Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

Rats were tested in the forced swim test in 35 or 20 cm of water or in an open field to evaluate the effects of different intensities of stress on blood gases, electrolytes, and metabolic indices, compared to nontested controls. Animals tested in the open field did not differ from controls on any measure. Immersion in deep water resulted in a greater mixed metabolic and respiratory acidemia (low pH, low bicarbonate, high pCO2), higher glucose and higher lactate levels than immersion in shallow water which in turn resulted in greater metabolic acidemia (low pH, low bicarbonate), and higher glucose and lactate levels than occurred in open field or control animals. In contrast to immersion in deep water, immersion in shallow water resulted in an initial hypocapnia followed by a hypercapnia. Immersion in deep water also resulted in higher potassium levels, lower bicarbonate and total carbon dioxide levels, and a higher anion gap than immersion in shallow water, testing in the open field, or in controls. In a second study, lactate infusion resulted in a metabolic alkalemia (increased pH and bicarbonate levels) and an increase in total carbon dioxide levels. These results indicate that test parameters from forced swim testing (e.g., water depth) can significantly affect the rat's physiological response to testing. The effects of forced swim testing are not simply due to general stress; and the physiological changes seen in conjunction with forced swim testing (e.g., acidemia) are not due to lactate alone.
...
PMID:A further analysis of physiological changes in rats in the forced swim test. 780 Jul 51

We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demonstrate that chronic, but not acute, respiratory acidosis stimulates activity of both renal proton ATPases. By contrast, both acute and chronic respiratory alkalosis decrease the two renal proton pumps. The stimulatory effect of hypercapnia and the inhibitory effect of hypocapnia on the renal ATPases appear to be potassium and aldosterone independent. Although the precise mechanisms for these results are not known, a direct effect of PCO2, pH, or changes in bicarbonate delivery may be involved.
...
PMID:Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes. 809 53

Volatile anaesthetics may modulate cerebrovascular resistance, but their direct actions on human cerebral arteries are unknown. In the present study, we have evaluated the effects of halothane and isoflurane at different MAC (0.4, 1.0 and 2.0) on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated ring segments of human pial arteries. Neither halothane nor isoflurane had significant effects on potency (unaffected EC50 value) or the maximum response (Emax) in potassium-contracted arteries, even though there was a general tendency to attenuation of Emax. Similarly, the potency of prostaglandin F2 alpha was unchanged (unaffected EC50 value). However, the Emax value for prostaglandin F2 alpha at normocapnia (mean PCO2 4.3 (SEM 0.1) kPa, pH 7.41 (0.01)) and addition of halothane (0.4, 1.0 and 2.0 MAC) was significantly attenuated to 96 (2)%, 91 (3)% and 84 (4)% at the respective MAC concentrations. Isoflurane at 2 MAC and normocapnia also reduced Emax to 94 (3)%. During hypocapnia (PCO2 2.7 (0.1) kPa, pH 7.64 (0.01)), the vasodilator effect of halothane was reduced, whereas isoflurane at 0.4 and 1.0 MAC enhanced the contraction induced by prostaglandin F2 alpha.
...
PMID:Influence of halothane and isoflurane on the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries. 819 13

Moderate hypoglycemia (MH) may be associated with blunting of cerebral hypocapnic vasoconstriction. Coincident with this change, electroencephalogram (EEG) flattening occurs. Previous reports show that brain extracellular potassium activity ([K+]o) increases in association with the onset of isoelectricity during severe hypoglycemia and that K+ increases cause pial vessel vasodilation. Using a model of MH, we tested the hypothesis that increases in [K+]o (approximately 15 mM) correlate with blunting of cerebral hypocapnic vasoconstriction. Cerebral blood flow (CBF), [K+]o, and EEG were measured during normocapnia [arterial Pco2 (Paco2) = 35 Torr)] and hypocapnia (PaCO2 = 15 Torr) in MH (< 2 mM) and normoglycemic dogs. During MH, increases in [K+]o occurred in association with EEG flattening (from 4.2 +/- 0.5 to 13.8 +/- 3.8 mM). During normoglycemia and MH without [K+]o elevations, hypocapnic vasoconstriction occurred. [K+]o elevations with MH were associated with increased CBF and decreased vascular resistance (146 +/- 5 and 42 +/- 2% of control, respectively) during normocapnia, and blunting of cerebral hypocapnic vasoconstriction (93 +/- 16% normocapnic control) when [K+]o increased during hypocapnia. This study shows that increases in [K+]o during MH are necessary for both normocapnic increases in CBF and blunting of cerebral hypocapnic vasoconstriction. Increases in [K+]o may represent a mechanism for decreases in cerebral vascular resistance during MH.
...
PMID:Extracellular potassium activity and cerebral blood flow during moderate hypoglycemia in anesthetized dogs. 832 5

To determine the effect of changes in potassium (K+) flux on airway constriction, we studied effects of lemakalim, a K+ channel opener, and glibenclamide, an ATP-sensitive K+ channel blocker. A wedged bronchoscope technique was used to measure peripheral airway resistance (Rp) in anesthetized dogs. Rp was measured before and after constriction of the airways by hypocapnic challenge, acetylcholine aerosol, or dry air hyperpnea. Lemakalim (5 micrograms/kg i.v.) was administered, and the challenge was repeated. Lemakalim attenuated responses to hypocapnia by 72 +/- 7% (n = 6, P = 0.0007) and to dry air challenge by 37 +/- 8% (n = 6, P = 0.005) but not to acetylcholine. On separate days, sublobar segments were pretreated with aerosolized glibenclamide (2 mg/ml), and responses to hypocapnic challenge were measured before and after lemakalim (5 micrograms/kg i.v.), nifedipine (20 micrograms/kg i.v.), or albuterol (1 microgram/kg i.v.). In the presence of glibenclamide, lemakalim had no significant effect on responses to hypocapnia; however, both nifedipine (n = 6, P = 0.0003) and albuterol (n = 6, P = 0.0001) attenuated responses to hypocapnic challenge. These findings suggest that lemakalim attenuated hypocapnic bronchoconstriction by promoting K+ efflux through ATP-sensitive K+ channels.
...
PMID:Lemakalim attenuates hypocapnia- and dry air-induced bronchoconstriction in canine peripheral airways. 837 5

Previous studies suggest that desflurane may increase cerebrospinal fluid (CSF) formation rate (Vf) and volume, particularly during conditions of hypocapnia combined with elevated CSF pressure. The present study was designed to determine whether treatments routinely used in patients during anesthesia for neurological surgery would decrease Vf during desflurane anesthesia in rabbits. Three groups of six rabbits each were examined at four experimental conditions. Condition 1 was the combination of isoflurane, normocapnia, and normal CSF pressure (baseline, all groups). Condition 2 was the combination of isoflurane (group 1) or desflurane (groups 2 and 3), hypocapnia, and elevated CSF pressure (27 and 33 cm H2O). Conditions 3 and 4 were the same as condition 2 with the addition of furosemide, dexamethasone, mannitol, or fentanyl in groups 2 and 3. Vf, resistance to reabsorption of CSF (Ra), and systemic values were determined at each experimental condition, and brain water content was determined at the end of the study. Mean baseline Vf was 9.8 +/- 2.6 microliters.min-1. During the combination of desflurane, hypocapnia, and elevated CSF pressure, furosemide decreased Vf to 3.2 +/- 1.7 microliters.min-1, mannitol increased plasma osmolality and decreased plasma sodium concentration, and fentanyl decreased heart rate and increased plasma potassium concentration. Values for Ra and brain water content did not differ between groups. Of the four treatments examined, only furosemide decreased Vf during the combination of desflurane, hypocapnia, and elevated CSF pressure.
...
PMID:Furosemide decreases cerebrospinal fluid formation during desflurane anesthesia in rabbits. 910 Jan 89

Ten healthy Labrador Retrievers (4 females and 6 males aged 3-6.5 years [mean, 4.5 years]) training with a professional trainer were studied. The dogs were in training during the entire study. Dogs were monitored within 5 minutes after retrieving birds on land and in water on 2 consecutive days during training and on 2 consecutive days at the Atlanta Retriever Club Fall Field Trial. Baseline samples were taken in the morning on a separate day before the dogs were loaded onto a truck. Venous samples were analyzed with a portable blood analyzer. Measurements included hematocrit, sodium, potassium, chloride, blood urea nitrogen (BUN), glucose, lactate, blood pH, Pco2, Po2, HCO3, and TCO2 plus rectal temperature, pulse rate, and respiratory rate. Ambient temperatures were recorded. Distances and times were estimated. Compared to baseline, significant increases occurred in rectal temperature, pulse rate, respiratory rate, chloride, lactate, and pH postexercise (P < .05): sodium, potassium, BUN, Pco2, and TCO2 were significantly decreased postexercise. Blood pH was markedly higher after retrieves on land than after retrieves in water. Estimated mean speeds were 11.4 mph (18.3 km/h) during a triple retrieve on land and 5.6 mph (9.0 km/h) during a retrieve in water. Maximal ambient temperatures were 84-86 degrees F (29-30 degrees C). In summary, Labrador Retrievers training with a professional trainer had evidence of hyperthermia, respiratory alkalosis, hypocapnia, and mild metabolic acidosis monitored within 5 minutes postexercise during training and field trial competition when maximal ambient temperatures were 85 degrees F (29 degrees C). The results provide a baseline against which physiologic responses of dogs with poor performance can be compared.
...
PMID:Physiologic responses in healthy Labrador Retrievers during field trial training and competition. 1505 63

During voluntary hyperventilation in unanesthetized humans, hypocapnia causes coronary vasoconstriction and decreased oxygen (O(2)) supply and availability to the heart. This can induce local epicardial coronary artery spasm in susceptible patients. Its diagnostic potential for detection of early heart disease is unclear. This is because such hypocapnia produces an inconsistent and irreproducible effect on electrocardiogram (ECG) in healthy subjects. To resolve this inconsistency, we have applied two new experimental techniques in normal, healthy subjects to measure the effects of hypocapnia on their ECG: mechanical hyperventilation and averaging of multiple ECG cycles. In 15 normal subjects, we show that hypocapnia (20 +/- 1 mmHg) significantly reduced mean T wave amplitude by 0.1 +/- 0.0 mV. Hypocapnia also increased mean heart rate by 4 beats/min without significantly altering blood pressure, ionized calcium or potassium levels, or the R wave or other features of the ECG. We therefore provide the first unequivocal demonstration that hypocapnia does consistently reduce T wave amplitude in normal, healthy subjects.
...
PMID:Hypocapnia reduces the T wave of the electrocardiogram in normal human subjects. 1576 Nov 87

Modified Hb solutions have been developed as O(2) carrier transfusion fluids, but of concern is the possibility that increased scavenging of nitric oxide (NO) within the plasma will alter vascular reactivity even if the Hb does not readily extravasate. The effect of decreasing hematocrit from approximately 30% to 18% by an exchange transfusion of a 6% sebacyl cross-linked tetrameric Hb solution on the diameter of pial arterioles possessing tight endothelial junctions was examined through a cranial window in anesthetized cats with and without a NO synthase (NOS) inhibitor. Superfusion of a NOS inhibitor decreased diameter, and subsequent Hb transfusion produced additional constriction that was not different from Hb transfusion alone but was different from the dilation observed by exchange transfusion of an albumin solution after NOS inhibition. In contrast, abluminal application of the cross-linked Hb produced constriction that was attenuated by the NOS inhibitor. Neither abluminal nor intraluminal cross-linked Hb interfered with pial arteriolar dilation to cromakalim, an activator of ATP-sensitive potassium channels. Pial vascular reactivity to hypocapnia and hypercapnia was unaffected by Hb transfusion. Microsphere-determined regional blood flow indicated selective decreases in perfusion after Hb transfusion in the kidney, small intestine, and neurohypophysis, which does not have tight endothelial junctions. Administration of a NOS inhibitor to reduce the basal level of NO available for scavenging before Hb transfusion prevented further decreases in blood flow to these regions compared with NOS inhibition alone. In contrast, blood flow to skeletal and left ventricular muscle increased, and cerebral blood flow was unchanged after Hb transfusion. This cross-linked Hb tetramer is known to appear in renal lymph but not in urine. We conclude that cell-free tetrameric Hb does not scavenge sufficient NO in the plasma space to significantly affect baseline tone in vascular beds with tight endothelial junctions but does produce substantial constriction in beds with porous endothelium. The data support increasing the molecular size of Hb by polymerization or conjugation to limit extravasation in all vascular beds to preserve normal vascular reactivity.
...
PMID:Role of nitric oxide scavenging in vascular response to cell-free hemoglobin transfusion. 1589 76

The regulation of cerebral blood flow (CBF) is a complex process that is altered significantly with altitude exposure. Acute exposure produces a marked increase in CBF, in proportion to the severity of the hypoxia and mitigated by hyperventilation-induced hypocapnia when CO(2) is uncontrolled. A number of mediators contribute to the hypoxia-induced cerebral vasodilation, including adenosine, potassium channels, substance P, prostaglandins, and NO. Upon acclimatization to altitude, CBF returns towards normal sea-level values in subsequent days and weeks, mediated by a progressive increase in PO2, first through hyperventilation followed by erythropoiesis. With long-term altitude exposure, a number of mechanisms play a role in regulating CBF, including acid-base balance, hematological modifications, and angiogenesis. Finally, several cerebrovascular disorders are associated with altitude exposure. Existing gaps in our knowledge of CBF and altitude, and areas of future investigation include effects of longer exposures, intermittent hypoxia, and gender differences in the CBF responses to altitude.
...
PMID:Cerebrovascular responses to altitude. 1754 54


<< Previous 1 2 3 Next >>

---