Hypoxia caused

Bronchiolar smooth muscle is sensitive to changes in carbon dioxide levels. Excess carbon dioxide causes bronchodilation and reduced carbon dioxide causes bronchoconstriction. Pulmonary vascular smooth muscle is sensitive to changes in oxygen levels excess oxygen causes vasodilation and insufficient oxygen (hypoxia) causes vasoconstriction. The changes in bronchiolar and vascular smooth muscle tone alter the amount of ventilation and perfusion in a lung unit to return the V/Q ratio to one. 

Draw and label the axes. Plot a point at a normal Pao2 and CBF as shown. Draw a horizontal line extending to the right of this point. This demonstrates that for values > 8 kPa on the x axis, CBF remains constant. Below this point, hypoxia causes cerebral vasodilatation and CBF rises rapidly. At flow rates >100 ml.l00g 1.min 1, maximal blood flow will be attained and the curve will tail off. Remember that the vasodilatory effect of hypoxia will override any other reflexes to ensure maximal oxygenation of the brain tissue. 

Dehler M, Zessin E, Bartsch P, Mairbaurl H (2006) Hypoxia causes permeability oedema in the constant pressure perfused rat lung. Eur Respir J 27 600-606. 

Rodriguez-Jimenez FJ, Moreno-Manzano V, Lucas-Dominguez R et al (2008) Hypoxia causes downregulation of mismatch repair system and genomic instabUity in stem cells. Stem CeUs 26 2052-2062... 

Cyanide toxicity, overshoot hypotension, and myocardial ischaemia. Hypoxia caused by increased ventilation-perfusion mismatch due to pulmonary vasodilatation and inhibition of hypoxic pulmonary vasoconstriction. Rebound hypertension after discontinuation of SNP infusion. 

Arai, A., Vanderklish, P., Kessler, M., Lee, K., and Lynch, G., A brief period of hypoxia causes proteolysis of cytoskeletal proteins in hippocampal slices, Brain Res., 555,276, 1991. 

Under normal conditions, lactate is metabolized in the liver and the blood lactate level is between 1 and 2 mM. Lactate accumulation in body fluids can be due to increased production and/or decreased utilization. Blood lactate-to-pyruvate ratio below 25 suggests defects in a gluconeogenic enzyme (Chapter 15) or pyruvate dehydrogenase (discussed later). A common cause of lactic acidosis is tissue hypoxia caused by shock, cardiopulmonary arrest, and hypoperfusion. Inadequate blood flow leads to deprivation of oxygen and other nutrients to the tissue cells as well as to the removal of waste products. Oxygen deprivation leads to decreased ATP production and accumulation of NADH, which promotes conversion of pyruvate to lactate. 

The inhibition of cytochrome c oxidase, and resultant disturbance of electron transport, results in decreased mitochondrial O2 utilization and decreased ATP (Olsen and Klein, 1947). Anaerobic metabolism leads to an accumulation of lactic acid and lactate acidosis, and the combination of lactate acidosis and cytotoxic hypoxia causes severe metabolic disturbances, particularly in the central nervous system (CNS), resulting in disturbances of perception and consciousness. 

Seizure-induced muscular contractions and hypoxia cause lactic acid release that can produce a severe acidosis that may be accompanied by hypotension and shock. Muscle contractions can be so severe that rhabdomyolysis with secondary hyperkalemia and acute tubular necrosis may occur. The airway may be obstructed, and the patient may become cyanotic or hypoxic at any time. Additionally, an increase in salivation and tracheal and pulmonary secretions may result in aspiration pneumonia. Although transient pleocytosis (i.e., white blood cell counts up to 20,000/mm ) may develop, it should not be attributed to GCSE until infectious causes have been eliminated. 

Hydrogen ion concentration can also be measured in fetal blood to assess fetal distress during labour. Capillary blotxl samples can be obtained directly from the baby s scalp once the cervix is sufficiently dilated. Fetal hypoxia causes a lactic acidosis and elevated hydrogen ion concentration.. VleasLirement of fetal PO, can be obtained directly using a transcutaneous oxygen electrode. 

Previous Work. As shown by the results of many experimentors, cerebral blood flow rate (under normal blood pressure conditions) is primarily determined by the C02 tension in arterial blood (12,14, 21, 22, 45, 46). The pH value of the extracellular fluid in brain is regarded as an essential factor for regulating vascular diameter (47, 48, 49,50). Cerebral hypoxia causes the C02-dependent regulation of the cerebral blood flow to change or vanish (9, 21, 25, 40, 45, 46, 51, 52). 

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