the experiments. However, treatment with SCH 42495 lowered the blood pressure compared to previously non-treated rats. In conclusion, long-term administration of the neutral endopeptidase inhibitor SCH 42495 prevented previously shown changes in cardiac function as well as myocardial mass after 40 consecutive exposures to 5 bar.

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Diving and long-term cardiovascular health

Åsmul

Irgens

Grønning

et al. 2017

Occupational Medicine

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BackgroundShort-term cardiovascular effects from ambient pressure exposure are known. However, long-term cardiovascular effects from diving in humans have been less studied.AimsTo examine possible long-term cardiovascular health effects from occupational diving.MethodsWe compared the prevalence of cardiovascular disease in former divers to non-divers. We obtained data on male former divers with a certificate valid for professional diving after 1980, from the Norwegian Diver 2011 project, and matched data on the general male population from the HUNT3 Survey. We also compared former divers with high and low grades of diving exposure.ResultsData were available on 768 former divers. The prevalence of self-reported high blood pressure in former divers who often omitted a dive-free day after 3 days of strenuous diving was 28% compared with 18% in those who rarely violated these regulations [relative risk (RR) 1.47, confidence interval (CI) 1.01–2.15]. Also, the prevalence of myocardial infarction/angina pectoris was 11% in divers with >150 professional dives/year compared with 4% in divers with ≤50 professional dives/year [RR adj. 2.91 (CI 1.23–6.87)] and 16% in divers with >2000 air dives in total relative to 3% in divers with ≤2000 dives [RR adj. 3.05 (CI 1.47–6.34)].ConclusionsThe prevalence of some cardiovascular symptoms and diseases may be higher in male former divers than in the general population. Diving might have adverse long-term cardiovascular effects. Whether this is associated with diving per se or strenuous physical activity requires further studies.

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Repeated normoxic hyperbaric exposures induce haemodynamic and myocardial changes in rats

Cited by 4 publications

References 21 publications

Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

Effects of SCH 42495, a neutral endopeptidase inhibitor, on cardiac function and mass in rats after repeated hyperbaric exposures

Diving and long-term cardiovascular health

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