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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acid-base values of 13 patients with stable carbon dioxide tensions under controlled ventilation have been used to define the response to chronic hypocapnia in man. These patients had a respiratory paralysis and no apparent complicating disorders. Over a range of carbon dioxide tensions from 24 to 40 millimetres of mercury, the arterial blood hydrogen ion concentration decreased linearly by 0.32 nanomole per litre per millimetre of mercury decrement in carbon dioxide tension. Of primary interest was the finding that the slope of the regression line in chronic hypocapnia is close to that already reported for chronic hypercapnia. The physiological response to chronic hypocapnia in man is defined by a band that is approximately 10 nanomoles per litre (0.09 pH unit) wide for hydrogen ion concentration and 6 millimoles per litre wide for bicarbonate concentration. These significance bands may be used to differentiate additional acid-base disorders in patients with chronic hypocapnia over a clinically useful range of carbon dioxide tensions.
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PMID:Acid-base response to chronic hypocapnia in man. 2 Jan 87

Cerebral vasodilation in response to hypotension is necessary to maintain adequate cerebral blood flow. This study in newborn pigs examines the hypothesis that endothelial injury in vivo inhibits cerebral vasodilation in response to hypotension in newborn pigs, thus suggesting that this response is endothelium dependent. Chloralose-anesthetized piglets with closed cranial windows were studied before and after injury caused by light/dye or before and after dye only sham control. Light/dye injury was produced by injecting sodium fluorescein i.v. and passing filtered light from a mercury arc lamp through the cranial window. Measurements of pial arteries and arterioles were made during normotensive and hypotensive periods. Hemorrhagic hypotension (to 50% of the mean arterial control value) caused pial arterial and arteriolar diameters to increase 49 +/- 8% and 66 +/- 8%, respectively. After the light/dye injury, dilation in response to hypotension was absent, whereas dilations in response to isoproterenol and constriction in response to hypertension (3.33 to 4.0 kPa increase in arterial pressure) and hypocapnia were retained. These findings are consistent with the hypothesis that hypotension-induced cerebral arteriolar vasodilation is dependent on endothelial signals influencing adjacent smooth muscle.
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PMID:Light/dye microvascular injury eliminates pial arteriolar dilation in hypotensive piglets. 770 Jul 23

The effect of experimental meningitis on regional cerebral blood flow (rCBF), cerebral metabolic rate for oxygen (CMRO2), and cerebrovascular responsiveness to CO2 was determined in pentobarbital-anesthetized rabbits. The animals were inoculated intracisternally with saline (control) or log-phase Haemophilus influenzae type b (Hib). Eighteen hours later rCBF was determined with radiolabeled microspheres at normocapnia, hypocapnia, and hypercapnia. Cerebrovascular responses to hypocapnia and hypercapnia were assessed by calculating the change in cerebrovascular resistance per millimeter mercury change in PaCO2. At all CO2 levels, meningitis (M) was associated with elevated CBF compared with control (C: 47.5 +/- 3.0, M: 60.9 +/- 4.5 ml.100 g-1.min-1 at normocapnia, P < 0.01). Regional differences were present. In forebrain, the hyperemia in meningitis was confined to the superficial cortical grey matter. When compared with control, meningitis was not associated with altered vasoreactivity during hypocapnia (C: -0.026 +/- 0.006, M: -0.026 +/- 0.008 mmHg.ml-1 x 100 g-1.min-1.mmHg PaCO2(-1)) or hypercapnia (C: -0.037 +/- 0.004, M: -0.026 +/- 0.008 mmHg.ml-1 x 100 g.min.mmHg PaCO2(-1)). CMRO2 in meningitis was not significantly different from control (C: 3.53 +/- 0.29, M: 3.51 +/- 0.22 ml O2.100 g-1.min-1). These findings indicate that cerebrovascular responsiveness to CO2 is preserved in experimental Hib meningitis. Furthermore, enhanced CBF together with unchanged CMRO2 indicates that "luxury" cerebral perfusion is present in this model of bacterial meningitis.
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PMID:Cerebrovascular responsiveness to CO2 in Haemophilus influenzae type b meningitis in rabbits. 820 76