Effect of acute hypoxia on microcirculatory and tissue oxygen levels in rat cremaster muscle

2005 ◽  
Vol 98 (4) ◽  
pp. 1177-1184 ◽  
Author(s):  
Paul C. Johnson ◽  
Kim Vandegriff ◽  
Amy G. Tsai ◽  
Marcos Intaglietta
Keyword(s):  
Acute Hypoxia ◽  
Hypoxic Exposure ◽  
Cremaster Muscle ◽  
Tissue Oxygen ◽  
Oxygen Levels ◽  
Oxygen Fraction ◽  
Arterial Blood ◽  
S Period ◽  
Inspired Oxygen

Repeated exposure to brief periods of hypoxia leads to pathophysiological changes in experimental animals similar to those seen in sleep apnea. To determine the effects of such exposure on oxygen levels in vivo, we used an optical method to measure Po2 in microcirculatory vessels and tissue of the rat cremaster muscle during a 1-min step reduction of inspired oxygen fraction from 0.21 to 0.07. Under control conditions, Po2 was 98.1 ± 1.9 Torr in arterial blood, 52.2 ± 2.8 Torr in 29.0 ± 2.7-μm arterioles, 26.8 ± 1.7 Torr in the tissue interstitium near venous capillaries, and 35.1 ± 2.6 Torr in 29.7 ± 1.9-μm venules. The initial fall in Po2 during hypoxia was significantly greater in arterial blood, being 93% complete in the first 10 s, whereas it was 68% complete in arterioles, 47% at the tissue sites, and 38% in venules. In the 10- to 30-s period, the fall in normalized tissue and venular Po2 was significantly greater than in arterial Po2. At the end of hypoxic exposure, Po2 at all measurement sites had fallen very nearly in proportion to that in the inspired gas, but tissue oxygen levels did not reach critical Po2. Significant differences in oxyhemoglobin desaturation rate were also observed between arterial and microcirculatory vessels during hypoxia. In conclusion, the fall in microcirculatory and tissue oxygen levels in resting skeletal muscle is significantly slower than in arterial blood during a step reduction to an inspired oxygen fraction of 0.07, and tissue Po2 does not reach anaerobic levels.

In vivo Monitoring of Oxygen Levels in Human Brain Tumor Between Fractionated Radiotherapy Using Oxygen-enhanced MR Imaging

2020 ◽  
Vol 16 (4) ◽  
pp. 427-432
Author(s):  
Junchao Qian ◽  
Xiang Yu ◽  
Bingbing Li ◽  
Zhenle Fei ◽  
Xiang Huang ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Tumor Cells ◽  
Normal Tissue ◽  
Oxygen Level ◽  
Tissue Oxygen ◽  
Human Brain Tumor ◽  
Fractionated Radiotherapy ◽  
Oxygen Levels ◽  
Oxygen Breathing

Background:: It was known that the response of tumor cells to radiation is closely related to tissue oxygen level and fractionated radiotherapy allows reoxygenation of hypoxic tumor cells. Non-invasive mapping of tissue oxygen level may hold great importance in clinic. Objective: The aim of this study is to evaluate the role of oxygen-enhanced MR imaging in the detection of tissue oxygen levels between fractionated radiotherapy. Methods: A cohort of 10 patients with brain metastasis was recruited. Quantitative oxygen enhanced MR imaging was performed prior to, 30 minutes and 22 hours after first fractionated radiotherapy. Results: The ΔR1 (the difference of longitudinal relaxivity between 100% oxygen breathing and air breathing) increased in the ipsilateral tumor site and normal tissue by 242% and 152%, respectively, 30 minutes after first fractionated radiation compared to pre-radiation levels. Significant recovery of ΔR1 in the contralateral normal tissue (p < 0.05) was observed 22 hours compared to 30 minutes after radiation levels. Conclusion: R1-based oxygen-enhanced MR imaging may provide a sensitive endogenous marker for oxygen changes in the brain tissue between fractionated radiotherapy.

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis

2002 ◽  
Vol 92 (5) ◽  
pp. 2097-2104 ◽  
Author(s):  
Claudia Höhne ◽  
Willehad Boemke ◽  
Nora Schleyer ◽  
Roland C. Francis ◽  
Martin O. Krebs ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Respiratory Alkalosis ◽  
High Sodium ◽  
Low Sodium ◽  
Oxygen Fraction ◽  
Arterial Blood ◽  
Inspiratory Oxygen

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium · kg body wt−1 · day−1) or high-sodium (HS = 7.5 mmol sodium · kg body wt−1 · day−1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial Po 2 34.4 ± 2.1 Torr), plasma pH increased from 7.37 ± 0.01 to 7.48 ± 0.01 ( P < 0.05) because of hyperventilation (arterial Pco 2 25.6 ± 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

Chronic hypoxia increases fetoplacental vascular resistance and vasoconstrictor reactivity in the rat

2008 ◽  
Vol 294 (4) ◽  
pp. H1638-H1644 ◽  
Author(s):  
Vít Jakoubek ◽  
Jana Bíbová ◽  
Jan Herget ◽  
Václav Hampl
Keyword(s):  
Vascular Resistance ◽  
Intrauterine Growth Restriction ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Hypoxic Exposure ◽  
High Dose ◽  
Key Factors ◽  
Intrauterine Growth ◽  
The Relationship

An increase in fetoplacental vascular resistance caused by hypoxia is considered one of the key factors of placental hypoperfusion and fetal undernutrition leading to intrauterine growth restriction (IUGR), one of the serious problems in current neonatology. However, although acute hypoxia has been shown to cause fetoplacental vasoconstriction, the effects of more sustained hypoxic exposure are unknown. This study was designed to test the hypothesis that chronic hypoxia elicits elevations in fetoplacental resistance, that this effect is not completely reversible by acute reoxygenation, and that it is accompanied by increased acute vasoconstrictor reactivity of the fetoplacental vasculature. We measured fetoplacental vascular resistance as well as acute vasoconstrictor reactivity in isolated perfused placentae from rats exposed to hypoxia (10% O2) during the last week of a 3-wk pregnancy. We found that chronic hypoxia shifted the relationship between perfusion pressure and flow rate toward higher pressure values (by ∼20%). This increased vascular resistance was refractory to a high dose of sodium nitroprusside, implying the involvement of other factors than increased vascular tone. Chronic hypoxia also increased vasoconstrictor responses to angiotensin II (by ∼75%) and to acute hypoxic challenges (by >150%). We conclude that chronic prenatal hypoxia causes a sustained elevation of fetoplacental vascular resistance and vasoconstrictor reactivity that are likely to produce placental hypoperfusion and fetal undernutrition in vivo.

Diuretic response to acute hypoxia in the conscious dog

1982 ◽  
Vol 243 (5) ◽  
pp. F440-F446 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Respiratory Alkalosis ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Hypoxic Exposure ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Prostaglandin Release ◽  
Diuretic Response

Experiments were performed to determine the renal effects of acute hypoxia in conscious normovolemic dogs. Dogs were made hypoxic and also became hypocapnic through increased ventilation. Hypocapnic hypoxia was associated with increased urine flow, arterial blood pressure, cardiac output, PAH and inulin clearance, and electrolyte excretion. Urinary excretion of prostaglandin E2 (PGE2) also increased during hypocapnic hypoxia. To test whether the respiratory alkalosis accompanying hypoxic exposure was important in mediating the observed response, experiments were conducted in which the dogs were hypoxic but remained isocapnic via addition of CO2 to the inspired gas. Urine flow increased and was associated with changes in renal function and hemodynamics similar to those during hypocapnic hypoxia. Experiments were also conducted to determine whether the increased PGE2 release in hypoxia was functionally significant. Dogs were pretreated with meclofenamate and then made hypoxic. Prostaglandin synthesis inhibition did not alter the renal response to hypocapnic hypoxia. Dogs were also treated chronically with propranolol in an attempt to blunt the rise in blood pressure during hypoxia. In dogs with only a small transient increase in blood pressure, the diuresis was blocked. It is concluded that systemic hypoxia results in a mild diuresis in the conscious normovolemic dog. This response occurs independent of changes in arterial pH or renal prostaglandin release. The diuretic effect of hypoxia is probably due to increased renal perfusion pressure and resultant increased filtration.

Inspired Oxygen and Nitrous Oxide Concentrations in Volunteers during Nitrous Oxide Sedation with a Hudson Mask

1988 ◽  
Vol 16 (4) ◽  
pp. 423-426 ◽  
Author(s):  
B. J. Anderson ◽  
A. Dyson ◽  
A. M. Henderson
Keyword(s):  
Nitrous Oxide ◽  
Variable Amount ◽  
Oxygen Levels ◽  
Oxygen Fraction ◽  
Carbon Dioxide Concentrations ◽  
End Tidal Carbon Dioxide ◽  
Oxide Concentration ◽  
End Tidal ◽  
Nitrous Oxide Concentration ◽  
Inspired Oxygen

Ten volunteers were given varying ratios of oxygen and nitrous oxide at 4,6 and 8 litres per minute using a Hudson mask delivery system. Maximum and minimum inspired oxygen concentrations, maximum inspired nitrous oxide concentrations and end tidal carbon dioxide concentrations were measured using the Datex Cardiocap CCI-104 monitor. Although pharyngeal oxygen fraction varies with the Hudson mask because the inspiratory flow exceeds the entrainment of the mask by a variable amount during much of the cycle, at 8 litres/minute flow with a ratio of 3 to 5, oxygen to nitrous oxide, safe levels of oxygen were delivered (range of means 26–31%) with basal nitrous oxide levels (mean maximum inspired N 2 O, 34%). When nitrous oxide sedation is used clinically, nitrous oxide must be used with consideration of safe oxygen levels. This study did not detect unsafe pharyngeal oxygen levels in the ratios investigated, where the maximum delivered nitrous oxide concentration was 75%.

scholarly journals The Effect of Combined Hypoxemia and Cephalic Hypotension on Fetal Cerebral Blood Flow and Metabolism

1991 ◽  
Vol 11 (1) ◽  
pp. 99-105 ◽  
Author(s):  
A. Roger Hohimer ◽  
Conrad R. Chao ◽  
John M. Bissonnette
Keyword(s):  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Glucose Utilization ◽  
Fetal Sheep ◽  
Oxygen Fraction ◽  
Arterial Blood ◽  
Arterial Blood Oxygen ◽  
Cerebral Vasodilation ◽  
Inspired Oxygen ◽  
Cerebral Vascular Resistance

The effect of hypoxemia and cephalic hypotension, alone and in combination, on hemispherical CBF and metabolism was examined in seven chronically catheterized fetal sheep. Hypoxemia was induced by lowering the maternal inspired oxygen fraction and cephalic hypotension was generated by partial occlusion of the fetal brachiocephalic artery. CBF was measured with radionuclide-labeled microspheres. During control, the arterial blood oxygen content (Cao2) was 3.2 ± 1.0 (SD) m M and CBF averaged 131 ± 21 (SD) ml min−1 100 g−1. The cephalic perfusion pressure (PP, mean cephalic arterial - sagittal venous) was 40 ± 4 mm Hg and cerebral vascular resistance (CVR, PP/CBF) was 0.31 ± 0.06 mm Hg ml−1 min 100 g. During induced hypoxemia, Cao2 was 1.4 ± 0.7 m M and CBF was elevated to 223 ± 60 ml min−1 100 g−1. PP was not different from control and CVR was lower at 0.19 ± 0.04 mm Hg ml−1 min 100 g, reflecting cerebral vasodilation. With cephalic hypotension alone (PP = 21 ± 4 mm Hg; Cao2 = 3.4 ± 0.9 m M), CBF fell to 83 ± 23 ml min−1 100 g−1 and there was no significant change in CVR (0.26 ± 0.05 mm Hg ml−1 min 100 g). During combined hypoxemia and hypotension (Cao2 = 1.5 ± 0.8 m M and PP = 18 ± 4 mm Hg), CBF was significantly greater than during hypotension alone (100 ± 6 ml min−1 100 g). CVR was 0.19 ± 0.05 mm Hg ml−1 min 100 g, identical to that measured in normotensive hypoxemia and significantly less than found during hypotension alone. Cerebral oxygen consumption was lower during combined hypoxemia and cephalic hypotension than during hypoxemia alone. Cerebral glucose uptake was significantly higher than control in both the hypoxemic and combined hypoxemic-hypotensive conditions. The glucose:oxygen quotient (6 × molar glucose uptake/molar oxygen consumption) was not different from unity during control or hypotension but was 2.31 ± 1.16 and 3.63 ± 1.99 during the hypoxemic and hypoxemic-hypotensive conditions, respectively, suggesting an anaerobic glucose utilization. No significant lactate efflux could be measured in any of these conditions.

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

2013 ◽  
Vol 304 (8) ◽  
pp. L540-L548 ◽  
Author(s):  
Daniela Parrau ◽  
Germán Ebensperger ◽  
Emilio A. Herrera ◽  
Fernando Moraga ◽  
Raquel A. Riquelme ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Resistance ◽  
Vascular Reactivity ◽  
Chronic Hypoxia ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Arterial Blood ◽  
Low Altitude

We determined whether store-operated channels (SOC) are involved in neonatal pulmonary artery function under conditions of acute and chronic hypoxia, using newborn sheep gestated and born either at high altitude (HA, 3,600 m) or low altitude (LA, 520 m). Cardiopulmonary variables were recorded in vivo, with and without SOC blockade by 2-aminoethyldiphenylborinate (2-APB), during basal or acute hypoxic conditions. 2-APB did not have effects on basal mean pulmonary arterial pressure (mPAP), cardiac output, systemic arterial blood pressure, or systemic vascular resistance in both groups of neonates. During acute hypoxia 2-APB reduced mPAP and pulmonary vascular resistance in LA and HA, but this reduction was greater in HA. In addition, isolated pulmonary arteries mounted in a wire myograph were assessed for vascular reactivity. HA arteries showed a greater relaxation and sensitivity to SOC blockers than LA arteries. The pulmonary expression of two SOC-forming subunits, TRPC4 and STIM1, was upregulated in HA. Taken together, our results show that SOC contribute to hypoxic pulmonary vasoconstriction in newborn sheep and that SOC are upregulated by chronic hypoxia. Therefore, SOC may contribute to the development of neonatal pulmonary hypertension. We propose SOC channels could be potential targets to treat neonatal pulmonary hypertension.

4-Chloro-m-cresol is a Trigger of Malignant Hyperthermia in Susceptible Swine

1999 ◽  
Vol 90 (6) ◽  
pp. 1733-1740. ◽  
Author(s):  
Frank Wappler ◽  
Jens Scholz ◽  
Marko Fiege ◽  
Kerstin Kolodzie ◽  
Christiana Kudlik ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Malignant Hyperthermia ◽  
Carbon Dioxide Concentration ◽  
Central Venous ◽  
Mechanically Ventilated ◽  
Oxygen Fraction ◽  
Animal Care ◽  
Inspired Oxygen

Background 4-Chloro-m-cresol (4-CmC) induces marked contractures in skeletal muscle specimens from individuals susceptible to malignant hyperthermia (MHS). In contrast, 4-CmC induces only small contractures in specimens from normal (MHN) patients. 4-CmC is a preservative within a large number of commercially available drug-preparations (e.g., insulin, heparin, succinylcholine), and it has been suggested that 4-CmC might trigger malignant hyperthermia. This study was designed to investigate the effects of 4-CmC in vivo and in vitro in the same animals. Methods After approval of the animal care committee, six Pietrain MHS and six control (MHN) swine were anesthetized with azaperone 4 mg/kg intramuscularly and metomidate 10 mg/kg intraperitoneally. After endotracheal intubation, lungs were mechanically ventilated (inspired oxygen fraction 0.3) and anesthesia was maintained with etomidate 2.5 mg x kg(-1) x h(-1) and fentanyl 50 microg x kg(-1) x h(-1). Animals were surgically prepared with arterial and central venous catheters for measurement of hemodynamic parameters and to obtain blood samples. Before exposure to 4-CmC in vivo, muscle specimens were excised for in vitro contracture tests with 4-CmC in concentrations of 75 and 200 microM. Subsequently, pigs were exposed to cumulative administration of 3, 6, 12, 24, and 48 mg/kg 4-CmC intravenously. If an unequivocal episode of malignant hyperthermia occurred, as indicated by venous carbon dioxide concentration &gt; or = 70 mmHg, pH &lt; or = 7.25, and an increase of temperature &gt; or = 2 degrees C, the animals were treated with dantrolene, 3.5 mg/kg. Results All MHS swine developed malignant hyperthermia after administration of 4-CmC in doses of 12 or 24 mg/kg. Venous carbon dioxide concentration significantly increased and pH significantly decreased. Temperature increased in all MHS animals more than 2 degrees C. Blood lactate concentrations and creatine kinase levels were significantly elevated. All MHS swine were treated successfully with dantrolene. In contrast, no MHN swine developed signs of malignant hyperthermia. After receiving 4-CmC in a concentration of 48 mg/kg, however, all MHN animals died by ventricular fibrillation. The in vitro experiments showed that both concentrations of 4-CmC produced significantly greater contractures in MHS than in MHN specimens. Conclusions 4-CmC is in vivo a trigger of malignant hyperthermia in swine. However, the 4-CmC doses required for induction of malignant hyperthermia were between 12 and 24 mg/kg, which is about 150-fold higher than the 4-CmC concentrations within clinically used preparations.

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