Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Labetalol is a drug possessing both alpha and beta adrenergic receptor blocking properties. Its possible use in induced hypotension during halothane anaesthesia has been investigated. It causes a satisfactory decrease in arterial pressure unaccompanied by tachycardia. The circulatory effects of the drug during halothane anaesthesia, both with spontaneous and controlled respiration, have been measured and compared with those of halothane alone. In patients anaesthetised with 1% halothane, labetalol, with both spontaneous and controlled ventilation, was associated with a reduction in MAP from 71.5 mmHg to 54.0 mmHg (P less than 0.001) and 66.8 mmHg to 50.4 mmHg (P less than 0.001) respectively. This reduction was associated with decreases in Qt of 18% and 12% respectively. In the presence of labetalol, with 3% halothane and spontaneous respiration, the depressant effects of the anaesthetic on the heart became rapidly apparent: Qt was reduced by a further 28%. In patients not receiving labetalol, the depressant effects of 3% halothane were frequently countered by the positive inotropic effects of hypercarbia.
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PMID:Circulatory effects of labetalol during halothane anaesthesia. 63 71

On the basis of microsphere distribution, inert gas washout, and standard clearance data, the effects of acute hypoxia and hypercapnia on the kidney were studied in anesthetized, mechanically ventilated rats. Moderate hypoxia (mean PO2, 48 mm Hg) did not significantly change diuresis, GFR, and tubular sodium rejection. Due to a decrease in renal vascular resistance (R) from 40.1 to 31.8 mm Hg ml-1 min, mean renal blood flow stayed constant in spite of a significant drop in mean arterial blood pressure. Hypoxic changes in R were not accompanied by significant changes in intrarenal distribution of blood flow (IDBF). In severe hypoxia (PO2 less than 45 mm Hg) with oliguria and marked arterial hypotension, R was the lowest of all groups (28.8 mm Hg ml-1 min). Hypercapnia did not significantly change the renal excretory parameters, although an increase in R (without change in IDBF), together with a decrease in MAP caused a marked drop in mean renal blood flow. From these studies we conclude: 1) in the anestheized rat, acute hypoxia caused significant changes in intrarenal hemodynamics without changes in excretory function, 2) hypoxic renal vasodilation persists even in severe hypotension with oliguria and anuria, 3) in acute hypoxia and hypercapnia, changes in renal blood flow and renal vascular resistance are not accompanied by significant changes in IDBF.
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PMID:Renal function and intrarenal hemodynamics in acutely hypoxic and hypercapnic rats. 68 25

The newborn brain, and even more so the brain of the premature child, can be considered as an authentic target organ for numerous pathological conditions, some of which exist outside the central nervous system (changes involving primarily both respiratory function and cardiocirculatory function with serious repercussions at encephalic level). In the premature, this greater "vulnerability" is related to the reduced or absent capacity for self-regulation of the cerebral blood low (mechanism influenced negatively by hypoxia, hypercapnia and metabolic acidosis conditions) and the important role played by numerous factors in protecting newborns from haemorrhagic damage. Of these the most important are the state of prematurity, the presence of vascular, intravascular and extravascular changes, the effects exerted on cerebral haemodynamics by mechanical ventilation and by certain drugs employed in treatment. In mechanically ventilated newborns and premature, prevention of haemorrhagic damage (periendoventricular) is currently based on the application of clear-cut protocols of intensive and rehabilitative treatment. The following form part of these protocols: low damage ventilation techniques (high frequencies, low PJP, low MAP), curarisation (to avoid fluctuations in cerebral blood flow), neuroprotection (phenobarbital), the use of substances and drugs which, by exploiting different mechanisms, go to reduce the extent of the haemorrhage (vitamin E, indomethacin, ethamosylate, tranexamic acid).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention of hemorrhagic cerebral injury in newborn and premature infants subjected to mechanical ventilation]. 269 3

CPP reflects perfusion problems related to increased ICP or inadequate MAP. CPP is a most helpful and practical management tool. The relationship of CBF and CPP depends on cerebral vascular resistance (flow equals pressure divided by resistance). At present, we do not have a practical method to measure vascular resistance or CBV. A close relationship between an increase in CBV and increase in ICP exists. However, the relationship between CBF and ICP is more complex. Whereas CBV is strongly dependent on vasodilation and venous return, CBF is influenced by CPP, vascular resistance, viscosity changes, and focally or diffusely increased ICP. For instance, in hypotensive shock one finds a low CBF with an elevated CBV (and ICP) from vasodilation related to hypercapnia, anoxia, or acidosis. Nevertheless, about two thirds of patients with increased ICP after head injury have increased CBF (hyperemia) and increased CBV. This frequent hyperemia is one rationale for the wide usage of hyperventilation to treat increased ICP. It must be recognized that a group of patients may have ischemia caused by excessive hyperventilation therapy for increased ICP. The PaCO2 must not be allowed to decrease to 20 mmHg or lower, but in some patients a PaCO2 level of 21 to 25 may be predisposing to ischemia. Strong consideration is thus given to monitoring CBF and cerebral oxygen metabolism (arteriovenous oxygen content difference [AVDO2], CMRO2) in states of coma and increased ICP. In such patients, continuous infusion of mannitol may result in improved CBF, and hyperventilation therapy can be less aggressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonsurgical management of increased intracranial pressure. 270 May 10

Radiolabeled microspheres were employed to measure the cerebrovascular response to severe anaphylactic-induced hypotension in pentobarbital-anesthetized dogs. A rapid drop in mean arterial pressure (MAP, 140 to below 50 mm Hg) coincided with total and regional cerebral blood flows (CBF) that were not significantly different from prechallenge values. While blood flow to the occipital region (highest measured region of the brain) was significantly greater than that of brainstem regions prior to and during the shock regimen, no major redistributional phenomena occurred to any cerebral region. These findings were in contrast with other reports that demonstrated a loss in CBF and a redistribution of regional CBF as perfusion pressures declined below 55 to 60 mm Hg. To investigate whether the maintenance of CBF during severe anaphylactic hypotension was associated with cerebral hypoxia or hypercapnia, we employed in a second group of dogs the technique of venous drainage from the confluens sinus, so that the cerebral arterial-venous difference for blood gases and other blood components could be determined. Similar to our previous findings, CBF was maintained to perfusion pressures of 39 +/- 4 mm Hg. The drop in cerebral vascular resistance during the severe hypotensive period was not associated with a significant decline in arterial PO2, or a significant increase in arterial PCO2, A-V PO2, or V-A PCO2. Our results suggest that the fall in cerebral vascular resistance during anaphylactic-induced hypotension would not be associated with a severely altered cerebral metabolism.
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PMID:The cerebral circulatory response during canine anaphylactic shock. 309 90

The technique of high-frequency oscillatory ventilation (HFOV) was successfully used in a preterm infant with severe hyaline membrane disease and in a term neonate presenting with intrauterine pneumonia and associated severe pneumomediastinum. None of the infants could adequately be ventilated by conventional ventilation; both of them deteriorated owing to severe hypoxaemia and hypercapnia. In the preterm infant with HMD a rapid and progressive improvement of oxygenation had been observed immediately after the beginning of HFOV, and he was successfully weaned off the ventilator after 71 hours on HFOV. His recovery was uncomplicated and definitive. In the term neonate presenting with IUP and associated severe PM, an improvement in oxygenation was detected, whereas the retention of paCO2 remained unaltered. On leaving the MAP unchanged but doubling the flow rate, paCO2 and arterial pH also normalised. No sign of PM was seen on the X-ray picture 17.5 hours after the start of HFOV. This patient was weaned off the ventilator after 29 hours on HFOV and his recovery was also uncomplicated. It is believed that recovery of the PM was secondary to the low MAP and to the higher arterial pO2 levels, and that HFOV may also have a direct role in the treatment of preexisting air leaks and perhaps also in their prevention. In our patients HFOV resulted in a definitive recovery, while no improvement had occurred on using conventional ventilation. To determine the exact mechanism of action, the clear cut fields of indications and the possible side effects of HFOV, further investigations are needed.
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PMID:High-frequency oscillatory ventilation (HFOV) in the treatment of neonatal respiratory disturbances: case reports of two infants. 393 21

To evaluate the effect of prostagrandin E1 (PGE1)-induced hypotension on cerebral blood flow (CBF) and carbon dioxide (CO2) reactivity of CBF, regional cerebral hemoglobin oxygen saturation (rSo2) was measured in non-neurosurgical patients (n = 10) under sevoflurane-anesthesia using near infrared spectroscopy. PGE1 was infused intravenously to maintain arterial pressure at a level of about 75% of the MAP (hypotensive group) under sevoflurane-anesthesia alone (normotensive group). Ventilation was controlled to adjust PaCO2 to hypocapnia (25-30 mmHg), normocapnia (35-40 mmHg) and hypercapnia (45-50 mmHg) in both normotensive and hypotensive groups. rSo2 during hypotension did not change by hypocapnia and normocapnia, but significantly increased by hypercapnia, compared with rSo2 during normotension. Significant correlations between rSo2 and PaCO2 during both normotensive and hypotensive groups were observed. Slope of the regression line of rSo2 and PaCO2 did not differ between the normotensive and hypotensive groups. When arterial oxygen content and cerebral metabolic rate of oxygen are constant, changes in rSo2 correlate with those of CBF. Therefore, CBF and CO2 reactivity of CBF that indicates autoregulation in response to changes in CO2 during hypotension were maintained as those during normotension. The results show that PGE2-induced hypotension maintains CBF and CO2 reactivity well in non-neurosurgical patients under sevoflurane anesthesia.
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PMID:[Prostagrandin E1-induced hypotension well maintains cerebral circulation and carbon dioxide reactivity in non-neurosurgical patients under sevoflurane-anesthesia]. 907 Nov 2

Recently we have found that hypercapnia induces nuclear protein (FOS) expression in the brainstem chemosensitive neurons, including catecholamine-containing cells. In the present studies we examined the role of protein kinase C (PKC) pathway in CO2-induced c-fos expression. Because of the complexity of the CNS system, experiments were performed in pheochromocytoma cells (PC12 cells). These cells originate from neuronal crest and express catecholaminergic traits. We depleted PKC from PC12 cells by prolonged (48 h) exposure to high concentration of phorbol 12-myristate, 13-acetate (PMA, 100 nM), and then determined the expression of: (1) c-fos mRNA by Northern blot (2) PKC isoforms, tyrosine phosphorylated and unphosphorylated MAP (mitogen activated protein) kinases by Western blot. Depletion of PKC abolished the effect of CO2 on c-fos mRNA expression, inhibited MAP kinases tyrosine phosphorylation and suppressed the expression of PKC(alpha) and PKC(zeta). These results suggest that MAP kinases, PKC(alpha) and/or PKC(beta) might be involved in CO2-induced c-fos mRNA expression.
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PMID:A possible role for protein kinase C in CO2/H+-induced c-fos mRNA expression in PC12 cells. 957 65

The effects of hypoxemia and hypercapnia in acute cardiovascular response to periodic non-obstructive apneas were explored in seven preinstrumented, sedated paralyzed and ventilated pigs under three conditions: room air breathing (RA), O2 supplementation (O2), and supplementation with O2 and CO2 (CO2). EEG monitoring showed no arousal under any conditions. RA apneas increased mean arterial pressure (MAP, from baseline 95.9 +/- 4.5 to late apnea 124.4 +/- 7.8 Torr, P < 0.01), left ventricular end-diastolic pressure, end-diastolic and end-systolic myocardial fiber lengths and systemic vascular resistance, but decreased cardiac output (CO, 3.09 +/- 0.34-2.37 +/- 0.26 L/min, P < 0.01), heart rate (HR, 115.1 +/- 7.5-102.0 +/- 7.8 bpm, P < 0.01), and stroke volume (SV, 29.6 +/- 0.7 21.1 +/- 1.8 ml, P < 0.01). 02 apneas produced similar decreases in HR (114.0 +/- 11.8-105.4 +/- 8.7 bpm, P < 0.05) as with RA apneas, but smaller increases in MAP (94.5 +/- 1.8-103.4 +/- 2.8 Torr, P < 0.01) and in the variables of pre- and after-load. CO and SV remained unchanged with O2 apneas. CO2 was associated with higher MAP, CO, and HR at baseline relative to RA, but similar cardiovascular response during apneas in direction and magnitude to those of O2 apneas. We conclude that in this model hypoxemia is a major but not the sole determinant of the pressor response during apneas. Hypercapnia cannot explain the pressor response seen when hypoxemia is abolished. The HR fall during apneas is independent of hypoxemia, hypercapnia and the pressor response.
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PMID:Role of hypoxemia and hypercapnia in acute cardiovascular response to periodic apneas in sedated pigs. 962 31

Six horses were randomly assigned to receive either frusemide (F) (0.5 mg/kg i.v.) or an equivalent volume of saline (S) i.v., 4 h prior to treadmill exercise. Horses were instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) carotid arterial pressures, pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), blood gases, and cardiac output (CO). Plasma (PV) and blood volumes (BV) were measured using 2 injections of Evan's Blue dye. Baseline parameters were recorded while the horse stood quietly. Horses were then administered F or S. Four hours later, they were warmed up for 3 min at 4 m/s and then exercised to the point of fatigue at 115% VO2max. Horses were anaesthetised immediately following exercise by administration of detomidine (0.04 mg/kg bwt i.v.) followed 5 min later by tiletamine-zolazepam (1.25 mg/kg bwt i.v.). After transporting the horse to a recovery stall, anaesthesia was maintained with isoflurane in 100% O2. Data were analysed using a 2-way ANOVA with repeated measures with post hoc differences identified using the Student-Newman-Keul's procedure. Exercise was associated with increases in HR, SAP, MAP, DAP, PAP, CVP, TEMP, PCV, and BV, and decreases in PV, pH, arterial bicarbonate and base excess. Anaesthesia was associated with marked hypercapnia, a decrease in HR following detomidine administration, and persistent pulmonary hypertension despite carotid arterial pressure which returned to baseline. No effects attributable to F were identified at any time during the study.
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PMID:Effects of pre-exercise frusemide administration and post exercise anaesthesia on cardiopulmonary and acid-base parameters and blood and plasma volumes in horses exercised supramaximally to fatigue. 1065 46


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