Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the past decade, the survival rate of infants with congenital diaphragmatic hernia (CDH) treated in the intensive care unit of the Royal Children's Hospital, Melbourne, has remained unchanged at 56% +/- 6%. Newer forms of treatment, such as extracorporeal membrane oxygenation (ECMO), high-frequency oscillation, and surfactant and nitric oxide therapy, are now available. The exact role of these therapies in the management of infants with CDH has not been determined. This study examines five clinical parameters derived from an infant's best preoperative ventilatory and blood gas data in the first 24 hours of life. One hundred twenty-five CDH infants were admitted to the intensive care unit between January 1, 1981 and December 31, 1991. Criteria for inclusion in the study were (1) CDH diagnosed within 6 hours of delivery, (2) ventilation before repair, and (3) no associated lethal congenital abnormality. Of the 90 cases studied in detail, there were 38 deaths (42% mortality rate). All five parameters were analyzed by receiver operating curve analysis to determine the optimum value of each parameter in predicting survival. An oxygenation index (MAP x FIO2/PaO2) of less than 0.08 predicted a 94% chance of survival, with a sensitivity of 96% and a specificity of 95%. Similarly, a modified ventilation index (PIP x RR x CO2/1,000) of less than 40 predicted a 91% chance of survival, with a sensitivity of 94% and a specificity of 86%. By stratifying each criterion according to outcome, three groups of infants were identified according to their response to conventional therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Predictors of survival for infants with congenital diaphragmatic hernia. 784 17

The mass discharges of the splanchnic sympathetic (SND) and phrenic nerves (PND) were recorded in urethananesthetized rats with resected vagal and aortic nerves. Carotid chemoreceptor (CC) stimulation with N2 inhalation (4-12 s) or cyanide (50-100 micrograms/kg iv) activated SND in bursts synchronized with the postinspiratory phase (mean SND increase: 105 +/- 8%), raised AP, and increased PND rate and amplitude (n = 40). Brain transection at superior collicular level produced no effect. The sympathetic (SChR) and respiratory chemoreflexes (RChR) were reduced after transections through the pons. Lesions of the dorsolateral pons (dl-pons) produced CO2-dependent apneusis and/or tachypnea at rest. After such lesions, CC stimulation produced expiratory apnea and a 30% increase in SChR due to tonic activation of SND. In contrast, bilateral lesions of the ventrolateral pons (vl-pons) reduced the SChR by 54-76%. Muscimol (Mus) injections (bilateral, 175 pmol/side) into vl-pons did not change resting SND, MAP, baroreflex, and RChR but reduced the SChR (54-82%). In conclusion, under anesthesia: 1) the pathway of the carotid chemoreflex is confined to the pons and medulla, 2) the dl-pons exerts indirect control over the SChR via its role in respiratory rhythmogenesis, and 3) neurons in the vl-pons contribute selectively to the SChR but not to PND activation during CC activation.
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PMID:Role of the pons in the carotid sympathetic chemoreflex. 806 62

A randomized, blinded, crossover study was designed to evaluate the respiratory, cardiovascular, and behavioral effects of butorphanol given postoperatively to oxymorphone-premedicated and surgically stimulated dogs. Nine healthy adult dogs were premedicated intramuscularly with atropine (0.04 mg/kg), acepromazine (0.10 mg/kg), and oxymorphone (0.2 mg/kg). Anesthesia was induced with thiamylal (12 mg/kg) and maintained with halothane in oxygen. According to the protocol of a concurrent study, all dogs had percutaneous endoscopic gastrostomy (PEG) feeding tubes placed during the first anesthetic episode and removed during the second anesthetic episode. All dogs received postoperatively either butorphanol tartrate (0.2 mg/kg) or an isovolumetric dose of saline placebo, both given intravenously. Respiratory rate (RR), tidal volume (TV), minute ventilation (MV), end-tidal CO2 concentration (ETCO2), heart rate (HR), and indirect diastolic (DP), systolic (SP) and mean arterial (MAP) blood pressures were measured at times 0, 2, 5, 10, 20, 40, 80, and 120 minutes after injection. The time from injection of the test drug until extubation was recorded. RR, MV, HR, and DP were significantly (P < .05) increased, while ETCO2 was significantly decreased, for a minimum of 30 minutes in butorphanol-treated dogs compared with saline controls. TV, SP, and MAP were transiently (< or = 15 minutes) increased in butorphanol-treated dogs compared with saline controls. There was no significant difference between the times to extubation in the butorphanol-treated dogs versus the saline control dogs.
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PMID:Butorphanol tartrate for partial reversal of oxymorphone-induced postoperative respiratory depression in the dog. 814 Jul 42

Within one year 3 newborns with meconium-aspiration and 4 infants with bronchopulmonary dysplasia (BPD) were treated with HFP, synchronous with conventional ventilation (CMV). The entrance criteria were insufficient oxygenation (PO2/FiO2 < 50 mmHg) and/or CO2-elimination (> 60 mmHg), respectively peak inspiratory pressure Pi > 40 mmHg and mean airway pressure MAP > 20 mbar during CMV. All three cases of meconium-aspiration have shown a striking improvement in oxygenation and ventilation, in one case starting from a disastrous situation with PCO2 > 90 mmHg, PO2 30 mmHg (FiO2 100%). After a HFO period of 9 to 10 hours Pi, MAP and CMV-frequency could be reduced. The patients could be extubated after 1-2 weeks. In severe BPD only in one case continuous improvement and extubation in the 4. week of life were possible. Here the pulmonary artery pressure in doppler-echocardiography slightly was elevated (30-35 mmHg). In a further case extubation was possible after several trials with HFO. Indeed chronic respiratory insufficiency, progredient pulmonary emphysema on x-ray and clearly elevated pulmonary artery pressure (> 40 mmHg) persisted. In 2 further cases there was no longstanding improvement of ventilation. One child died after 8 months, one after 6 months. In both cases there was a right-to-left shunt over foramen ovale and pulmonary artery pressures at systemic level. HFO led to an improvement in oxygenation and ventilation in all three cases of meconium-aspiration and probably prevented a fatal outcome in one case. The effect seems to depend on improved secretolysis and gas exchange.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[High frequency oscillation in meconium aspiration and bronchopulmonary dysplasia]. 819 11

The hemodynamic effects of argon pneumoperitoneum were studied to define its possible role as an alternative gas for intraperitoneal insufflation during minimally invasive surgery. Adult pigs were anesthetized and placed on mechanical ventilation. Parameters measured or determined included mean arterial (MAP), pulmonary arterial (PAP), pulmonary arterial wedge (PAWP), right atrial (CVP), and inferior vena cava venous (IVC) pressures, total excretion of CO2 (VCO2), oxygen consumption (VO2), minute ventilation, and arterial blood gases. Also determined were cardiac output, stroke volume, and systemic vascular resistance all indexed to weight (CI, SVI, SVRI). Data were recorded during a 1-h baseline, 2 h of insufflation with argon gas at a constant pressure of 15 mmHg, and 1 h recovery after desufflation. There was no significant change from baseline in VCO2, VO2, MAP, PAP, PAWP, CVP, PaCO2, or arterial pH. Argon pneumoperitoneum significantly increased systemic vascular resistance index and exerted a depressant effect on stroke volume index and cardiac index by 25% and 30% from baseline values, respectively (P < 0.05). Inferior vena cava pressure increased as a reflection of the intraabdominal pressure. Argon insufflation had no effect on respiratory function. Argon gas may not be physiologically inert, and in patients with cardiovascular disease its effects may be clinically important.
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PMID:Hemodynamic effects of argon pneumoperitoneum. 820 3

A prototype armoured laryngeal mask airway (LMA) was compared with tracheal intubation (ETT) for anaesthesia for adenotonsillectomy. Fifty-five children were randomised into the LMA group and 54 into the ETT group. During insertion of the LMA, peripheral oxyhaemoglobin desaturation (SpO2) < 94% occurred in ten patients (18.2%) and in seven patients (13%) during tracheal intubation (NS). After opening the Boyle-Davis gag, airway obstruction occurred in ten patients (18.2%) in the LMA group and in three patients (6%) in the ETT group (P = 0.07). In five patients (9%) the LMA was abandoned in favour of tracheal intubation. In all others (91%), when the need for adequate depth of anaesthesia was realized, a satisfactory airway was achieved more rapidly than with tracheal intubation (P < 0.001), and maintained throughout surgery. Manually assisted ventilation was required in all patients in the ETT group, mean duration 373 +/- 385 sec, and in 26 patients (52%) in the LMA group, mean duration 134 +/- 110 sec, P < 0.001. Mean end-tidal CO2 (PetCO2) was 45.5 +/- 6.21 mmHg in the ETT group and 46.6 +/- 6.09 in the LMA group (NS). The LMA did not limit surgical access. Heart rate, MAP and blood loss in the LMA group were 110 +/- 21, 74 +/- 9 mmHg and 1.92 +/- 1.22 ml.kg-1 respectively, compared with 143 +/- 13 (P < 0.001), 85 +/- 12 mmHg (P < 0.001) and 2.62 +/- 1.36 ml.kg-1 (P < 0.05) with tracheal intubation. Fibreoptic laryngoscopy at the end of surgery in 19 patients in the LMA group revealed no blood in the larynx.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anaesthesia for adenotonsillectomy: a comparison between tracheal intubation and the armoured laryngeal mask airway. 792 29

The goal of therapy in patients with severe head injury is to avoid secondary brain damage. Analgesia and sedation are an essential part of the therapy, and several drugs are in current use. However, few controlled clinical trials have been performed so far, and none of these drugs has proved to be superior. Although in the past the therapy has been focused on controlling elevated intracranial pressure (ICP), many authors emphasize the role of cerebral ischaemia in the prognosis of patients. Therefore, cerebral perfusion pressure (CPP) i.e. the difference between ICP and mean arterial pressure (CPP = MAP-ICP), seems to be more important than ICP alone. Analgesics and sedatives reduce the cerebral metabolic rate (CMR), and the consequent decrease in cerebral oxygen uptake might prevent ischaemic damage in regions with low perfusion. Moreover, a decrease in CMR is often associated with a decrease of cerebral blood flow (CBF) in regions with normal perfusion and, as a result, ICP is also reduced. Basically, the cerebral effects (on ICP, CMR, and CBF) and the haemodynamic effects with respect to maintenance of a sufficient CPP are most important in the selection of drugs for analgosedation. In addition, the effects on general intensive care management must be considered (pulmonary function, immunreactivity bowel motility). The purpose of this paper is to describe drugs commonly used for analgosedation in severe head injury. Barbiturates bring about the most pronounced decrease of CMR and ICP. In the past these drugs were used routinely in high doses ("barbiturate coma"). However, no improvement in outcome was demonstrable, and vitally dangerous side effects, such as infection, pulmonary dysfunction, arterial hypotension, and renal failure often occurred. High-dose barbiturate therapy is therefore only indicated in exceptional cases, such as refractory increase in ICP with preserved CO2 response of cerebral vessels. The effect is dependent on CMR at the start of this therapy. Benzodiazepines are frequently used in patients with head injury. They cause only a moderate decrease of CMR and ICP. In general, side effects are negligible. However, a possible decrease of MAP by reduced central sympathetic drive has to be taken into account. Opioids are also frequently used in patients with head trauma. The observed cerebral effects are inconsistent. Some authors have described increases in ICP, CBF, and CMR, but in most studies no influence on these values, or a decrease, has been observed. In any case, cautious titration of these drugs and cerebral monitoring are therefore desirable. As with benzodiazepines, a decrease in MAP due to central effects is possible. In addition, opioids inhibit bowel motility. Ketamine is generally used because of its favourable circulatory effects, bronchodilatation and absence of inhibition of bowel motility. In patients with increased ICP, however, it is often considered contraindicated, since it can be associated with cerebral vasodilation and ICP increase. Other studies did not confirm an increase of ICP when controlled ventilation and additional sedation were applied. More recent studies have demonstrated the role of neuroexcitatory NMDA-receptors in ischaemic and traumatic brain damage. Since ketamine exerts an antagonistic effect on N-methyl-D-aspartate receptors (NMDA) and studies in animals have demonstrated a protective effect of ketamine against ischaemic and traumatic brain damage, controlled clinical studies in patients with head injury are desirable. Propofol results in a profound decrease of CMR and a significant decrease of ICP, but often also in haemodynamic depression. Few results obtained during long-term administration are available, but it seems to be beneficial. More clinical studies are warranted. Gamma-hydroxybutyrate (GHB) is a physiological substance, which has only sporadically been investigated for sedation in patients with head trauma. The few available studies show beneficial res
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PMID:[Analgesia and sedation in patients with head-brain trauma]. 859 67

Near-infrared spectrophotometry-determined cerebral (ScO2) and muscle oxygen saturations (SmO2) were followed in 15 volunteers during passive 50 degrees head-up-tilt-induced central hypovolaemia, and in nine volunteers during ventilatory manoeuvres affecting arterial carbon dioxide tension. During head-up tilt, mean arterial pressure [MAP, 88 (77-118) to 97 (80-136) mmHg, median and range] and heart rate [HR; 66 (49-77) to 87 (42-132) beats min-1 P < 0.01] increased, but after 22 (1-45) min they declined [to 61 (40-91) mmHg and 69 (38-109) beats min-1, respectively, P = 0.001] and pre-syncopal symptoms developed. Central hypovolaemia was indicated by an increased thoracic electrical impedance, and a decreased cardiac output and central venous oxygen saturation. The arterial oxygen saturation, pulmonal oxygen uptake and skin temperatures remained constant. The ScO2 remained stable at 72 (62-77)% until the pre-syncopal incidence, when it decreased to 62 (31-73)% (P = 0.001), and tilt down made it increase to 75 (36-87)% (P < 0.05) before the recovery value was established. In contrast, SmO2 decreased during tilting [75(70-87) to 65 (53-70)%], and recovered to 70 (53-83)%, P < 0.01) during the hypotensive episode. The end-tidal CO2 tension decreased only during tilt-up. The ScO2 decreased, and SmO2 increased during hyperventilation, and ScO2 increased during breathing of 5% carbon dioxide. Rebreathing from a bag made SmO2 decrease and resulted in a biphasic ScO2 response: it first increased and subsequently decreased. Cardiovascular changes during tilt were not reflected in skin temperature. The ScO2 reflected the maintained autoregulation of cerebral blood flow until the perfusion pressure decreased markedly. In contrast, SmO2 mirrored muscle vasoconstriction early during tilt, and vasodilatation when pre-syncopal symptoms appeared.
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PMID:Brain and muscle oxygen saturation during head-up-tilt-induced central hypovolaemia in humans. 884 72

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

In the present study we sought to determine the contribution of endogenous brain stem angiotensin to renal sympathetic reflexes in conscious rabbits. Initial studies determined the subtype of receptor involved in the pressor response to angiotensin II (ANG II) administration into the fourth ventricle (4V). The AT1 antagonist losartan (0.001-10 micrograms 4V) had no effect on blood pressure alone but caused a dose-dependent blockade of the pressor effect of ANG II, with complete blockade produced by 10 micrograms, an effect that lasted for at least 3 h. The AT2 antagonist PD-123319 (0.1-1,000 micrograms) and vehicle had no effect on the ANG II pressor response. The effect of losartan (10 micrograms) on the baroreceptor, chemoreceptor, and trigeminal reflexes was examined in eight rabbits that had been implanted with 4V catheters and an electrode for recording renal sympathetic nerve activity (RSNA) 1 wk earlier. Baroreflex assessments were made during normoxia and two conditions of hypoxia (10% O2 and 10% O2 + 3% CO2) before and after 10 micrograms losartan or vehicle, on separate experimental days. During normoxia and hypoxia+CO2 losartan increased resting RSNA, the range, and upper plateau of the RSNA-MAP baroreflex curves. By contrast the marked increase in RSNA due to activation of trigeminal afferents was not affected by losartan. In conclusion the effect of losartan to increase RSNA activity in conscious rabbits, particularly during hypoxia and baroreceptor unloading, suggests that endogenous ANG II via AT1 receptors normally inhibits renal sympathetic baroreceptor and chemoreceptor reflexes.
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PMID:Role of endogenous angiotensin II on sympathetic reflexes in conscious rabbits. 922 95


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