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

We measured CBF and CO2 reactivity after traumatic brain injury (TBI) produced by controlled cortical impact (CCI) using magnetic resonance imaging (MRI) and spin-labeled carotid artery water protons as an endogenous tracer. Fourteen Sprague-Dawley rats divided into TBI (CCI; 4.02 +/- 0.14 m/s velocity; 2.5 mm deformation), sham, and control groups were studied 24 hours after TBI or surgery. Perfusion maps were generated during normocarbia (Paco2 30 to 40 mm Hg) and hypocarbia (PaCO2 15 to 25 mm Hg). During normocarbia, CBF was reduced within a cortical region of interest (ROI, injured versus contralateral) after TBI (200 +/- 82 versus 296 +/- 65 mL.100 g-1.min-1, P < 0.05). Within a contusion-enriched ROI, CBF was reduced after TBI (142 +/- 73 versus 280 +/- 64 mL.100 g-1.min-1, P < 0.05). Cerebral blood flow in the sham group was modestly reduced (212 +/- 112 versus 262 +/- 118 mL.100 g-1.min-1, P < 0.05). Also, TBI widened the distribution of CBF in injured and contralateral cortex. Hypocarbia reduced cortical CBF in control (48%), sham (45%), and TBI rats (48%) versus normocarbia, P < 0.05. In the contusion-enriched ROI, only controls showed a significant reduction in CBF, suggesting blunted CO2 reactivity in the sham and TBI group. CO2 reactivity was reduced in the sham (13%) and TBI (30%) groups within the cortical ROI (versus contralateral cortex). These values were increased twofold within the contusion-enriched ROI but were not statistically significant. After TBI, hypocarbia narrowed the CBF distribution in the injured cortex. We conclude that perfusion MRI using arterial spin-labeling is feasible for the serial, noninvasive measurement of CBF and CO2 reactivity in rats.
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PMID:Assessment of cerebral blood flow and CO2 reactivity after controlled cortical impact by perfusion magnetic resonance imaging using arterial spin-labeling in rats. 929 May 84

This study on conscious rats with occluded left carotid artery investigates the influence of cerebral edema after acute carbon monoxide (CO) poisoning on cerebrospinal fluid pressure (CSFp) and evaluates the therapeutic effectiveness of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2). The CSFp was continuously recorded via a cannula placed in the left cerebral ventricle before, during, and for up to 6 h after exposure to 0.27% CO for 1 h. A non-sustained small increase in the CSFp and identical degrees of hypoxemia, hypocapnia, arterial hypotension, and acidosis were found during the exposure in all rats. After the CO exposure, all non-edema control rats without carotid artery ligation (n = 7) recovered completely with normal CSFp, behavior, and brain water content. All untreated (n = 7) and NBO2-treated rats (n = 7) developed a severely increased CSFp (> 50 mmHg) with neurologic motor dysfunction, and died of a severely increased CSFp (> 100 mmHg) with considerable cerebellar herniation. Except in one rat, the CSFp did not reach a dangerous level (> 25 mmHg) after the HBO2 session (300 kPa O2 for 1 h, beginning at 20 min post CO). All HBO-treated rats (n = 7) survived with less neurologic motor dysfunction and less left hemispheric edema than those in untreated and NBO2-treated rats. The results demonstrated that the increase in the CSFp was related to the left hemispheric edema, and that the cerebellar herniation was the predominant cause of death after the CO exposure. HBO2, but not NBO2, prevented the severe increase in the CSFp and thus saved the life after the CO exposure.
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PMID:Cerebrospinal fluid pressure changes after acute carbon monoxide poisoning and therapeutic effects of normobaric and hyperbaric oxygen in conscious rats. 944 57

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
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PMID:[The internal environment and intracranial hypertension]. 975 May 95

Respiratory inhibition following laryngeal water administration was investigated by breath-by-breath analysis of inspiratory ventilation (VI) and central inspiratory drive (P0.1) in 15 unanesthetized lambs studied in 0.21 FIO2 (PaO2: 82-92 torr, PaCO2 41-43 torr) and in 0.1 FIO2 (Pao2 30-34 torr, PaCO2 32-33 torr). During the 30 sec period after stimulation, VI decreased significantly compared to prestimulation levels both in 0.21 FIO2 (-22, -21 and -18%) and in 0.1 FI(O2), (-16, -23 and -19%) at 5, 16 and 29 days, respectively. In contrast, P0.1 remained at prestimulation levels during normoxia in all age groups (1, 10 and 9%, NS), but decreased significantly during hypoxia (-11 and -13%, P < 0.05) at 16 and 29 days, respectively. Poststimulation apnea duration was significantly related to the decrease in VI (P < 0.001) but not to the change in P0.1. Laryngeal stimulation during hypoxemia/hypocapnia induces a prolonged decrease of central inspiratory drive in postneonatal lambs, a finding of potential significance for the mechanisms of sudden infant death syndrome.
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PMID:Reduced inspiratory drive following laryngeal chemoreflex apnea during hypoxia. 1042 Oct 32

Hypercapnia and hypocapnia produce cerebral vasodilation and vasoconstriction, respectively. However, regional differences in the vascular response to changes in Paco2 in the human brain are not pronounced. In the current study, these regional differences were evaluated. In each of the 11 healthy subjects, cerebral blood flow (CBF) was measured using 15O-water and positron emission tomography at rest and during hypercapnia and hypocapnia. All CBF images were globally normalized for CBF and transformed into the standard brain anatomy. t values between rest and hypercapnia or hypocapnia conditions were calculated on a pixel-by-pixel basis. In the pons, cerebellum, thalamus, and putamen, significant relative hyperperfusion during hypercapnia was observed, indicating a large capacity for vasodilatation. In the pons and putamen, a significant relative hypoperfusion during hypocapnia, that is, a large capacity for vasoconstriction, was also observed, indicating marked vascular responsiveness. In the temporal, temporo-occipital, and occipital cortices, significant relative hypoperfusion during hypercapnia and significant relative hypoperfusion during hypocapnia were observed, indicating that cerebral vascular tone at rest might incline toward vasodilatation. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve by hypercapnia and in the correction of CBF measurements for variations in subjects' resting Paco2.
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PMID:Regional differences in cerebral vascular response to PaCO2 changes in humans measured by positron emission tomography. 1095 Mar 85

A study was made on acid-base metabolism in early posthemorrhagic period as exemplified by examination of patients presenting with gastrointestinal hemorrhage. It has been ascertained that hemorrhage is accompanied by a mixed variant of the acid-base state (ABS) deviation, namely metabolic lactate-acidosis and respiratory alkalosis. In the time-related course of posthemorrhagic period such deviations persist in patients with lethal outcome; with the disease running a favourable course the above deviations are found to return to normal quite soon. The development of complications leads to staging in ABC, its stages being as follows: stage I--the initial stage, stage II--persisting metabolic acidosis and respiratory alkalosis, stage III--alkalosis, stage IV--normalization, with stage III of ABS being encouraged by hypocapnia caused by function disorders of the lungs in early posthemorrhagic period, normalization of cell metabolism, increase in the rate of urination as a reflection of the third earlier identified stage of water metabolism, with the H+ excretion in the urine at the previous level. The identified ABS stage III threatens coming trouble, being accompanied by metabolic deviations together with a risk of function disorder of the myocardium.
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PMID:[An unexpected stage of alkalosis in the dynamics of the early posthemorrhagic period]. 1103 59

In addition to metabolic CO2 production and gill ventilatory flow rate, expired water PCO2 is very dependent on water acid-base balance in a complex way. This is particularly true in carbonated waters at low ambient PCO2 and high pH, where CO2 excreted in the gill water may be buffered by carbonate ions, leading to an increased CO2 capacitance coefficient. The higher the carbonate alkalinity (CA) and the lower the inspired PCO2 (i.e., the higher the inspired water pH), the stronger the carbonate buffering and the smaller the increase of PCO2 in the gill water during respiratory CO2 exchanges. As a consequence, as shown by a number of reported data, increasing the CA leads to blood hypocapnia and respiratory alkalosis at constant low, but not at high, inspired PCO2. In the low range of inspired PCO2, internal PCO2 becomes very sensitive to even small changes of water PCO2, which may explain at least in part the large variability of reported blood PCO2 values in gill breathers. Water CA also influences the amplitude of respiratory acid-base disturbances caused by changes of the gill ventilatory flow rate. Carbonate buffering of excreted CO2 and thus dependence of blood PCO2 on water alkalinity requires catalysis of CO2 hydration by carbonic anhydrase, that must be available from the water side of the gill epithelium.
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PMID:Effect of water alkalinity on gill CO2 exchange and internal PCO2 in aquatic animals. 1125 77

Thirty-four dogs suffering from severe babesiosis caused by Babesia canis rossi were included in this study to evaluate acid-base imbalances with the quantitative clinical approach proposed by Stewart. All but 3 dogs were severely anemic (hematocrit <12%). Arterial pH varied from severe acidemia to alkalemia. Most animals (31 of 34; 91%) had inappropriate hypocapnia with the partial pressure of CO2 < 10 mm Hg in 12 of 34 dogs (35%). All dogs had a negative base excess (BE; mean of - 16.5 mEq/L) and it was below the lower normal limit in 25. Hypoxemia was present in 3 dogs. Most dogs (28 of 34; 82%) were hyperlactatemic. Seventy percent of dogs (23 of 33) were hypoalbuminemic. Anion gap (AG) was widely distributed, being high in 15, low in 12, and normal in 6 of the 33 dogs. The strong ion difference (SID; difference between the sodium and chloride concentrations) was low in 20 of 33 dogs, chiefly because of hyperchloremia. Dilutional acidosis was present in 23 of 34 dogs. Hypoalbuminemic alkalosis was present in all dogs. Increase in unmeasured strong anions resulted in a negative BE in all dogs. Concurrent metabolic acidosis and respiratory alkalosis was identified in 31 of 34 dogs. A high AG metabolic acidosis was present in 15 of 33 dogs. The lack of an AG increase in the remaining dogs was attributed to concurrent hypoalbuminemia, which is common in this disease. Significant contributors to BE were the SID, free water abnormalities, and AG (all with P < .01). Mixed metabolic and respiratory acid-base imbalances are common in severe canine babesiosis, and resemble imbalances described in canine endotoxemia and human malaria.
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PMID:The mixed acid-base disturbances of severe canine babesiosis. 1159 31

The hypoxic ventilatory response during hypocapnia has been studied with divergent results. We used volume-cycled ventilation in spontaneously breathing normal subjects to study their hypoxic ventilatory response under conditions of stable hypocapnia. Subjects were studied at three different levels of end-tidal (partial) carbon dioxide pressure (PETCO2), eucapnia and 6 and 12 mm Hg below eucapnia (mild and moderate hypocapnia, respectively). The response to hypoxia was assessed by changes in muscle pressure output (Pmus) and respiratory rate. Compared with the Pmus response at eucapnia (0.53 +/- 0.59 cm H2O/percentage oxygen saturation [% O2sat]), the response at mild hypocapnia was attenuated (0.26 +/- 0.33 cm H2O/% O2sat), whereas the response at moderate hypocapnia was negligible (0.003 +/- 0.09 cm H2O/% O2sat). Similar reductions were seen with the respiratory rate (eucapnia, 0.17 +/- 0.2 breaths/minute/% O2sat; mild hypocapnia, 0.11 +/- 0.11 breaths/minute/% O2sat; moderate hypocapnia, 0.01 +/- 0.06 breaths/minute/% O2sat). The Pmus and respiratory rate responses at the three levels of PETCO2 were significantly different (p < 0.05, analysis of variance). The responses at moderate hypocapnia were not significantly different from zero. We conclude that when apnea occurs under conditions in which central PCO2 is well below the CO2 setpoint, subjects are at risk of developing dangerous hypoxemia due to absence of a hypoxic ventilatory response.
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PMID:Hypoxic respiratory response during acute stable hypocapnia. 1510 5

During brain activation, local control of oxygen delivery is facilitated through microvascular dilatation and constriction. A new functional MRI (fMRI) methodology is reported that is sensitive to these microvascular adjustments. This contrast is accomplished by eliminating the blood signal in a manner that is independent of blood oxygenation and flow. As a consequence, changes in cerebral blood volume (CBV) can be assessed through changes in the remaining extravascular water signal (i.e., that of parenchymal tissue) without need for exogenous contrast agents or any other invasive procedures. The feasibility of this vascular space occupancy (VASO)-dependent functional MRI (fMRI) approach is demonstrated for visual stimulation, breath-hold (hypercapnia), and hyperventilation (hypocapnia). During visual stimulation and breath-hold, the VASO signal shows an inverse correlation with the stimulus paradigm, consistent with local vasodilatation. This effect is reversed during hyperventilation. Comparison of the hemodynamic responses of VASO-fMRI, cerebral blood flow (CBF)-based fMRI, and blood oxygenation level-dependent (BOLD) fMRI indicates both arteriolar and venular temporal characteristics in VASO. The effect of changes in water exchange rate and partial volume contamination with CSF were calculated to be negligible. At the commonly-used fMRI resolution of 3.75 x 3.75 x 5 mm(3), the contrast-to-noise-ratio (CNR) of VASO-fMRI was comparable to that of CBF-based fMRI, but a factor of 3 lower than for BOLD-fMRI. Arguments supporting a better gray matter localization for the VASO-fMRI approach compared to BOLD are provided.
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PMID:Functional magnetic resonance imaging based on changes in vascular space occupancy. 1287 2


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