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:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progesterone administration increase VE in man, but its effects on ventilatory response to hypercapnia and hypoxia have not been well documented. Accordingly, VE, HVR, and HCVR were measured during placebo and MPA administration in 11 normal men. The effect of MPA (20 mg orally q 8 hr for 32 hr) on T degrees, metabolic rate (VO2 and VCO2) was also determined. With MPA, T degrees, rose 0.4 degrees C +/- 0.0008 (S.E.M.) p less than 0.0001), VE increased 0.46 +/- 0.16 L/min (p less than 0.01), and VO2 and VCO2 did not change significantly. HCVR (measured under hyperoxic conditions during rebreathing) increased significantly (P less than 0.01) from 2.9 +/- 0.33 L/min/mm Hg (placebo) to 4.0 +/- 0.29 (MPA). HVR was measured as the shape parameter A, so that when A increased, HVR was augmented. During MPA, HVR increased from A = 132 +/- 19.1 to 179 +/- 20.5 (P less than 0.02). We conclude that 60 mg of MPA daily in normal men increases VE and chemosensitivity as measured by the ventilatory response to hypercapnia and hypoxia.
...
PMID:Effects of progesterone on chemosensitivity in normal men. 35 85

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.
...
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.
...
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)
...
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)
...
PMID:Nonsurgical management of increased intracranial pressure. 270 May 10

Previous studies have shown that some patients with chronic obstructive lung disease and hypercapnia will respond to medroxyprogesterone with improvement in arterial blood gases. The exact mechanism of this effect is unclear but it is presumed to be a result of ventilatory stimulation. To determine whether the ability to correct arterial blood gas abnormalities by voluntary hyperventilation would predict a subsequent favourable response to progesterone, we studied 11 subjects with chronic obstructive lung disease and chronic hypercapnia. Five subjects had chronic obstructive lung disease of moderate severity with mean (SE) FEV1 1.8 (0.34) 1 maximum voluntary ventilation (MVV) 40.4 (7.16) 1/min-1, arterial oxygen tension (Pao2) 53.8 (2.40 mm Hg, and arterial carbon dioxide tension Paco2) 49.6 (3.91) mm Hg, and were able to normalise their blood gas tensions during voluntary hyperventilation (Pao2 85.4 (8.01) mm Hg; Paco2 32.8 (3.43) mm Hg). Six subjects had severe chronic obstructive lung disease with FEV1 0.77 (0.12) 1, MVV 19 (3.09) 1/min-1, Pao2 60.0 (2.89) mm Hg and Paco2 50.5 (1.38) mm Hg, and they could not significantly alter their blood gases with voluntary hyperventilation (Pao2 62.5 (3.19) mm Hg, Paco2 49.7 (1.84) mm Hg). The groups were similar in age, height, weight, and resting Pao2 and Paco2. Each subject received one month of oral placebo and one month of medroxyprogesterone acetate (Provera). 20 mg orally thrice daily, given in a randomised, double blind fashion. The groups responded similarly with a significantly higher Pao2 and lower Paco2 while having medroxyprogesterone acetate than while having placebo. Two patients with polycythaemia showed a reduction in haemoglobin concentration while taking progesterone. It is concluded that the response to medroxyprogesterone is not predictable from spirometric or blood gas changes after voluntary hyperventilation.
...
PMID:Oral progesterone treatment in chronic obstructive lung disease: failure of voluntary hyperventilation to predict response. 294 45

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.
...
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.
...
PMID:High-frequency oscillatory ventilation (HFOV) in the treatment of neonatal respiratory disturbances: case reports of two infants. 393 21

A 62 year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation of provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary ventilation. Progesterone (200 mg/d during 3 weeks) or naloxone did not improve either arterial blood gases (ABG) or the P 0.1/PCO2 curve. Hypoxemia and hypercapnia were not corrected during metabolic acidosis provoked by acetazolamide (250 mg/d). Nasal CPAP did not control hypoventilation periods. Mechanical ventilation was initiated with negative pressure (NPV) through a poncho. The patient presented severe discomfort with NPV and obstructive apneas were verified during it. She refused to continue NPV. Mechanical ventilation was initiated with positive intermittent pressure (IPPV) through a nasal mask. The patient had excellent tolerance to the procedure. SpO2 during IPPV was always higher than 95%. During sleep induction (under IPPV), respiration in phase with the ventilator 1: 1 was observed; instead, during consolidated sleep there was a complete dependence of the ventilator with apnea for over 2 min when IPPV was interrupted (Fig. 1). After 2 months of treatment, a relief of right ventricular failure occurred and hematocrit fell to 39%. There was an improvement of day-time ABG (Table I). The P. 0.1/PaCO2 curve 3 months after IPPV was the same as the previous one (Fig. 2). The patient has been for 18 months on home ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Central alveolar hypoventilation with cor pulmonale: successful treatment by non-invasive intermittent positive pressure ventilation]. 771 33

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.
...
PMID:[Prostagrandin E1-induced hypotension well maintains cerebral circulation and carbon dioxide reactivity in non-neurosurgical patients under sevoflurane-anesthesia]. 907 Nov 2


1 2 3 4 Next >>

---