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

Serial magnification angiography under hypocapnia and hypertension was performed in 200 cases of cerebral tumours and cerebrovascular lesions. The advantages over conventional angiography are evident; the extent of a tumour is easier to determine as well as in most cases the nature of the mass lesion.
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PMID:Serial magnification angiography under hypocapnia and hypertension. 20 8

Two groups of anesthetized, splenectomized, and paralyzed dogs were hyperventilated (Vt 40 ml/kg). Normocapnia was maintained in one group (mean Paco2 37.6 mm"h'g, mean p"h '7.41) and respiratory alkalosis (mean Paco2 8 mmHg, mean pH 7.75) in the other. Splanchnic hemodynamic responses were similar in both groups. Average hepatic venous pressure increased from 3.2 to 6.4 mmHg in the normocapnic group and from 3.8 to 7.7 mmHg in the hypocapnic group. Average portal venous pressure increased from 10.7 to 12.0 mmHg and 10.8 to 12.7 mmHg in the normocapnic and hypocapnic groups, respectively. Mesenteric vascular resistance increased in 93 per cent of dogs. A decrease in functional intestinal capillary surface area during hyperventilation was indicated by a significant reduction in mesenteric Vo2 (from 15 to 11 ml/min, average 30 per cent), and a concomitant reduction in mesenteric O2 extraction ratio. Changes in mesenteric Vo2 were reflected in calculated splanchinic Vo2. Hepatic O2 uptake was essentially unchanged by tidal hyperventilation with or without hypocapnia.
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PMID:Splanchnic hemodynamic response to passive hyperventilation. 23 21

Nitroglycerin was administered to a group of 11 patients with chronic obstructive pulmonary disease in a dose of 0.4 mg sublingually. Arterial blood gases and blood pressure and pulse were measured at 5-min intervals for 30 min after nitroglycerin. There was a slight decrease in arterial O2 tension for the duration of the study; the maximal change was from a mean pre-nitroglycerin value of 53.5 mm Hg to 50.3 mm Hg at 20 min. In addition, there was a slight reduction in arterial CO2 tension and bicarbonate for 25 min. It is postulated that decreased O2 transport (due to increased hypoxemia and probably decreased cardiac output) plus hypocapnia were a sufficient stimulus to raise blood lactate. It is recommended that in patients receiving nitroglycerin who have obstructive airway disease, attention be directed toward the effect on arterial blood gases.
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PMID:The effect of nitroglycerin in gas exchange on chronic obstructive pulmonary disease. 23 14

Records of all patients with a clinical diagnosis of septic shock were reviewed retrospectively; cases occurred from August 1968-July 1971 in a general teaching hospital with 667 beds. In the 3-year period, 80 patients (38 males and 42 females) presented with 82 episodes of septic shock; this represented 14% of total hospital admissions to Intensive Care. The age range was from 15-78 years, with a mean of 52+ or -16 years. The incidence of the syndrome increased with age, reaching a maximum in the 7th decade. 66 (0f 71) of the surgical/gynecological referrals followed operative procedures, of which 1/2 were undertaken electively. By the time of referal to the Intensive Care Unit, pyrexia, hyperventilation, cyanosis, vasoconstriction, pallor, and sweating were commonly present, although 16 patients presented with warm hypotension; moderate hypotension was present in 48 patients, and severe hypotension was present in 18. Dehydration, oliguria, and azotemia were frequently present on admission. Abnormalties in serum electrolytes were common. Blood gas analysis on admission revealed that marked hypoxemia was commonly present in association with hypocapnia and metabolic acidosis. Blood cultures were performed in 62 patients and positive results were obtained in 38 on at least 1 occasion. Of a total of 47 positive blood cultures, 33 were gram-negative organisms and 5 were gram-negative anaerobic bacilli. The former were sensitive to gentamisin and the latter were resistant to both the cephalosporins and ampicillin. Gram-positive organisms were sensitive to cloxacillin and cephalosporins. Initial mortality was 64%, which increased to 70% including late deaths after return to wards. Nonsurvivors were significantly older than survivors (P .005); they were more frequently dehydrated (P .005); and they were more subject to the development of tachycardia and cardiac arrhythmias. Nonsurvivors were also considerably more hypoxemic than survivors. There was a marked difference between nonsurvivors and survivors in mode of presentation and infection source; nonsurvivors were characterized by either mediastinitis as a consequence of leakage of an esophageal anasotmosis or fecal peritonitis.
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PMID:A three year retrospective analysis of septic shock in a general hospital. 23 90

Thirty-five asthmatic patients (average age 28 years) who attended a pulmonary function laboratory when their mean ratio of forced expiratory volume in one second: forced vital capacity was 81 per cent (within the normal range for their age group) had arterial hypoxaemia and hypocapnia. These were probably secondary to lung hyperinflation and pulmonary ventilation/perfusion imbalance. The pulmonary abnormalities of bronchial asthma are not always detected by simple spirometric tests and the results of such tests should be interpreted cautiously.
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PMID:Pulmonary function in asthmatic patients in remission. 23 66


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