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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured rat brain cortex PO2 (PtO2) with gold microelectrodes (tip diameter 5--10 micron) for up to 2 hours after 16 min of transient global brain ischemia with and without thiopental 90 mg/kg infused iv over 60 min beginning at 5 min postischemia. Seventeen rats were immobilized and mechanically ventilated on 1% halothane in oxygen with continuous monitoring of PtO2, ECG, end-expiratory CO2, rectal temperature, and arterial blood pressure. Global ischemia was induced by trimethaphan hypotension to an MAP of about 50 torr and a neck tourniquet inflated to 1500 torr. Postischemia, nine control rats (11 PtO2 measurements) were untreated and eight rats (8 PtO2 measurements) received thiopental 90 mg/kg. Preischemia, PtO2 values in both groups ranged from less than 5--70 torr with values of greatest frequency between 10 and 15 torr. Postischemia, PtO2 in control rats peaked at 45 +/- 8 (SEM) torr at 20 min. In thiopental treated rats, peak PtO2 was 24 +/- 6 torr at 10 min postischemia. Relative frequency histograms of PtO2 revealed that PtO2 in thiopental treated rats was lower (p less than 0.05) between 15 and 30 min postischemia. The magnitude of the decrease in PtO2 between 105 and 120 min postischemia appeared to correlate directly with the absolute preischemic value (i.e., the higher the preischemic PtO2, the greater the decrease in PtO2 postischemia). These results suggest that thiopental administered in large doses in early postischemia does not improve brain oxygenation secondary to a reduction in brain oxygen consumption. The relevance of the correlation between the magnitude of the fall in PtO2 postischemia and the magnitude of the preischemic value is discussed.
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PMID:Postischemic brain oxygenation with barbiturate therapy in rats. 3 43

The placental diffusing capacity for carbon monoxide was measured in unanaesthetized monkeys (M. Mulatta). Maternal and fetal blood was sampled from chronically placed catheters while the mother breathed 50 or 100 parts per million of CO. Diffusing was calculated from the amount of CO taken up by the fetus divided by the partial pressure difference across the placenta, it averaged 0.646 plus or minus 0.062 (SEM) ml x min(-1) x torr(-1) x kg(-1) of fetal weight. The significance of this index of respiratory gas exchange in the monkey placenta is discussed with respect to previous measurements in other species and with respect to fetal growth.
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PMID:Placental diffusing capacity and its relation to fetal growth. 26 82

Oxprenolol is a beta-adrenergic blocker with intrinsic sympathomimetic activity. Such drugs are not currently available in the United States, although they have the advantage of less negative inotropic effect than the available propranolol. In 18 patients with mild essential hypertension, oxprenolol (9 patients) or propranolol (9 patients) was added to thiazide in random double-blind fashion and continued for 7 wk during which supine heart rate, blood pressure, and noninvasively measured cardiac output (by CO2 rebreathing) were determined weekly. With thiazide dosage constant throughout, maximal dose titration to 386. +/- 52.1 (SEM) mg/day of oxprenolol and 360.0 +/- 45.4 mg/day of propranolol was achieved over the first 5 wk. Blood pressure fell with both (141.8 +/- 4.8/96.0 +/- 2.3 to 128.0 +/- 5.1/87.2 +/- 1 mm Hg on oxprenolol, p less than 0.01; 150.8 +/- 5.5/98.0 +/- 1.7 to 129.9 +/- 5.5/86.8 +/- 3.4 mm Hg on propranolol, p less than 0.01). Cardiac output fell from 6.85 +/- 0.63 to 5.77 +/- 0.45 1/min (p less than 0.01) on oxprenolol, and from 6.79 +/- 0.61 to 5.37 +/- 0.37 1/min (p less than 0.02) on propranolol. Oxpranolol. Oxprenolol reduced heart rate from 76.4 +/- 2.0 to 65.6 +/- 2.1 beats/min (p less than 0.001) and it fell from 82.0 +/- 3.8 to 65.3 +/- 3.7 beats/min (p less than 0.001) with propranolol; the fall in heart rate was less but not significantly so for oxprenolol (-14.2 +/- 1.8% and -19.8 +/- 2.8%, p less than 0.1). Thus oxprenolol is equivalent to propranolol in antihypertensive action; minor hemodynamic differences between the two drugs might reflect intrinsic sympathomimetic activity of oxprenolol. Oxprenolol should be considered as an alternative to propranolol.
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PMID:Hemodynamic effects of oxprenolol and propranolol in hypertension. 38 30

Six patients with chronic obstructive pulmonary disease (COPD) (forced expiratory volume in one second, 1.01 +/- 0.08 L [mean +/- SEM] ) were given either 1 mL of 100% alcohol per kilogram of body weight in an aqueous solution or a similar volume of water in a crossover design on consecutive days. All subjects became intoxicated and the peak alcohol concentration was 137 +/- 11 mg/dL, 40 minutes after ingestion. No significant difference was found in either PaO2 or PaCO2 between the alcohol and control period. A significant decrease in arterial pH occurred following alcohol (P less than .05), and represented a mild metabolic acidosis. Alcohol ingestion resulted in an increase in oxygen consumption (P less than .05) and carbon dioxide production (P less than .05) but no change in respiratory rate. It appears that small to moderate amounts of alcohol will not cause marked changes in oxygen tension or alveolar hypoventilation in patients with severe COPD who do not have marked hypercapnia. Nevertheless, other effects of alcohol on the cardiopulmonary system and the concomitant use of sedatives have to be considered before condoning the use of alcohol.
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PMID:Moderate alcohol dose and chronic obstructive pulmonary disease: not a cause of hypoventilation. 43 97

The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p less than 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 +/- 16 mueq/min (mean +/- SEM) to 310 +/- 49 mueq/min (p less than 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O/(CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV. UKV fell acutely from 91 +/- 13 to 45 +/- 5 mueq/min (p less than 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 +/- 15 to 143 +/- 18 microgram/min and fractional excretion of calcium increased from 0.55 +/- 0.13 to 1.24 +/- 0.21% (p less than 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 +/- 0.05 to 4.30 +/- 0.03 mg/dl (p less than 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independetn of changes in parathyroid hormone (as reflected by urinary cAMP).
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PMID:Effect of acute metabolic acidemia on renal electrolyte transport in man. 45 20

We measured placental diffusing capacity for carbon monoxide (DpCO) in 10 unanesthetized sheep with catheters chronically implanted in maternal and fetal vessels. Serially measured DpCO during the last third of gestation averaged 0.55 +/- 0.02 (SEM) ml.(min.Torr.kg fetal wt)-1, essentially the same value as that previously reported in anesthetized, acutely operated animals. While placental CO diffusing capacity increased as a function of gestational age when expressed as ml.(min.Torr)(-1), it remained constant when calculated per kg fetal wt. In eight experiments, DpCO showed no change following the administration of several drugs which combine with cytochrome P450. We interpret this as evidence against the carrier hypothesis for placental CO exchange. We calculated the placental diffusing capacity for oxygen to be 0.68 ml.(min.Torr.kg)-1 and the mean maternal-to-fetal capillary Po2 difference to be 10 Torr. Caculations predict that maternal and fetal oxygen partial pressures equilibrate in end-capillary blood during the course of a single transit in placental exchange vessels; thus placental oxygen exchange is not limited by diffusion.
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PMID:Placental diffusing capacity for carbon monoxide and oxygen in unanesthetized sheep. 59 80

Umbilical PaO2 and PaCO2 were continuously monitored in vivo in acute fetal lamb preparations with a semipermeable membrane connected to a mass spectrometer. The response time of this system (0 to 90% of final value) was 36 sec. In seven pregnant sheep (128--135 days gestation) the maternal inspired mixture was abruptly changed and the following changes in fetal PaO2 and PaCO2 were observed: (1) 100% O2 to room air: PaO2 decreased from 21.5 +/- 0.8 (mean +/- SEM) to 14 +/- 1.1 mm Hg at a rate of 1.63 +/- 0.33 mm Hg/min. Following return to 100% O2 the PaO2 returned to 21 +/- 1.1 mm Hg at a rate of 2.44 +/- 0.4 mm Hg/min. (2) 100% O2 to 12% O2/10% CO2: after 6 min the PaO2 fell from 19.3 +/- 1.3 to 6.3 +/- 0.3 mm Hg at a rate of 4.65 mm Hg/min and the PaCO2 rose from 37 +/- 8 to 70 +/-5 mm Hg. At 100% O2 the PaO2 returned to 19 +/- 1.0 mm Hg at a rate of 11.76 +/- 0.086 mm Hg, the PaCO2 to 39 +/- 7 mm Hg. (3) 100% O2 to 90% O2/10% CO2. The PaO2 and PaCO2 increased by 4.7 and 22 mm Hg, respectively. The changes of fetal PaO2 and PaCO2 occurred after 1 minute of changing in maternal inspired mixture except in the transition from 12% O2/10% CO2 to 100% O2 (34 +/- 12 sec). Following the reinstitution of 100% the fetal PaO2 and PaCO2 returned to their previous values within 4 and 16 min, respectively.
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PMID:The effects of changes of maternal PaO2 and PaCO2 on the fetal PaO2 and PaCO2--in vivo study. 62 13

We studied the arterial blood gas determinations done on the first hospital day in 14 narcotic addicts with bacterial endocarditis (group 1) and six addicts with other medical complications of narcotic addiction (group 2). The arterial oxygen tension (PaO2) was 67.3 +/- 3.3 mm Hg (SEM) in group 1, and 75.0 +/- 6.4 mm Hg in group 2, with no statistically significant difference (P less than .20) between the groups. The arterial CO2 tension (PaCO2), 27.8 +/- 1.7 mm Hg, in group 1 was significantly lower (P less than .005) than that of group 2, 40.1 +/- 3.7 mm Hg. The arterial blood pH, 7.47 +/- 0.01 units, in group 1 was significantly higher (P less than .025) than that of group 2, 7.36 +/- 0.06 pH units. Abnormal blood gas values were found in each of the patients in group 1 with a normal admission chest roentgenogram. Arterial blood gas determinations may be useful in the initial examination of ill narcotic addicts.
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PMID:Bacterial endocarditis in narcotic addicts: analysis of arterial blood gases. 66 29

The mechanical properties of cardiac muscle during ultrasonic irradiation have been studied in vitro. Left anterior papillary muscle from normal rats was suspended in buffered lactated Ringers solution equilibrated with 95% O2, and 5% CO2 and maintained at 20 degrees C. The muscles were stimulated to contract isometrically three times per minute at the length which produced maximum tension. Each muscle was irradiated with a MHz ultrasound at an average power of 2.4 Wcm-2 for a period of 10 min with a 10 min recovery period. Irradiation caused an average increase in temperature of the muscle of 1.7 +/- 0.2 degrees C (mean +/- SEM). Irradiation caused the resting tension (1.46 +/- 0.13g) to decrease by 17.8 +/- 4.7% and the developed tension (3.33 +/- 0.61g) to decrease by 4.1 +/- 0.9%. Since changes in contractile properties have been reported with temperature the bath temperature was raised and changes in contraction observed. When compensated for effects of temperature, the changes in resting tension became - 13.3 +/- 4.1% while the change in developed tension became + 1.6 +/- 2.3%. The change in resting tension is highly significant (p less than 0.05 paired t-test) while the change in developed tension is not. Thus 1 MHz ultrasound at an intensity of 2.4 Wcm-2 appears to affect resting tension of cardiac muscle without affecting the active tension. Since changes in cardiac mechanics of this type have not been described previously the effects of ultrasound appears to be unique.
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PMID:The effects of ultrasound on the mechanical properties of rat cardiac muscle. 67 75

At operation the body temperature of mechanically ventilated infants was initially decreased to 25--22 degrees C with surface cooling and further lowered to 16 degrees C by total body perfusion. During circulatory arrest, averaging 40 min, repair of complex intracardiac deformities was carried out. Rewarming to 36 degrees C was achieved by 35--65 min of total body perfusion. Of 29 infants, 23 under 10 kg survived their correction; normothermic ventilation without added CO2 was given throughout the cooling period. The following measurements were made: gas exchange, lung mechanics, heart rate, arterial pressure, right atrial pressure, cardiac output (Qt), ECG, core and nasopharyngeal temperature, as well as biochemical determinations. During surface cooling O2 consumption (VO2), CO2 production (VCO2), endtidal CO2 (PETCO2) and PaCO2 decreased proportionally and linearly with body temperature. Inspiratory resistance, total compliance, physiological dead space (VD/VT), and the single breath CO2 curve did not reveal disturbed lung function. Mean arterial pressure was 98, 90, and 70 mm Hg and heart rate was 141, 107, and 76 beat/min, at temperature 35, 30, and 25 degrees C, respectively. Cardiac index was 2.2 +/- 0.2 liter/min/m2 (mean +/- SEM, n = 25) 2 hours after surgery. Arterial lactate reached peak values of 4.1 +/- 0.3 mM/liter (n = 17), during rewarming but returned to normal. Respiratory alkalosis caused by hyperventilation during cooling caused no apparent harm. No neurological damage was observed. It is concluded that surface cooling performed with normothermic ventilation under guidance of core temperature, VO2, PETCO2, and VCO2, is a safe method.
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PMID:Cardiorespiratory and metabolic effects of profound hypothermia. 72 92


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