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Biomedical subjects

J Ponte

Publications and source records attributed to J Ponte.

At least 55 records · Page 3Linked to original sources
PubMed1988

Comparison of a total intravenous anaesthetic technique using a propofol infusion, with an inhalational technique using enflurane for day case surgery.

A total intravenous anaesthetic technique with a propofol infusion for maintenance of anaesthesia was compared with an inhalational technique that used oxygen, nitrous oxide and enflurane in 98 unpremedicated patients who presented for day case surgery. Overall quality of anaesthesia during induction and maintenance was comparable in both groups. Quality of maintenance of anaesthesia in the propofol group was improved by an increase of the initial infusion rate from 12 to 15 mg/kg/hour. There was a larger decrease in arterial blood pressure after induction in the propofol group but no difference in blood pressure between the groups during maintenance. Recovery times and scores using the Steward scoring system were not significantly different. Nausea and vomiting were slightly less frequent in the propofol group.

Adult↗
PubMed1988

Sedation.

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Anesthesia, Dental↗
PubMed1987

Drift in vivo of transcutaneous dual electrodes.

TcPO2 and tcPCO2 monitoring is widely used but the in vitro drift of the new combined sensors is unknown. We tested the in vivo stability of 3 such electrodes in six adults, compared to nasal endtidal values from a mass spectrometer. Each electrode was remembraned within 5 days and had a 2 point dry gas calibration at 45 degrees C before fixing to the subjects' right arms. TcPO2, tcPCO2 and endtidal values were averaged over four minutes after 30 minutes equilibration, and then at seven subsequent 20 minute intervals. We observed that (1) Endtidal values remained stable (2) tcPCO2 differed from baseline by less than 3 torr (3) tcPO2 rose significantly in all three electrodes by an average of 16 to 21% and, (4) in vivo drift greatly exceeded separately determined in vitro changes. We discuss the possible explanations for the observed results, and conclude that skin permeability changes may play an important role. In the light of the large in vivo tcPO2 drift, transcutaneous dual electrodes are not reliable trend indicators of blood gases in adults.

Adult↗
PubMed1987

Monitoring oxygenation.

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Blood Gas Monitoring, Transcutaneous↗
PubMed1986

Anaesthetic temperature and shivering in epidural anaesthesia.

The mechanism of shivering during epidural analgesia remains unclear. This study investigates the role of the temperature of the local anaesthetic injected extradurally. Forty patients admitted for elective caesarean section under epidural anaesthesia were studied; 20 were given bupivacaine warmed to 37 degrees C (warm group) and 20 were given bupivacaine stored at 4 degrees C (cold group); the occurrence of shivering in both groups was recorded. The overall incidence of shivering was 27.5%; two patients of the warm group and nine patients of the cold group shivered. This difference was statistically significant (P less than 0.03). The results suggest that there are thermosensory mechanisms in the human spinal canal. In our view, epidural anaesthetic solutions should be warmed to body temperature prior to injection to reduce the incidence of shivering.

Adult↗
PubMed1986

The new formulation of I.C.I. 35868 (propofol) as the main agent for minor surgical procedures.

Thirty unpremedicated patients for day-case surgery were anaesthetized with 2.5 mg kg-1 of a new formulation of I.C.I. 35868 (propofol: Diprivan--I.C.I.) in a lipid emulsion. An initial bolus of fentanyl (1-1.5 micrograms kg-1) was given. Anaesthesia was maintained with intermittent boluses of propofol (1 mg kg-1) with no other agent added. The significant problems were: a high incidence of pain on injection (30%) and apnoea following induction lasting more than 30 s (57%). Cardiovascular depression was significant but not considered excessive. Recovery from the drug was rapid and uneventful, with no reported hangover effect.

Adolescent↗
PubMed1984

Pathways to complement activation during cardiopulmonary bypass.

Complement activation was assessed in 34 patients undergoing cardiopulmonary bypass. Arterial concentrations of complement fragments Ba and C3d rose in all patients, the increase in Ba preceding that of C3d. At the same time as complement fragments were being generated the arterial neutrophil count fell. These findings suggest (a) that complement activation is initiated by the alternative pathway during cardiopulmonary bypass and (b) that complement activation mediates loss of neutrophils during bypass. Complement mediated loss of neutrophils during the analogous setting of haemodialysis is the result of leucosequestration in the pulmonary vasculature. During cardiopulmonary bypass the lungs are out of circuit, so that activated leucocytes may sequester in other target organs. This may be an aetiological factor in the multi-organ failure occasionally seen after uneventful cardiopulmonary bypass.

Adult↗
PubMed1982

Adrenergic mechanisms and chemoreception in the carotid body of the cat and rabbit.

1. The effect of beta-adrenergic and dopaminergic agonists and antagonists on the chemoreceptor response to graded hypoxia and hypercapnia was tested in nineteen cats and ten rabbits anaesthetized either with chloralose-urethane or pentobarbitone sodium, paralysed with pancuronium bromide and artificially ventilated.2. The inhibitory action of dopamine was confirmed. The inhibition following intra-arterial bolus injection was blocked by haloperidol; dopamine then excited and this excitation was blocked with propranolol. Adrenaline or noradrenaline caused a transient inhibition followed by a marked excitation. The inhibition was blocked with haloperidol and the excitation blocked with propranolol or metoprolol. Isoprenaline excited without inhibition and this was blocked with propranolol or metoprolol.3. A novel finding was that the chemoreceptor response to hypoxia was markedly reduced or even abolished with propranolol or metoprolol. The response was enhanced with a constant infusion of isoprenaline, adrenaline or noradrenaline in proportion to the degree of hypoxia, an effect mimicked by raising CO(2). The chemoreceptor response to hypoxia was similarly enhanced by haloperidol and depressed by a constant infusion of dopamine in proportion to the degree of hypoxia.4. The effect of these drugs on the chemoreceptor response to hypercapnia was less constant. In the majority of tests the aminergic agonists and antagonists caused a parallel shift of the CO(2) response curves in the same direction as the O(2) response curves and by amounts proportional to the degree of hypoxia. In some tests these drugs caused a change in the slope of the CO(2) response curves but only if P(a, O2) was less than 60 mmHg.5. One interpretation of these results is that hypoxia exerts a presynaptic action, causing the release of noradrenaline and dopamine from Type I cells, and that these substances act upon aminergic receptors on the sensory fibre, causing a change in potential and discharge frequency proportional to the rates of dopamine and noradrenaline release.6. An additional or alternative interpretation is that O(2) and CO(2) (the latter most probably acting on intracellular pH) alter the sensitivity of the aminergic receptors to their agonists.

Action Potentials↗
PubMed1981

Prolongation of the Q-T interval (Romano-Ward syndrome): anaesthetic management.

The anaesthetic management is described of a patient with prolonged Q-T interval which had been complicated by ventricular fibrillation at induction of general anaesthesia for a previous operation. This complication was prevented by effective premedication with i.v. propranolol and block of the left stellate ganglion.

Adult↗
PubMed1980

Activity of carbonic anhydrase in stored blood.

The activity of carbonic anhydrase in blood stored in CPD at 4 degrees C for up to 31 days was measured electrometrically at 5-day intervals and compared with that in fresh blood taken from four normal subjects. No change in activity in stored red cell lysates was observed over this period. There was a clear increase in activity in serum from stored blood with time. These results are discussed in the context of alveolar-to-arterial carbon dioxide gradients seen occasionally in patients following massive transfusions of stored blood.

Blood Preservation↗
PubMed1980

Fluctuations of Pa, CO2 with the same period as respiration in the cat.

1. A CO2 sensor using mass spectrometry is described. It responds linearly to O2 and CO2 with a time constant of 0.5 sec: it is not affected by pressure or flow in the physiological range: its temperature coefficient is 4 mm Hg PCO2 per degree C at 37 degrees C. 2. When this sensor and its through flow cuvette were placed in a common carotid artery-to-jugular vein loop in anaesthetized cats breathing spontaneously or being ventilated artificially, fluctuations of Pa, CO2 which had the same period as respiration were readily observed. 3. The amplitude of these fluctuations varied inversely with respiratory frequency being less than 1.5 mmHg Pa, CO2 in the range of normal respiratory frequencies in the cat, 25--35 min-1. The amplitude also varied with the mixed venous-to-end tidal CO2 difference which was altered either by giving the cat CO2 to inhale or infusing CO2 intravenously. 4. We have concluded that these fluctuations of Pa, CO2 are unlikely to provide a significant drive to ventilation at normal respiratory frequencies but they may provide a signal that gas exchange in the lung is less than optimal.

Animals↗
PubMed1980

Changes in partial pressure of carbon dioxide with time in carotid arterial blood in cats.

1. A rapidly responding CO2 sensor and cuvette were placed in the carotid artery of anaesthetized cats and changes of PCO2 in post-pulmonary capillary blood were recorded when flow through the cuvette was suddenly stopped. 2. Under control conditions when the cats breathed spontaneously or were ventilated artificially, stop-flow caused Pa, CO2 to decay by 2--5 mmHg reaching a new equilibrium in 10--15 sec. The amount by which CO2 decayed was reduced by the inhalation of high O2. The decay was enhanced by hypoxia, the inhalation or infusion of CO2. It was reversed by the administration of acetazolamide: now with stop-flow, Pa, CO2 rose by 8--15 mmHg. 3. the mechanism of this decay is uncertain. We propose that it is due to the transfer of CO2 from plasma to red cells in post-capillary blood in response to the reduction of [H+]i as H+ binds to Hb following the oxylabile release of CO2 from Hb.

Acetazolamide↗
PubMed1978

Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat.

1. Respiratory responses were measured in forty-seven cats, made decerebrate or anaesthetized with pentobarbitone or chloralose-urethane, to changes in the level of CO(2) infused into the inferior vena cava via an external oxygenator circuit or to changes in the volume of venous return or to the inhalation of CO(2).2. No consistent difference was found between the respiratory response to the increase in the level of CO(2) infused or CO(2) inhaled provided that the volume of venous return during both sets of tests was held constant at normal levels.3. If the volume of venous return was increased and the level of CO(2) infused maintained at levels such that V(CO2) did not increase, ventilation increased with a fall in P(a, CO2), a response lying approximately on the isometabolic curve.4. If the volume of venous return and the level of CO(2) infusion were raised together, a spectrum of intermediate respiratory responses was obtained which reproduced all those seen in earlier papers, in muscular exercise or other hypermetabolic states.5. None of the steady-state respiratory responses was significantly affected by bilateral vagotomy or section of the sinus nerves, though sinus nerve section slowed the responses to infused or inhaled CO(2) and they were then less precisely controlled.6. Additional experiments indicated that where CO(2) was infused or inhaled, the effective stimulus to respiration was an increase in mean P(a, CO2) in proportion to the CO(2) added and that the respiratory response to CO(2) was enhanced by reduced blood volume. How the changes in venous return were sensed and affected respiration, remains unclear.7. These results may explain why previous workers have obtained exaggerated respiratory responses to the infusion of CO(2) and why respiration increases rapidly at the start of exercise and is then maintained at high levels without discernible change in the chemical stimulus in arterial blood.

Animals↗