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47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoregulation of cerebral (CBF) and cerebellar blood flow (CeBF) was studied before, during and after acutely induced cerebral ischemia in spontaneously hypertensive rats. Cerebral ischemia of the supratentorial portion was induced for one hour by bilateral carotid artery ligation (BCL). The animals were artificially ventilated and the blood flow was measured with a hydrogen clearance technique. To test the autoregulation, the blood pressure was stepwise lowered by bleeding and maintained at a new level, i.e. 15% or 30% lower than the baseline values before, during and after cerebral ischemia. At the preischemic state, CBF and CeBF were 52.1 +/- 6.2 and 58.9 +/- 4.6 ml/100 g/min (mean +/- SEM), of which autoregulations were normally preserved. Following BCL, CBF was markedly decreased to about 10% of control value while CeBF was minimally reduced to 46.9 +/- 8.6 ml/100 g/min (80%). At the ischemic state, CBF became almost zero flow during hypotension. CeBF was also reduced to 74% and further to 58% of the resting value by 15% and 30% decrease in the blood pressure, respectively, indicating impaired CeBF autoregulation. At the 30 min post-ischemic state, CBF was recovered to 48.0 +/- 4.9 and CeBF to 53.9 +/- 5.4 ml/100 g/min. Autoregulation of CBF was still abolished, whereas CeBF was kept constant by 15% fall of blood pressure and slightly reduced to 84% by 30% hypotension, indicating almost recovery of CeBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral and cerebellar blood flow autoregulations in acutely induced cerebral ischemia in spontaneously hypertensive rats--transtentorial remote effect. 381 Jul 34

The effect of pirenzepine on 24 hour intragastric acidity was studied in 10 healthy volunteers using ambulatory 24 hour intragastric pH-monitoring in a double blind crossover study. Tests were performed on the seventh day of ingestion of either placebo, 75 mg pirenzepine or 150 mg pirenzepine per day. The drugs were given at two doses at 8.30 am and 8.30 pm. Mean nocturnal hydrogen ion activity during placebo treatment was 68 mmol/l +/- 9 SEM and was reduced by 75 mg (26%, p less than 0.01) and 150 mg of pirenzepine (36%, p less than 0.01), respectively. Mean diurnal hydrogen ion activity was 32 mmol/l +/- 6 SEM and was not significantly reduced (p greater than 0.1) by either dose of pirenzepine (4% and 12% respectively). Thus, the effect of pirenzepine on intragastric acidity is small, even with high doses of the drug, and becomes apparent only during the night.
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PMID:Evaluation of pirenzepine on gastric acidity in healthy volunteers using ambulatory 24 hour intragastric pH-monitoring. 388 25

Monomers which promote adhesion not only to enamel but also to dentine have been prepared. They have both hydrophilic and hydrophobic groups. The monomers are 2-hydroxy-3-beta-naphthoxypropyl methacrylate, 2-methacryloxyethyl phenyl hydrogen phosphoric acid and 4-methacryloxyethyl trimellitate anhydride. Chemical reaction between monomers and tooth substrates did not lead to adhesion. Cleaning of the ground tooth surface to remove the smeared layer with aqueous 10 per cent citric acid and 3 per cent ferric chloride solution prior to adhesion is recommended. Then, the lipophilic monomers will promote the inter-penetration of monomers into the hard tissues. The infiltrated methacrylates polymerize there and good adhesion takes place. The layer has good resistance against acid and is, in effect, a resin reinforced dentine and enamel as demonstrated by SEM and TEM. The tensile adhesive strength to the cleaned dentine was 18 MN/m2 and to the enamel 14 MN/m2. On the other hand, the value was reduced to 6 MN/m2 when the dentine had been etched by phosphoric acid or citric acid. The ferric chloride added to the citric acid protected dentinal collagen during demineralization. However, the ferric chloride provided ineffective protection against an acid as strong as phosphoric acid. The high bond strength was not dependent upon interlocking at the dentinal tubules as had been considered previously. The resin reinforced dentine and enamel is a hybrid of natural tissue and artificial material and is valuable in the prevention of secondary caries after restoration.
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PMID:Bonding of restorative materials to dentine: the present status in Japan. 389 41

After acute regional coronary occlusion, myocardial tissue PCO2, as measured by mass spectrometry, rises, reaches a peak, and then gradually falls. This late fall in myocardial tissue PCO2 could be due to (1) a gradual increase in tissue blood flow (and hence improved carbon dioxide washout), (2) a gradual consumption of tissue bicarbonate, (3) a gradual reduction in the production of carbon dioxide due to progressive cellular damage, or (4) an artifact caused by the continued presence of the mass spectrometer probe in the ischemic tissue. To determine which of these four mechanisms is responsible for the late fall in myocardial tissue PCO2, we subjected 27 anesthetized open-chest dogs to 3-hour occlusion of the left anterior descending coronary artery. Both myocardial tissue PCO2 and intramyocardial hydrogen ion concentration were measured in the myocardial segment supplied by the left anterior descending coronary artery. Ten dogs (group 1) were killed after the occlusion (occlusion I), and 11 dogs (group 2) underwent reocclusion (occlusion II) at the same site after a 45-minute period of reflow. Regional myocardial blood flow was measured periodically by the intramural injection of 127Xe. Changes in myocardial tissue PCO2 and hydrogen ion concentration were related to ultrastructural changes in the tissues adjacent to the myocardial tissue PCO2 probe. Regional myocardial blood flow remained unchanged throughout the 3-hour occlusion, ruling out increased carbon dioxide washout as a cause for its late fall. Tissue hydrogen ion concentration, as measured by a new lead glass electrode, correlated well with myocardial tissue PCO2, with the reduction in regional myocardial blood flow, and with ischemic damage assessed histologically. Myocardial hydrogen ion concentration also exhibited a late fall after the occlusion, from a peak of 199.8 +/- 27.8 nmol/liter to 91.9 +/- 12.1 nmol/liter (mean +/- SEM). This ruled out consumption of tissue bicarbonate as the cause for the late fall in myocardial tissue PCO2. Peak rise in myocardial tissue PCO2 after occlusion II (71.2 +/- 7.9 mm Hg) was significantly lower than peak myocardial tissue PCO2 after occlusion I (116.7 +/- 13.9 mm Hg, P less than 0.001). The difference between these latter two values, as well as the magnitude of fall in myocardial tissue PCO2 during occlusion I, related directly to the degree of histological damage observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The significance of the late fall in myocardial PCO2 and its relationship to myocardial pH after regional coronary occlusion in the dog. 391 63

Functional indices of distal acidification were assessed in five unrelated children with primary distal renal tubular acidosis. All patients were unable to lower urinary pH below 6.0 both during ammonium chloride-induced acidosis or after acute i.v. administration of furosemide. In these patients the urine minus blood Pco2 gradient failed to increase normally during acute sodium bicarbonate loading (mean +/- SEM: 5.8 +/- 2.0 mmHg), or after neutral phosphate administration (13 +/- 2.7 mmHg), despite adequate urinary concentrations or bicarbonate (72.2 +/- 14.6 mmol/L) and phosphate (25 +/- 2.3 mmol/L), respectively. They also failed to decrease urine pH below 5.5 with sodium sulfate (7.17 +/- 0.08), but urinary potassium excretion increased significantly. These results strongly suggest that the mechanism responsible for defective distal acidification is a failure of hydrogen ion secretion ("secretory' defect) and not an inability to establish a steep hydrogen ion gradient, as it was formerly believed.
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PMID:Pathophysiology of primary distal renal tubular acidosis. 392 6

Gastric bicarbonate secretion in humans was determined in vivo by using a gastric perfusion-aspiration system. A computer calculated the bicarbonate concentration every 30 s throughout the experiment from measurements of the pH and PCO2 in the aspirate. The total bicarbonate concentration was calculated according to the formula of Henderson and Hasselbalch as the sum of free bicarbonate plus the CO2 that was formed during reaction of bicarbonate with hydrogen ions. In 16 subjects basal gastric bicarbonate secretion was 410 +/- 39 mumol/h (mean +/- SEM). After sham feeding using the chew and spit technique to achieve physiologic vagal activation, the gastric bicarbonate secretion rate increased to 692 +/- 67 mumol/h (p less than 0.001). This response of bicarbonate secretion rate to vagal stimulation was independent of the intragastric pH (range 2-7). In 6 subjects the sham-feeding response was almost abolished (88% inhibition) by the anticholinergic drug benzilonium bromide, however, it was unaffected by premedication with indomethacin. The findings demonstrate that the increase in gastric bicarbonate secretion during the cephalic phase of gastric secretion occurs parallel to the increase in acid secretion. It may therefore be regarded as a physiologic response to reinforce the protective mucus-bicarbonate barrier. The response to vagal stimulation seems to be mediated by a muscarinic transmitter and to be independent of intragastric pH and endogenous prostaglandins.
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PMID:Vagal stimulation of human gastric bicarbonate secretion. 392 92

Fetal breathing movements (FBM) indicated by repetitive negative intrathoracic pressures and biparietal electrocorticograms (ECoG) were recorded from 8 fetal sheep for 3 h before (control) and 3 h after the administration of a carbonic anhydrase inhibitor, acetazolamide. FBM and the low voltage (LV) ECoG state occurred 36 +/- 5% (SEM) and 60 +/- 3% of the control period, respectively. Virtually no FBM occurred during high voltage (HV) ECoG while in 57 +/- 6% of the LV state the fetuses were making FBM. The peak magnitude of the negative intrathoracic (tracheal) pressure deflections was 4 +/- 1 Torr. Following acetazolamide the incidence of FBM rose to 53 +/- 4% (P less than 0.01) but there was no significant change in the incidence of the LV state (58 +/- 3%). Most of the increase in the incidence of FBM remained confined to periods of LV ECoG activity so that an increased proportion of this state (88 +/- 2%, P less than 0.001) was occupied with respiratory efforts. The amplitude of the FBM also increased to 8 +/- 1 Torr (P less than 0.05). The increased incidence and depth of FBM is most likely due to an elevated hydrogen ion concentration and differs from a fetal respiratory acidosis induced by increasing the inspired CO2 fraction to the ewe in that the respiratory stimulation induced by acetazolamide is not associated with an increased incidence of the permissive LV ECoG state.
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PMID:The effect of carbonic anhydrase inhibition on breathing movements and electrocortical activity in fetal sheep. 393 69

Red-cell lithium-sodium countertransport is increased in patients with essential hypertension. It has been proposed that sodium-hydrogen ion exchange in the brush border of the renal proximal tubules is analogous to red-cell countertransport. To investigate the rate of sodium reabsorption by the proximal renal tubules in hypertension, we measured lithium clearance (a measure of proximal tubular reabsorption of sodium), as well as red-cell countertransport, in 14 patients with untreated essential hypertension and in 31 controls. As a group, the hypertensive patients had a higher average (+/- SEM) rate of red-cell countertransport (0.378 +/- 0.030 mmol of lithium per liter of cells per hour, P less than 0.01) and a lower renal fractional lithium clearance (13.96 +/- 0.69 percent, P less than 0.01) than normotensive subjects (0.317 +/- 0.015 mmol of lithium per liter of cells per hour and 17.75 +/- 0.81 percent, respectively). Within the normotensive group, subjects with hypertension in at least one first-degree relative had significantly lower fractional lithium clearances than subjects with no hypertensive relatives (15.37 +/- 0.84 percent vs. 19.06 +/- 1.07 percent, P less than 0.05). We conclude that hypertensive patients have heightened proximal tubular reabsorption of sodium and that red-cell countertransport is a marker of the renal abnormality. Enhanced proximal tubular sodium reabsorption may precede the development of essential hypertension.
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PMID:Red-cell lithium-sodium countertransport and renal lithium clearance in hypertension. 394 8

Current requirements for the lactose breath hydrogen test (LBHT) include serial expired air samplings and multiple hydrogen (H2) determinations. One hundred thirty-two consecutive LBHTs were evaluated to determine whether multiple samplings are indeed necessary for detection of lactose malabsorption. Expired air samples were collected at 0, 30, 60, 90, 120, 150, and 180 min following ingestion of lactose. Fifty-five LBHTs were positive for lactose malabsorption. All tests showed abnormally elevated breath H2 concentrations at 120 min. The mean value of the change in parts per million (delta ppm) of H2 at 120 min (51.1 +/- 4.7 SEM) was higher than at any other time point. If only the 120-min samples were examined without subtracting the initial concentrations, four of the 77 negative tests (5.2%) would have been falsely positive. Thus, the values of H2 at 0 and 120 min were sufficient to define lactose malabsorption in all cases. We conclude that just as a single blood sample now suffices for determining xylose malabsorption, so expired air sampling at only 0 and 120 min during the LBHT is a reliable method for detecting lactose malabsorption and diminishes the need for acquiring and analyzing multiple samples.
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PMID:Two-hour lactose breath hydrogen test. 394 36

Autoregulation of cerebral blood flow was studied with the hydrogen clearance method during development of hypertension in young spontaneously hypertensive rats. To examine the influence of sympathetic nerves on autoregulatory range, the unilateral superior cervical ganglion was removed 2 hours or 2 or 5 weeks before the study. Wall-to-lumen ratio of cerebral arteries was determined with freeze substitution technique. Basal blood pressures were 87 +/- 1 mm Hg (mean +/- SEM) at 4 weeks of age, 105 +/- 2 at 6 weeks, and 126 +/- 3 at 9 weeks, although resting cerebral blood flow was unchanged. Initially, cerebral blood flow remained relatively constant when the blood pressure was raised by intravenous infusion of phenylephrine. The upper limits of cerebral blood flow autoregulation in these groups were 110 +/- 4 mm Hg, 126 +/- 7, and 159 +/- 6 respectively. Acute ganglionectomy significantly lowered the upper limits (p less than 0.05), but chronic denervation did not affect the autoregulatory range. The wall-to-lumen ratios of cerebral arteries were 0.136 +/- 0.007 at 4 weeks and 0.130 +/- 0.005 at 9 weeks. These differences were not significant, nor did sympathetic denervation alter the ratio. These results indicate that (1) the upward shift of the autoregulation is closely related to a rise in the basal blood pressure, (2) acute interruption of sympathetic nerves modulates the autoregulatory range, and (3) adaptation of cerebral blood flow autoregulation to early developmental hypertension may be attributed to factors other than vascular smooth muscle hypertrophy.
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PMID:Cerebral autoregulation in young spontaneously hypertensive rats. Effect of sympathetic denervation. 399 22


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