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)

In this experimental study, we investigated pathophysiology of respiratory failure with acute pancreatitis. Pancreatitis was induced by injection of 15% Na-taurocholate 1 ml/kg into the main pancreatic duct of the dogs. Experimental dogs were divided into two groups based on the value of Respiratory Index (R-Index). Group A included 9 dogs in whom respiratory failure was not recognized (R-Index less than 0.5) and Group B included 9 dogs with respiratory failure (R-Index less than 0.5). All the dogs were sacrificed 12 hours after induction of pancreatitis, and histological findings were examined. Quantity of water in the lung (Qwl) was also measured by gravimetric method. Group B showed severe hypoxia with hypocapnia, and increase of A-aDO2, R-Index, and decrease of a/A PO2. Qwl in Group B increased significantly comparing with Group A. In biochemical study, increase of serum lipase, triglyceride, free fatty acid, and angiotensin converting enzyme were observed in Group B. These results indicate that respiratory failure with acute pancreatitis is due to lung edema following injury of the capillary of the lung. The role of free fatty acid liberated by lipolysis was suggested in the mechanism of pulmonary damage with acute pancreatitis.
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PMID:[Experimental study of respiratory failure with acute pancreatitis in dogs]. 241

In the proximal tubules, fractional reabsorption remains essentially unchanged during variations in glomerular filtration rate (GFR). Glomerulotubular balance (GTB), defined as the linear relationship between proximal tubular reabsorption and GFR, is quantitatively the most important regulator of tubular reabsorption, which may be stopped by inhibiting Na, K-ATPase activity completely. However, ouabain in doses inhibiting 80% of the Na, K-ATPases, exerts no effect on proximal reabsorption of water, NaCl and NaHCO3. At constant plasma pH, the same relationship between filtered and reabsorbed bicarbonate is obtained whether bicarbonate reabsorption is altered by varying GFR or plasma concentration of bicarbonate. In contrast, a selective rise in plasma NaCl concentration at constant plasma pH (hypernatremia) reduces NaHCO3 reabsorption and fails to stimulate NaCl reabsorption. Other characteristics of proximal tubular reabsorption are that nonreabsorbable solutes, such as mannitol, inhibit water and NaCl reabsorption with little or no change in NaHCO3 reabsorption and renal oxygen consumption. Mannitol reduces the slope of the GTB curve for NaCl but not for NaHCO3. Hypertonic NaHCO3 exerts an osmotic effect on proximal water and NaCl reabsorption comparable to that of mannitol, whereas hypertonic NaCl is without osmotic effect. By reducing plasma pH (hypercapnia at high plasma bicarbonate concentration), the slope of the GTB curves for NaCl and NaHCO3 can be greatly increased. By raising plasma pH either by hypocapnia or bicarbonate loading, proximal reabsorption of NaHCO3 and NaCl is greatly depressed and remains almost unaltered during variations of GFR (abolished GTB). Similarly, carbonic anhydrase inhibitors, such as acetazolamide, reduce the reabsorption of NaCl and NaHCO3 in the same proportion as a rise in plasma pH, and abolish GTB. Examinations of proximal tubular oxygen consumption indicate that the energy requirement for NaHCO3 reabsorption is as expected for transcellular transport by Na, K-ATPases, whereas proximal NaCl reabsorption requires no additional energy. These data indicate that transcellular energy-requiring NaHCO3 reabsorption provides the main osmotic force across the tight junction for paracellular reabsorption of proximal tubular fluid containing NaCl and other solutes of low reflection coefficient. The main factors influencing GTB are the filtered load of bicarbonate, plasma pH and nonreabsorbable solutes in the proximal tubular fluid.
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PMID:Essentials of glomerulotubular balance. 267 97

High-frequency jet ventilation (HFJV) is used in respiratory distress syndrome (RDS) to avoid high airway pressures and barotrauma. This study was designed to find rational strategies to regulate oxygenation and alveolar ventilation at HFJV and to determine appropriate monitoring methods. Seven dogs were subjected to total lung lavage with saline to induce RDS. PEEP was increased at conventional intermittent positive-pressure ventilation until re-expansion was indicated by a PaO2 of 300 torr at an FIO2 of 1.0 HFJV at 4 and 15 Hz was each tried at 0 and 10 cm H2O PEEP. Intermittent low-frequency inflations were also added to HFJV at 0 PEEP. Lung expansion was maintained without circulatory depression by adjustment of minute ventilation (VE) delivered by the HFJ ventilator; external PEEP was a useful complement. PaCO2 was controlled by frequency adjustment. HFJV at 4 Hz resulted in hypocapnia; intermittent low-frequency inflations had no effect. VE monitoring, CO2 elimination monitoring, and PEEP adjustment was done with a standard ventilator during HFJV. This study illustrates that HFJV is efficient in RDS; VE and external PEEP strongly influence oxygenation and may be used to regulate this factor, and frequency affects CO2 elimination, thus suggesting a method of PaCO2 control.
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PMID:Setting and monitoring of high-frequency jet ventilation in severe respiratory distress syndrome. 267 44

Previous studies have shown that following experimental brain injury cerebral arterioles dilate and display endothelial lesions and reduced responsiveness to hypocapnia. These abnormalities are caused by cyclo-oxygenase-dependent free radical generation. There is evidence that the kallikrein-kinin system may in part stimulate the cyclooxygenase-dependent damage since bradykinin is a powerful stimulator of prostaglandin formation and it has recently been shown that a specific kinin receptor blocker decreases the arteriolar abnormalities caused by injury. In order to further examine the hypothesis that the kallikrein-kinin system is important in inducing damage, rat brain tissue was examined for kininogen, the precursor of kinins, at 10 minutes and 1, 3, 6, 15, 24, 48, and 72 hours after injury. A fluid-percussion brain injury device was attached over the right cerebral cortex of rats and a 1.6-atmosphere pressure injury was administered. The kininogen content was determined by a radioimmunoassay procedure in tissues which were free of intravascular blood. After injury, bleeding was confined mainly to the right hemisphere. The kininogen content in the right hemisphere was significantly elevated by one hour after injury, continued to rise until 15 hours after injury, then was significantly decreased by 2 days after injury. In the left hemisphere, kininogen was significantly elevated at 1 hour postinjury, returned toward control levels over the 3- to 6-hour period after injury, then was again elevated at 15 hours after injury. These studies also show that brain water and cerebrovascular permeability were greater at 15 hours postinjury than at earlier time points. The data further support a role for the kallikrein-kinin system in brain injury and, when considered with the results of other studies, suggest that a secondary event is occurring in the 12- to 24-hour period after neural injury. The authors hypothesize that this secondary event is related to endothelial and vascular repair and may be important for the return of normal cerebrovascular function.
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PMID:Brain kininogen following experimental brain injury: evidence for a secondary event. 276 94

Three awake dogs with chronic tracheostomies were used to study the effects of hypoxia (12% O2) on tracheal smooth muscle tone. Pressure changes within a water-filled cuff in an isolated portion of the cervical trachea reflected changes in tracheal tone. During spontaneous ventilation, hypoxia produced hyperventilation, but no significant change in tracheal tone. If hypocapnia was prevented with inspired CO2 during hypoxia, one of three dogs increased tracheal tone, and all dogs increased ventilation beyond that measured with hypoxia alone. When the awake dogs were ventilated mechanically to prevent changes in ventilation, hypoxia always increased tracheal tone. We made independent changes in ventilation and CO2 similar to the spontaneous responses to hypoxia to test these effects on tracheal tone. When the dogs were ventilated mechanically first with 2% CO2, and then with no CO2, the resulting drop in end-tidal CO2 always decreased tone. When the tidal volume on the ventilator was increased under hyperoxic, isocapnic conditions, tracheal tone always decreased. We conclude that the normal ventilatory response to hypoxia opposes the bronchoconstrictor effect of hypoxia, resulting in no net change in tracheal smooth muscle tone.
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PMID:Ventilatory responses to hypoxia nullify hypoxic tracheal constriction in awake dogs. 309 75

Eggs laid at sea level and incubated at high altitude are subject to hypoxia, hypocapnia, and excessive water loss, resulting in retarded development and poor hatchability. The effect of altitude hypocapnia alone was studied in two series of eggs incubated at a simulated altitude of 2,800 m, PB = 542 torr; the incubator was ventilated at a low flow rate with O2-enriched air; the relative humidity was 70-74%, PH2O 34.4-36.4 torr; ambient PO2 about 130 torr at the plateau stage. In the normocapnic series, CO2 produced by the embryos increased ambient PCO2 to 14 torr at 18-19 days; altitude hypoxia, hypocapnia, and excessive water loss were practically compensated for. In the hypocapnic series, ambient CO2 was almost completely absorbed by soda lime, so that only hypocapnia was not compensated for. In 17-19-day eggs with similar sea level mass specific shell conductances [sp GH2O = 0.26-0.25 mg [g.d.torr]-1], the measured PO2 in the gas space, hematocrit, hemoglobin concentration, lengths of beak and third toe, and masses of body and brain were essentially the same in both series. The masses of heart, liver, and left wing were slightly different on day 19. Altitude hypocapnia alone, without altitude hypoxia and excessive water loss, had almost no significant effect on the embryos' development and hatchability.
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PMID:Altitude hypocapnia at 2,800 m does not affect development of the chicken embryo. 311 Mar 64

The study examined the role of cerebral blood volume (CBV), cerebrospinal fluid (CSF) volume, and brain tissue water and electrolytes on CSF pressure during 4 h of hypocapnia in dogs. Group I (n = 6) was examined during hypocapnia (PaCO2 20 mm Hg), with no intracranial mass being present. Group II (n = 6) was examined with an intracranial mass present (epidural balloon, CSF pressure 35 cm H2O), but no hypocapnia. In group III (n = 6), an intracranial mass was present, and hypocapnia was used to lower CSF pressure. In group I, hypocapnia initially reduced CBV from 3.4 to 2.4 ml. With continued hypocapnia, CBV reexpanded to 3.4 ml by 4 h. CSF volume changed reciprocally, so that intracranial CSF pressure remained constant. In group II, CBV remained steady (2.7 ml), and CSF volume fell only slightly, so that CSF pressure remained elevated. In group III, hypocapnia initially reduced CBV from 2.8 to 2.2 ml, and CSF pressure fell from 35 to 19 cm H2O. With continued hypocapnia, CBV rose to 2.8 ml by 4 h, but CSF volume fell from 6.1 to 5.0 ml, so that CSF pressure remained low. Net intracranial absorption of CSF did not exceed net intracranial CSF production, suggesting that CSF volume fell because hypocapnia improved access of intracranial CSF to spinal sites of CSF reabsorption. Brain tissue composition was not different among groups. The results indicate that hypocapnia lowers elevated CSF pressure initially by lowering CBV. This CSF pressure-lowering effect is sustained (despite reexpansion of CBV) by a further reduction of CSF volume.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebral blood volume, cerebrospinal fluid volume, and brain tissue water and electrolytes. 311 69

We studied the effects of passive, isocapnic changes in ventilation on tracheal smooth muscle tone in 3 awake and 6 anesthetized dogs. Ventilation was altered using mechanical ventilation under hyperoxic conditions, and tracheal tone was measured using the pressure within a water-filled balloon in an isolated segment of trachea. Hypocapnia was prevented at increased VA by increasing FICO2. When f and VT were changed reciprocally, keeping VA constant, tracheal tone did not change. However, when either for VT was changed independently, tracheal tone decreased with an increase in VA. This effect was abolished following thoracic vagotomy. We conclude that tracheal tone is reflexly decreased during an increase in VA.
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PMID:Reflex effects of isocapnic changes in ventilation on tracheal tone in awake dogs. 311 52

Part I of these studies (Artru, 1987) examined how cerebral blood volume (CBV), CSF volume, and brain tissue water and electrolytes determined CSF pressure during 4 h of hypocapnia in sedated dogs. The three groups reported were: hypocapnia (PaCO2 20 mm Hg) with no intracranial mass (group 1), intracranial mass (epidural balloon, CSF pressure 35 cm H2O) but no hypocapnia (group 2), and intracranial mass with hypocapnia used to lower CSF pressure (group 3). It was found that in dogs with an intracranial mass (group 3) the CSF pressure-lowering effect of hypocapnia was sustained for 4 h due to improved reabsorption of CSF, decrease of CSF volume to offset reexpansion of CBV and no increase in the sum of CSF volume and CBV. The present Part II studies (groups 4-8) examine the effects of anesthetics on CSF pressure during conditions like those used for group 3, namely, intracranial mass present and hypocapnia used to lower CSF pressure. When halothane or enflurane were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was not sustained. CSF pressure increased from 17.3 +/- 4.7 and 19.0 +/- 4.1 cm H2O, respectively (mean +/- SD), at 10 min to 50.3 +/- 12.8 and 43.2 +/- 12.8 cm H2O, respectively at 4 h. Increase of CSF pressure was associated with increased resistance to reabsorption of CSF (Ra) and increase in the sum of CSF volume and CBV. With halothane the intracranial volume increase was comprised chiefly of cerebral blood and with enflurane the intracranial volume increase was comprised chiefly of CSF. When isoflurane, fentanyl, or thiopental were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was sustained. Ra did not increase and the sum of CBV and CSF volume remained reduced.
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PMID:Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebral blood volume, cerebrospinal fluid volume and brain tissue water and electrolytes. II. Effects of anesthetics. 313 52

Agents which depress respiration, such as alcohol, seem to increase the occurrence of obstructive apneas during sleep. It has been proposed that upper airway obstruction can result from an imbalance in the activity (or forces) produced by the upper airway muscles versus the chest wall muscles so that upper airway passages might be blocked when a disproportionate decrease in upper airway muscle activity occurs. This study examines the hypothesis that depression of respiration affects the activity of the hypoglossal nerve (the motor nerve to the tongue) more than the activity of the phrenic nerve (the motor nerve to the diaphragm). In addition, we examined the role of the putative central chemoreceptor area on the ventrolateral medullary surface (VMS) in maintaining phrenic and hypoglossal discharge. In chloralose-anesthetized, artificially ventilated, paralyzed cats, three methods of reducing respiratory drive were studied: hyperoxic hypocapnia (produced by mechanical hyperventilation), the application to the intermediate area of the ventral medullary surface of the respiratory depressant GABA and its agonist muscimol, and cooling the same area of the VMS (using a water-cooled thermode). All these interventions decreased hypoglossal nerve activity more than phrenic nerve activity (range of p values: p less than 0.001 to p less than 0.01). Moreover, the reduction in hypoglossal activity was greater with GABA and muscimol than with the other two maneuvers; this was statistically significant for both GABA versus VMS cooling (p less than 0.02) and muscimol versus VMS cooling (p less than 0.01). These results show that respiratory depression can differentially affect hypoglossal and phrenic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of hypoglossal and phrenic nerves to decreased respiratory drive in cats. 374 14


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