| 1. |
- Borg, T, et al.
(författare)
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Complement activation and its relationship to adult respiratory distress syndrome. An experimental study in pigs.
- 1984
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Ingår i: Acta Anaesthesiologica Scandinavica. - 0001-5172 .- 1399-6576. ; 28:2, s. 158-65
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Tidskriftsartikel (refereegranskat)abstract
- Pulmonary leucostasis induced by complement activation has been considered an important pathogenic factor in adult respiratory distress syndrome (ARDS). To determine whether complement activation per se could evoke pulmonary dysfunction similar to ARDS, pigs were repeatedly infused with complement-activated plasma (CAP). Complement activation was produced by incubation of plasma with zymosan. Three groups of animals were investigated. Control animals received non-activated plasma. Nine animals (Group II) were given four infusions of CAP at a rate of 7 ml X min-1, and another nine animals (Group III) received two CAP infusions at a rate of 7 ml X min-1 followed by two at a rate of 14 ml X min-1. In the control animals there were no changes in gas exchange or haemodynamic variables and the leucocyte counts gradually increased. Infusion of CAP resulted in transient peripheral leucopenia and a dose-rate-dependent reversible increase in pulmonary vascular resistance in all animals. In one animal of Group II and in six of Group III there was a significant infusion-related decrease in Pao2 due to increased venous admixture. These animals were characterized by an enhanced pulmonary vascular tone before the start of the first CAP infusion. They also displayed a more pronounced pulmonary vascular response to infusion of CAP. The changes in gas exchange variables and pulmonary haemodynamics showed no relation to the degree of leucopenia or decrease in platelet count. The increased venous admixture was caused by "dry" ventilation/perfusion mismatching and not by oedema. These results suggest that additional factors besides complement activation and pulmonary leucostasis are required for the development of increased microvascular permeability and the pulmonary oedema characterizing ARDS.
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| 2. |
- Bålfors, E., et al.
(författare)
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Droperidol inhibits the effects of intravenous ketamine on central hemodynamics and myocardial oxygen consumption in patients with generalized atherosclerotic disease
- 1983
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Ingår i: Anesth Analg. ; 62:2, s. 193-7
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Tidskriftsartikel (refereegranskat)abstract
- A 2-mg/kg dose of ketamine was administered intravenously to 16 patients with generalized atherosclerotic disease. Eight patients were given 200 mu/kg of droperidol intravenously 10 min before ketamine administration; eight patients not given droperidol served as controls. Central hemodynamics, coronary flow (thermodilution technique) and myocardial oxygen, lactate, hypoxanthine, and catecholamine balances were studied. In control patients, ketamine increased mean blood pressure by 42%, pulmonary capillary wedge pressure by 144%, mean right atrial pressure by 60%, heart rate by 15%, and systemic vascular resistance by 40% without changes in cardiac index, stroke volume index, or left ventricular stroke work index. These data indicate that cardiac performance did not increase in parallel with the rise in afterload. However, the 50% increase in myocardial oxygen demand was associated with a 48% increase in coronary blood flow without changes in coronary vascular resistance or myocardial oxygen extraction. Augmented sympathetic activity was manifested by 397% and 164% increases in plasma levels of epinephrine and norepinephrine, respectively. The hemodynamic and cardiometabolic effects of ketamine were abolished when patients were pretreated with droperidol. The increase in plasma epinephrine levels was likewise inhibited by droperidol; significantly lower plasma norepinephrine levels also were observed. These findings suggest that droperidol inhibits the cardiovascular effects of ketamine by a centrally mediated reduction in sympathetic activity and by peripheral alpha receptor blockade.
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| 3. |
- Reiz, S., et al.
(författare)
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Beta-blockers and thoracic epidural analgesia. Cardioprotective and synergistic effects
- 1982
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Ingår i: Acta Anaesthesiol Scand Suppl. ; 76, s. 54-61
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Tidskriftsartikel (refereegranskat)abstract
- Seven groups of patients with and without hypertension or with ischaemic heart disease, treated with different beta blockers were investigated to study the circulatory effects of neurolept anaesthesia alone or combined with thoracic epidural analgesia from T4 to T12/L2 during abdominal surgery. The combination of thoracic epidural analgesia and neurolept anaesthesia in hypertensive subjects treated with non-cardioselective beta blockers induced slightly lower blood pressure than measured in similar patients on cardioselective beta blockers with neurolept anaesthesia only. Patients on non-selective beta blockers with intrinsic stimulatory activity (ISA) had higher blood pressure and heart rate after neurolept anaesthesia induction than patients on cardioselective blockers. During surgery, heart rate remained at a higher level in the patients treated with ISA blockers, whereas blood pressure increased to the same level as in patients with cardioselective blockers. Cardiovascular stability was, however, best maintained in the epidural group, where myocardial energy expenditure during maximal surgical stress was comparable to that in a group of healthy subjects with the same format of anaesthesia and significantly lower than in healthy subjects with neurolept anaesthesia alone. No circulatory side effects of the combination of thoracic epidural analgesia and beta blockade were seen. In patients with ischaemic heart disease, with or without non-selective beta blockade, similar haemodynamic changes were recorded following neurolept anaesthesia. During maximal surgical stress, unmasking of alpha adrenergic activity with marked rise in blood pressure was seen in the beta-blocked patients. Despite the more accelerated haemodynamic changes in the blocked patients, a lower increase in myocardial oxygen consumption was recorded compared with the non-blocked patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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| 4. |
- Rydvall, A., et al.
(författare)
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Effects of enflurane on coronary haemodynamics in patients with ischaemic heart disease
- 1984
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Ingår i: Acta Anaesthesiol Scand. ; 28:6, s. 690-5
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Tidskriftsartikel (refereegranskat)abstract
- The effects of enflurane with and without nitrous oxide on coronary haemodynamics and myocardial oxygenation were investigated in 11 patients with generalised atherosclerotic disease. Enflurane decreased systemic blood pressure (-50%) mainly by systemic vasodilation (SVR -41%) and to a lesser degree by impairment of cardiac performance (CO -27%). A change from 1MAC enflurane-nitrogen-oxygen (70/30) to 1MAC enflurane-nitrous oxide-oxygen (70/30) decreased blood pressure and cardiac output further (-16% and -14%). Enflurane-nitrogen-oxygen decreased coronary blood flow (-29%) and perfusion pressure (-47%). Coronary vascular resistance fell (-20%) along with decreases in myocardial oxygen consumption and extraction (-40% and -16%). Regional coronary blood flow measurements in four of the patients revealed maldistribution of blood flow. During enflurane-nitrous oxide-oxygen, myocardial oxygen consumption and extraction decreased further (-29% and -12%) without change in coronary blood flow or resistance. Myocardial ischaemia was observed in four patients during enflurane-nitrogen. During enflurane-nitrous oxide, ischaemia disappeared in two of the previously ischaemic patients and appeared in two not previously ischaemic. The regional blood flow maldistribution was abolished with nitrous oxide. It is concluded that enflurane is a powerful coronary vasodilator and in this respect slightly less potent than isoflurane. Enflurane may induce myocardial ischaemia by redistributing coronary blood flow and/or by producing hypotension. Nitrous oxide added to enflurane depresses cardiac function and augments the coronary vasodilatory effect of enflurane to a level at which coronary blood flow becomes totally pressure dependent.
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| 5. |
- Smith, Maj‐Lis ‐L, et al.
(författare)
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Models for studying long‐term recovery following forebrain ischemia in the rat. 2. A 2‐vessel occlusion model
- 1984
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Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 69:6, s. 385-401
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Forskningsöversikt (refereegranskat)abstract
- ABSTRACT— A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long‐term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near‐zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory‐evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near‐complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.
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| 6. |
- Werner, Olof, et al.
(författare)
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Carbon dioxide elimination from each lung during endobronchial anaesthesia. Effects of posture and pulmonary arterial pressure
- 1984
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Ingår i: British Journal of Anaesthesia. - 1471-6771. ; 56:9, s. 995-1001
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Tidskriftsartikel (refereegranskat)abstract
- The ventilation and carbon dioxide elimination of each lung, and pulmonary arterial pressure, were studied in 17 patients during the early phases of anaesthesia for pulmonary surgery. The patients were ventilated mechanically to moderate hypocapnia. Expired tidal volume and carbon dioxide elimination rate of the lung to be operated on, and of the other lung, were similar in the supine position. There was a significant (P less than 0.01) increase in ventilation and a decrease in end-tidal PCO2 of the upper lung after turning the patient on to the side. Simultaneously, the physiological deadspace fraction of tidal volume (VD/VT) increased from 42 to 45% (P less than 0.05). Mean pulmonary arterial pressure (MPAP) increased slightly as surgery on the chest wall commenced. A concomitant increase of carbon dioxide elimination from the upper lung occurred also, although the distribution of ventilation, between the lungs, was unchanged in comparison with the conditions during undisturbed anaesthesia. Individual changes in MPAP (delta MPAP) and corresponding changes in VD/VT (delta (VD/VT)) were negatively correlated (r = -0.68, P less than 0.01). The regression equation was delta (VD/VT) (%) = 0.7 - 0.83 X delta MPAP (mmHg). It was concluded that variations in pulmonary arterial pressure during surgical stimulation may significantly affect the pattern of carbon dioxide elimination in the lungs. However, there was no evidence that these effects were important clinically.
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| 7. |
- Werner, Olof, et al.
(författare)
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Gas exchange and haemodynamics during thoracotomy
- 1984
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Ingår i: British Journal of Anaesthesia. - 1471-6771. ; 56:12, s. 1343-1350
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Tidskriftsartikel (refereegranskat)abstract
- Cardiac index, systemic and pulmonary arterial pressures, carbon dioxide elimination and ventilation of each lung were studied during thoracotomy. Seventeen patients, placed in the full lateral position, were ventilated mechanically through a Carlens' tube to moderate hypocapnia. Mean cardiac index increased by 12% as the pleura was opened (P less than 0.05), with no further change during surgery on the still ventilated upper lung. Mean arterial pressure was unchanged after opening the pleura, but decreased from 114 +/- 15 mm Hg (mean +/- 1 SD) to 104 +/- 18 mm Hg during surgery on the lung (P less than 0.01). Mean pulmonary artery pressure was unchanged. There was a significant (P less than 0.01) increase in carbon dioxide elimination from the upper lung when the pleura was opened. In addition, the ventilation of this lung increased significantly (P less than 0.05). Mean end-tidal PCO2 of the lower lung increased from 4.1 to 4.2 kPa after opening the pleura, while that of the upper lung increased from 3.0 to 3.6 kPa (P less than 0.01). VD/VT decreased from 43 to 38% as the pleura was opened (P less than 0.01). During surgical handling of the lung, marked decreases in ventilation, compliance, carbon dioxide elimination and end-tidal PCO2 were observed in the upper lung. We conclude that ventilation-perfusion mismatch decreased on opening the pleura, and that neither opening the pleura nor the subsequent lung surgery (both lungs being ventilated) caused any clinically important derangements in haemodynamics or oxygenation.
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