Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the influence of variations in arterial oxygen tensions (PaO2), arterial carbon dioxide tensions (PaCO2), and arterial pH on long bone medullary pressures, seven anaesthetized dogs were investigated. Comparing the control medullary pressures, i.e. the mean medullary pressures obtained at the normal range of PaO2 (75--110 mmHg) with the mean medullary pressures corresponding to the range of PaO2 of less than 75 mmHg, statistically significant (P less than 0.05) decreases were seen in both epiphyseal, metaphyseal and diaphyseal medullary pressures, from 27.6 +/- 5.0 to 15.5 +/- 3.6 mmHg, from 23.5 +/- 2.9 to 13.9 +/- 2.3 mmHg and from 27.7 +/- 3.9 to 18.3 +/- 2.5 mmHg (all mean values +/- s.e. mean), respectively. Hyperoxia, hypocapnia, hypercapnia or metabolic acidosis had no effect on medullary pressures in any of the regions studied.
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PMID:Observations on long bone medullary pressures in relation to arterial PO2, PCO2 and pH in the anaesthetized dog. 4 59

In a group of 21 cats, the middle cerebral artery pressure (MCAP) was recorded by means of a catheter introduced into the artery at its origin, just distal to the occlusion. The effects of hypertension, hypercapnia, and hypocapnia were studied. In a group of five cats, both middle cerebral arteries (MCA) were catherized and the pressure was recorded simultaneously on both sides. In another group of five cats, O2 tension measurements were made with the aid of oxygen electrodes in the brain tissue, the occluded MCA, and the common carotid artery. Some of the results obtained in this study are compared with the results of a previous study where monkeys were used as experimental animals.
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PMID:Haemodynamic changes in the cerebral circulation of the cat during occlusion of the middle cerebral artery. 10 Oct 24

Intravenous injection of CT 1341 (a mixture of alphaxalone and alphadolone dissolved in cremophor el) induced a decrease in cerebral blood flow (CBF) measured by 133Xe clearance in cats with artificial respiration (the mean reduction in CBF was 2 ml/100 g/mn for 1,2 mg/kg or CT 1341. So, CBF was decreased by 22% when CT 1341 (7,2 mg/kg) was intravenously injected, (mean Pa CO2 equals 30 mm Hg). Changes in CBF following CT 1341 intravenous injection seems to be caused by cerebral vascular constriction evidenced by the direct observation of pial vessels. Following intravenous injection of CT 1341 (from 7, 2 mg/kg to 19,2 mg/kg), the cerebrovascular reactivity to hypercapnia or hypocapnia was not affected, but autoregulation of cerebral blood flow was transiently abolished. In animals with free respiration, CBF was increased in relation with the elevation in Pa CO2 caused by the depression of respiration.
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PMID:[Effects of combination alfaxalone and alfadolone, anesthetic derivatives of pregnanedione, on cerebral hemodynamics in cats]. 12 19

Cerebral blood flow (CBF) was determined in the rat under 70% nitrous oxide anesthesia and pentobarbital anesthesia. The application of the Fick principle technique of Kety et al. was modified utilizing 133Xe infused intravenously steadily for 30 seconds, at which time the animal was decapitated and the head frozen in liquid nitrogen. A prior femoral artery to femoral vein shunt was led through a polyethylene catheter of 0.13 ml volume. This catheter passed as a coil in a NaI crystal well-counter with the arterial 133Xe concentration curve recorded by a ratemeter-recorder system. The results of the hemispheric blood flow (HBF) were: under 70% nitrous oxide anesthesia in normocapnia (Paco2 38 mm Hg), 86 +/- 15 ml/100 gm per minute; with hypocapnia (Paco2 20 mm Hg), 40 +/- 5 ml/100 gm per minute; with hypercapnia (Paco2 63 mm Hg), 187 +/- 10 ml/100 gm per minute; and with pentobarbital anesthesia (Paco2 38 mm Hg), 41 +/- 8 ml/100 gm per minute.
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PMID:The measurement of cerebral blood flow in the rat. 12 60

The fluorescence of reduced nicotinamide adenine dinucleotide (NADH) from cerebral cortex was measured before, during, and after middle cerebral artery (MCA) occlusion and then at death of the animal. In normal cortex, NADH remained constant throughout a wide range of variations in blood pressure and Paco2. In ischemic cortex, NADH levels were higher in hypovolemic hypotensive animals than in normotensive normovolemic animals. Neither hypercapnia nor hypocapnia was effective in decreasing NADH in regions of ischemia, but the latter was associated with a degree of hypotension that interfered with interpretation of data. NADH returned to normal with restoration of flow, supporting the reversibility of this degree of ischemia. The high levels of NADH at death, compared to those during ischemia, are consistent with incomplete ischemia in this model of cerebral infarction.
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PMID:Reduced nicotinamide adenine dinucleotide fluorescence and cortical blood flow in ischemic and nonischemic squirrel monkey cortex. 2. effects of alterations in arterial carbon dioxide tension, blood pressure, and blood volume. 16 73

To study the relationship between proximal tubular reabsorption of bicarbonate, sodium, and chloride, the effects of changes in plasma PCO2 were examined in anesthetized dogs. Distal tubular reabsorption was inhibited by ethacrynic acid; plasma bicarbonate concentration was kept constant at 33.4 +/- 0.3 mM; glomerular filtration rate (GFR) was varied over a wide range to examine glomerulotubular balance (constant fractional reabsorption). Hypercapnia (PCO2, 112.0 +/- 2.5 mmHg) increased bicarbonate reabsorption by about 30%, and hypocapnia (PCO2, 19.8 +/- 0.6 mmHg) decreased reabsorption of bicarbonate by more than 50% and altered reabsorption of sodium, chloride, and bicarbonate in the molar ratios 2.7:1.6:1, respectively. During hypercapnia the range of glomerulotubular balance was extended to a GFR 125% of control. During hypocapnia glomerulotubular balance was present only at GFR below 50% of control; reabsorption of bicarbonate sodium, and chloride was constant at GFR exceeding 50% of control. During metabolic acidosis hypercapnia had no significant effect on reabsorption of bicarbonate, sodium, and chloride. These observations support the hypothesis that bicarbonate reabsorption is the main driving force for osmotic reabsorption of water and NaCl in the proximal tubules.
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PMID:Coupling of NaHCO3 and NaCl reabsorption in dog kidneys during changes in plasma PCO2. 42 65

Acute experiments on cats demonstrated a suppression of the cerebral vessels reaction to hypercapnia under condithacin, while the reaction to hypocapnia persisted. It is assumed that the effects of hypo- and hypercapnia on the cerebral vessels were realized by different mechanisms, i. e. reduction of prostaglandin concentration decreased the cerebral vessels sensitivity to hypercapnia and increased their sensitivity to hypocapnia.
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PMID:[Cerebral blood flow reactions to hypo- and hypercapnia during indomethacin inhibition of prostaglandin biosynthesis]. 42 75

Eight awake cats have been studied before and after carotid denervation during air and oxygen breathing, and during hypercapnia. Analysis of the variables that characterize the spirogram shows that carotid denervation consistently results in a decrease of the mean inspiratory flow (VT/TI), causing a decrease in tidal volume (VT) and ventilation with a relative alveolar hypercapnia. In carotid-denervated animals, inhalation of oxygen results in an increase in ventilation due to an augmentation of VT/TI and VT and a relative hypocapnia. TI does not significantly change in the different conditions whereas TE is significantly affected. TE seems therefore to be more closely related to the rate of rise of inspiratory activity than to inspiratory duration.
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PMID:Effects of carotid body denervation on respiratory pattern of awake cats. 46 36

Ventilation, laryngeal resistance and electromyograms of the diaphragm, posterior cricoarytenoid (PCA) and thyroarytenoid (TA) muscles were recorded in anesthetized, spontaneously breathing cats during 100% O2 administration and during steady state inhalation of hypercapnic and hypoxic gas mixtures. As shown previously, hyperoxic hypercapnia lowered expiratory laryngeal resistance (RlarE). Isocapnic hypoxia also lowered RlarE, and hypercapnia superimposed on hypoxia decreased it further. Hypocapnia raised RlarE. Changes in inspiratory laryngeal resistance (RlarI) were similar to those in RlarE, but smaller. When ventilation was stimulated to the same extent by hypoxia and by hypercapnia, RlarE was lower under hypoxic than hypercapnic conditions in most animals. The electromyograms showed that the respiratory oscillations in laryngeal resistance and the laryngeal responses to hypercapnia and hypoxia were determined chiefly by the activity of the PCA muscle, the abductor of the vocal cords. The TA-a representative adductor muscle-was silent under all conditions studied. The results, considered with previous work, indicate that the larynx plays a part in determining the breathing pattern under resting conditions and during respiratory stimulation by hypercapnia and hypoxia.
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PMID:Effects of hypercapnia and hypoxia on laryngeal resistance to airflow. 49 50

The responses to hypocapnia and to hypercapnia of both the systemic and the coronary circulations have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia. In the absence of significant variations of myocardial contractility, the reduction of cardiac output, because of hypocapnia, was determined by the increase of systemic vascular resistance, while the increase of cardiac output because of hypercapnia was determined by an increase of heart rate without change of stroke volume. The alterations of coronary blood flow (reduction following hypocapnia, augmentation following hypercapnia) were considerably larger than the changes of cardiac output and of myocardial oxygen consumption. Such disparity between oxygen supply and demand, together with the effect of pH and PCO2 on the oxyhaemoglobin dissociation curve led to a marked reduction of coronary sinus PO2 in response to hypocapnia and a marked increase of coronary sinus PO2 in response to hypercapnia. The data suggests that PCO2 (or respiratory alterations of pH) may have a direct effect on the regulation of coronary blood flow. The low coronary sinus PO2 observed at hypocapnia may suggest the risk of myocardial ischaemia.
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PMID:Effect of CO2 on the systemic and coronary circulations and on coronary sinus blood gas tensions. 49 91


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