Open tube drainage of empyema thoracis.
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Drainage↗
Biomedical subjects
M V Braimbridge
Publications and source records attributed to M V Braimbridge.
Malignant nerve sheath tumour arising in a ganglioneuroma.
A malignant nerve sheath tumour arising within a thoracic ganglioneuroma is described. This is only the seventh such case described in the literature and the first at this site. The previously documented cases are reviewed.
Adult↗
Ischemia- and reperfusion-induced arrhythmias in conscious rats--studies with prazosin and atenolol.
A conscious rat system has been developed to investigate the ability of alpha- and beta-adrenoceptor blocking agents to modify the severity of ischemia- and reperfusion-induced arrhythmias. Ischemia-induced arrhythmias were studied during a 30 min period of occlusion of the left anterior descending (LAD) coronary artery, and 100% of control animals (n = 24) exhibited ventricular tachycardia and 63% ventricular fibrillation. Beta-adrenoceptor blockade with atenolol (1 mg/kg body weight) significantly reduced the incidence of ventricular fibrillation to 17% (p less than 0.05). In contrast, alpha-adrenoceptor blockade with prazosin (0.01, 0.1 or 1 mg/kg body weight) failed to reduce the incidence of arrhythmias and actually increased mortality. This higher mortality with prazosin was associated with bradyarrhythmias. Administration of atenolol (1 mg/kg body weight) also reduced the incidence of reperfusion-induced ventricular fibrillation after a 5 min period of ischemia from 100% to 58% (p less than 0.05). Prazosin could not be tested due to the high mortality during coronary occlusion. Autopsy studies of hearts from the control, atenolol and prazosin groups indicated that all groups had similar occluded zone volumes. In conclusion, in conscious rats beta-blockade with atenolol reduced the incidence of both ischemia- and reperfusion-induced arrhythmias, whereas alpha-blockade with prazosin at the 3 doses studied failed to exert a protective effect and actually increased mortality.
Animals↗
Optimal myocardial protection during crystalloid cardioplegia. Interrelationship between volume and duration of infusion.
There is often a large difference between volumes of crystalloid cardioplegic solution used clinically (2 to 4 ml/gm myocardium) and experimentally (in rat heart preparations, volumes of 30 ml/gm or more are used). In an attempt to reconcile these differences and define the minimum volume and/or duration of infusion of the St. Thomas' Hospital cardioplegic solution consistent with maximal myocardial protection, we have used the isolated working rat heart to characterize the relationships between myocardial protection and (1) the duration of cardioplegic infusion and (2) the volume of cardioplegic infusion. Hearts (n = 6 per group, weighing 0.90 +/- 0.06 gm) were subjected to 0, 5, 10, 15, 30, 45, 60, 120, 180, 240, or 300 seconds of cardioplegic infusion (mean infusion volumes = 0, 1.3 +/- 0.1, 2.0 +/- 0.1, 2.8 +/- 0.2, 5.0 +/- 0.1, 8.3 +/- 0.2, 10.5 +/- 0.8, 21.8 +/- 2.1, 22.7 +/- 1.3, 32.3 +/- 2.1, and 39.1 +/- 1.8 ml per heart, respectively) before 30 minutes of normothermic ischemia. They recovered 3.9% +/- 2.3%, 9.7% +/- 5.0%, 22.8% +/- 5.8%, 34.6% +/- 4.6%, 54.7% +/- 6.6%, 64.0% +/- 5.0%, 67.4% +/- 4.0%, 56.6% +/- 11.1%, 60.0% +/- 5.8%, 51.6% +/- 7.0%, and 68.0% +/- 7.8% of their preischemic cardiac output on reperfusion. Creatine kinase leakage, tissue adenosine triphosphate and creatine phosphate content, and other indices of cardiac function supported this observation. To assess volume of infusion rather than duration, we infused hearts (n = 6 per group) with 1.0, 1.5, or 2.0 ml of cardioplegic solution over 120 seconds. Although recovery of cardiac output with 2.0 ml (56.2% +/- 6.8%) was not significantly different from that (56.6% +/- 11.1%) observed with large volumes of solution (21.9 +/- 2.1 ml), infusion of 1.5 and 1.0 ml resulted in poor recovery of cardiac output (40.1% +/- 4.6% and 21.8% +/- 3.9%, respectively). To assess duration (with low volumes) rather than volume of infusion, we infused hearts (n = 6 per group) with 2.0 ml of cardioplegic solution over 10, 30, 60, or 120 seconds. Maximal protection was observed with 30, 60, and 120 seconds of infusion (recovery of cardiac output = 56.7% +/- 5.9%, 45.1% +/- 7.9%, and 56.2% +/- 6.8%, respectively). Our results suggest that, for maximum myocardial protection, the St. Thomas' Hospital solution should be infused at a rate of not less than 2.0 ml/gm wet weight of heart and that the duration of infusion should be not less than 30 seconds.
Animals↗
Improved myocardial protection by oxygenation of St. Thomas' Hospital cardioplegic solutions. Studies in the rat.
The effect of oxygenation (100% oxygen) of the St. Thomas' Hospital cardioplegic solutions No. 1 (MacCarthy) and No.2 (Plegisol, Abbott Laboratories, North Chicago, Ill.) was examined in the isolated working rat heart subjected to long periods (3 hours for studies with solution No. 1 and 4 hours for studies with solution No. 2) of hypothermic (20 degrees C) ischemic arrest with multidose (every 30 minutes) cardioplegic infusion. At the aortic infusion point the oxygen tension of the oxygenated solutions (measured at 20 degrees C) was in the range of 320 to 560 mm Hg whereas that of the nonoxygenated solutions was less than 150 mm Hg. Twenty hearts (10 oxygenated and 10 nonoxygenated) were studied for each solution. The studies with solution No. 1 demonstrated that oxygenation led to a significant (p less than 0.05) reduction in the incidence of persistent ventricular fibrillation during postischemic reperfusion. Oxygenation of the cardioplegic solution also improved postischemic functional recovery so that the recovery of aortic flow was improved from 18.7% +/- 8.9% (of its preischemic control level) in the nonoxygenated group to 54.6% +/- 6.6% in the oxygenated group (p less than 0.025). Creatine kinase leakage was also significantly reduced from 27.5 +/- 4.8 to 9.9 +/- 0.6 IU/15 min/gm dry weight (p less than 0.005). Studies with solution No. 2 indicated that protection was better than with solution No. 1, even in the absence of oxygenation. A better degree of functional recovery was obtained after 4 hours of arrest with solution No. 2 than that obtained after only 3 hours of arrest with solution No. 1, and persistent ventricular ventricular fibrillation was never observed with solution No. 2. However, despite the superior performance with solution No. 2, further improvements could be obtained by oxygenation, with that time from the onset of reperfusion to the return of regular sinus rhythm being reduced from 55 +/- 8 to 35 +/- 2 seconds (p less than 0.01), postischemic recovery of aortic flow increasing from 59.8% +/- 7.4% to 85.7% +/- 2.5% (p less than 0.005), and creatine kinase leakage being reduced from 38.1 +/- 7.3 to 16.2 +/- 1.5 IU/15 min/gm dry weight (p less than 0.005). It is concluded that oxygenation of the St. Thomas' Hospital cardioplegic solutions improves their ability to protect the heart against long periods of ischemia and that this is manifested by improved postischemic electrical stability, functional recovery, and reduced creatine kinase leakage.
Animals↗
Free radicals and cardioplegia: the absence of an additive effect with allopurinol pretreatment and the use of antioxidant enzymes in the rat.
The isolated perfused working rat heart model of cardiopulmonary bypass was used to assess whether (a) allopurinol pretreatment enhances resistance to normothermic (30 min) or hypothermic (4 h) ischemia; (b) addition of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) to cardioplegic and/or reperfusion solutions are protective; (c) any protective effects are additive. With normothermic ischemia, allopurinol pretreatment improved recovery of aortic flow from its control value of 25 +/- 3% to 48 +/- 6% (P less than 0.05). Similarly, SOD plus CAT used during both ischemia and reperfusion improved recovery of aortic flow from a control value of 28 +/- 4% to 48 +/- 6% (P less than 0.05). However, various combinations of the two types of intervention afforded no additive protection. Under hypothermic (21 degrees C) conditions, allopurinol pretreatment was not effective, whereas SOD and CAT added during ischemia and reperfusion improved recovery of aortic flow from its control value of 53 +/- 4% to 69 +/- 5% (P less than 0.05). This value was similar to allopurinol pretreatment and SOD plus CAT added during ischemia and reperfusion (69 +/- 6%: P less than 0.05). These results provide further evidence that reperfusion-induced free radical formation may adversely affect postischemic recovery of function. The absence of an additive effect suggests a common mechanism of action, which is likely to involve the free radical-generating enzyme xanthine oxidase; however, other mechanisms may exist. Our results further support the use of antifree radical intervention in conjunction with cardioplegia to protect the heart during ischemia and reperfusion.
Allopurinol↗
Free radicals and cardioplegia: allopurinol and oxypurinol reduce myocardial injury following ischemic arrest.
Oxygen-derived free radicals generated by xanthine oxidase may represent a major cause of myocardial injury during ischemia and reperfusion. We have used the isolated working rat heart model of cardiopulmonary bypass and ischemic arrest to assess whether allopurinol or oxypurinol, which should prevent free radical formation through their ability to inhibit xanthine oxidase, can improve postischemic myocardial recovery when the drugs are administered either chronically (pretreatment) or acutely (as an addition to the cardioplegic or reperfusion solution). With normothermic ischemic arrest, both drugs, when given either chronically or acutely, significantly improved postischemic recovery of function. However, under hypothermic conditions, allopurinol conferred no protection when given either as pretreatment or during reperfusion, but it was effective when added to the cardioplegic solution. When administered under the appropriate conditions, both allopurinol and oxypurinol enhanced the protective effect afforded by the St. Thomas' Hospital cardioplegic solution, possibly by inhibiting xanthine oxidase activity and preventing the formation of oxygen-derived free radicals.
Allopurinol↗
Free radicals and cardioplegia. Free radical scavengers improve postischemic function of rat myocardium.
Oxygen-derived free radicals, such as the superoxide (O2-) anion, hydrogen peroxide (H2O2) and the hydroxyl (OH.) radical, may be involved in exacerbating myocardial injury during reoxygenation of ischemic tissue. The naturally occurring antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), prevent the formation of the cytotoxic OH. radical during physiological conditions but may not be able to cope with the free radical generation that follows ischemia and reperfusion. We have used the isolated perfused working rat heart model of cardiopulmonary bypass and ischemic arrest to assess whether exogenous addition of SOD (20 IU/ml) and CAT (100 IU/ml) during ischemia and/or reperfusion can improve postischemic recovery of function following normothermic or hypothermic global ischemic arrest induced by St. Thomas' Hospital cardioplegic solution. Under conditions of normothermia, the addition of SOD alone or CAT alone to both the cardioplegic solution (CS) and the reperfusion solution (RS) had no effect on postischemic recovery (after 20-min working reperfusion) of aortic flow (27.9 +/- 2.7% and 16.1 +/- 6.3%, respectively) when compared with the nontreated control value of 28.1 +/- 3.7%. However, recovery was improved when SOD plus CAT were added to the CS alone (39.3 +/- 8.7%) and was significantly improved when they were added either to both the CS and the RS (48.4 +/- 6.0%; P = less than 0.02) or to the RS alone (51.3 +/- 3.7%; P = less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Prosthetic valve endocarditis.
About 2% of patients with a prosthetic valve will develop endocarditis. This may occur within a few weeks of the valve replacement operation (early) or many months or years later (late). The infecting organisms, pathogenicity and prognosis differ in the two groups. The incidence of early prosthetic valve endocarditis (PVE) is under 1%; the predominant organisms are staphylococci that are acquired in the operating theatre or in the intensive therapy unit. Early PVE usually follows wound sepsis that may initially appear trivial. The mortality rate is around 70%, but such infections should be preventable by stringent antisepsis, good surgical technique and (perhaps) perioperative antistaphylococcal antibiotics. The incidence of late PVE is about 1% per annum. The infecting organisms are similar to those causing native valve endocarditis, predominantly streptococci. The commonest source of these organisms is the mouth and regular dental care and appropriate prophylactic antibiotics should help to prevent infection. The mortality rate of late PVE is around 10%. Failure of medical treatment in PVE is an indication for surgery to remove the infected valve(s) and this should not be delayed. The optimum length of treatment for PVE is unknown but it is seldom necessary to give antibiotics for more than 6 weeks except in Coxiella burnetii infection.
Adult↗
Long-term survival rates after prolonged aortic cross-clamping with St. Thomas' Hospital cardioplegia.
Prolonged aortic cross-clamping (in excess of 120 min) was necessary in 154 cardiac surgical patients. St. Thomas' Hospital cardioplegia was used for myocardial preservation. Quantitative polarization microscopy enabling quantitative birefringence measurements to assess the change in birefringence of the muscle fibres in response to the addition of buffer containing ATP and calcium (i.e. myocardial contractility) was used to detect whether there had been any deterioration in right or left ventricular myocardium during the bypass period. 30 day survival was 90%, long-term (60 months) survival was 80%. In single valve replacements, patients with aortic valvular replacement had 100% survival up to 92 months, whereas patients with mitral valvular replacement had survival rates of 83% after 12 months and 27% after 60 months. Survival rates after 60 months were 89% for coronary artery bypass grafting, 80% for multiple valve replacements, and 74% for combined valvular and coronary artery bypass grafting surgery. Quantitative birefringence assessment of function showed that in the surviving patients 5% had functional deterioration during bypass whereas in the non-surviving patients 70% had functional deterioration. It may be concluded that after cardiac surgery necessitating prolonged aortic cross-clamping--once the initial operative problems are overcome--reasonable long-term results can be obtained by using St. Thomas' Hospital cardioplegia.
Bicarbonates↗
Myocardial contractile force and catecholamines in patients undergoing open-heart surgery.
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Cardiac Surgical Procedures↗
Protection of the pediatric myocardium. Differential susceptibility to ischemic injury of the neonatal rat heart.
Myocardial protection during pediatric cardiac operations has been suggested to be less successful than in adult hearts. In the present study we have compared the resistance of adult, infant, and neonatal rat hearts to various periods of ischemic arrest with normothermic (37 degrees C) crystalloid cardioplegia. Isolated hearts with intraventricular balloons, from adult (50 to 60 days of age, heart weight 865 +/- 13 mg), infant (20 to 25 days of age, heart weight 251 +/- 3 mg), and neonatal rats (3 to 5 days of age, heart weight 40 +/- 1 mg) were subjected to 10, 20, 30, 40, 50, 60, 80, and 100 minutes of ischemia (n = 6 hearts for each time point and for each age group). St. Thomas' Hospital cardioplegic solution was infused at the onset of the period of arrest. With increasing durations of ischemia there was a declining postischemic recovery of function. Up to 40 minutes of ischemia there was no significant difference between the three age groups in postischemic recovery of left ventricular developed pressure: 40.3% +/- 4.4%, 45.4% +/- 6.5%, and 44.4% +/- 2.2% of preischemic control for adult, infant, and neonatal hearts, respectively. Beyond 40 minutes adult and infant hearts showed an identical deterioration with effectively no recovery beyond 60 minutes of ischemia. By contrast, neonatal hearts were much more resistant to ischemia. After 100 minutes of ischemia the mean recovery of left ventricular developed pressure was 20.9% +/- 1.1%, whereas in infant and adult hearts the values were 0.6% +/- 0.3% after 80 minutes of ischemia and 0% after 100 minutes, respectively. Analysis of creatine kinase leakage also indicated that with ischemic durations in excess of 40 minutes, the neonatal heart was far more resistant to ischemia, and creatine kinase leakage per gram dry weight was much less than in infant or adult rats. Analysis of the rates of recovery during reperfusion again revealed differences between neonatal hearts and hearts from the other two age groups. We conclude that in the normal rat the neonatal heart has a greater inherent tolerance to ischemia than that of the infant or adult rat.
Animals↗
The St. Thomas' Hospital cardioplegic solution. A comparison of the efficacy of two formulations.
Two commercially available formulations of St. Thomas' Hospital cardioplegic solutions, known as No. 1 (MacCarthy) and No. 2 (Plegisol, Abbott Laboratories, North Chicago, Ill.), were compared in the isolated working rat heart subjected to a long period (3 hours) of hypothermic ischemic arrest with multidose infusion. Solution No. 2 was found to be superior in nearly all respects. Of the 10 hearts infused with solution No. 1, persistent ventricular fibrillation during postischemic reperfusion occurred in six. Two of the six hearts, still in fibrillation after 15 minutes of reperfusion, were returned to regular rhythm by electrical defibrillation but failed to maintain an output. In contrast, in the 10 hearts infused with solution No. 2, ventricular fibrillation was short lasting (p less than 0.01). In comparing mechanical function in all hearts returning to regular rhythm (either spontaneously or after electrical defibrillation), the mean postischemic recoveries for aortic flow and rate of rise of left ventricular pressure (expressed as a percentage of its preischemic control) were significantly greater with solution No. 2 than with solution No. 1 (74.3% +/- 6.9% compared with 18.7% +/- 8.9%, p less than 0.01, and 98.0% +/- 6.0% compared with 63.0% +/- 9.0%, p less than 0.005, respectively). Creatine kinase leakage tended to be lower in hearts infused with solution No. 2 (19.7 +/- 4.7 IU/15 min/gm dry weight as opposed to 27.5 +/- 4.7 IU/15 min/gm dry weight), although this difference did not achieve a level of statistical significance. Consideration is given to the differences in formulation between solutions, which might account for the improved performance with solution No. 2, and it is concluded that the lower calcium content of solution No. 2 (1.2 as opposed to 2.4 mmol/L) is likely to be the most important factor.
Animals↗
Enhanced myocardial protection with high-energy phosphates in St. Thomas' Hospital cardioplegic solution. Synergism of adenosine triphosphate and creatine phosphate.
The potential for improving myocardial protection with the high-energy phosphates adenosine triphosphate and creatine phosphate was evaluated by adding them to the St. Thomas' Hospital cardioplegic solution in the isolated, working rat heart model of cardiopulmonary bypass and ischemic arrest. Dose-response studies with an adenosine triphosphate range of 0.05 to 10.0 mmol/L showed 0.1 mmol/L to be the optimal concentration for recovery of aortic flow and cardiac output after 40 minutes of normothermic (37 degrees C) ischemic arrest (from 24.1% +/- 4.4% and 35.9% +/- 4.1% in the unmodified cardioplegia group to 62.6% +/- 4.7% and 71.0% +/- 3.0%, respectively, p less than 0.001). Adenosine triphosphate at its optimal concentration (0.1 mmol/L) also reduced creatine kinase leakage by 39% (p less than 0.001). Postischemic arrhythmias were also significantly reduced, which obviated the need for electrical defibrillation and reduced the time to return of regular rhythm from 7.9 +/- 2.0 minutes in the control group to 3.5 +/- 0.4 minutes in the adenosine triphosphate group. Under more clinically relevant conditions of hypothermic ischemia (20 degrees C, 270 minutes) with multidose (every 30 minutes) cardioplegia, adenosine triphosphate addition improved postischemic recovery of aortic flow and cardiac output from control values of 26.8% +/- 8.4% and 35.4% +/- 6.3% to 58.0% +/- 4.7% and 64.4% +/- 3.7% (p less than 0.01), respectively, and creatine kinase leakage was significantly reduced. Parallel hypothermic ischemia studies (270 minutes, 20 degrees C) using the previously demonstrated optimal creatinine phosphate concentration (10.0 mmol/L) gave nearly identical improvements in recovery and enzyme leakage. The combination of the optimal concentrations of adenosine triphosphate and creatine phosphate resulted in even greater myocardial protection; aortic flow and cardiac output improved from their control values of 26.8% +/- 8.4% and 35.4% +/- 6.3% to 79.7% +/- 1.1 and 80.7% +/- 1.0% (p less than 0.001), respectively. In conclusion, both extracellular adenosine triphosphate and creatine phosphate alone markedly improve the cardioprotective properties of the St. Thomas' Hospital cardioplegic solution during prolonged hypothermic ischemic arrest, but together they act additively to provide even greater protection.
Adenosine Triphosphate↗
Particle-induced coronary vasoconstriction in the rat heart: pharmacological investigation of underlying mechanisms.
An isolated perfused rat heart preparation has been used in an attempt to define the mechanisms underlying the coronary vasoconstriction associated with the intraarterial infusion of cardioplegic solutions containing contaminant particles. Coronary infusion of commercially available intravenous solutions, compounded to create the St. Thomas' cardioplegic solution, resulted in a 40.3 +/- 1.9% decline in coronary flow rate at the end of a 20-minute period of infusion. Filtration of the solution through a 0.8 micron filter reduced this decline in flow rate to 23.4 +/- 2.3% of its control value. Inclusion of the 5HT2 receptor antagonist ketanserin (1.0 nanomoles/l), in the unfiltered cardioplegic solution, afforded the same protection as filtration. Inclusion of 5HT (0.1 micromole/l) in a filtered cardioplegic solution resulted in a reduction of coronary flow (49.7 +/- 1.9%) greater than that seen with the unfiltered solution. Studies with antagonists of the histamine receptor (mepyramine and cimetidine) and agonists and antagonists of adrenergic receptors suggested that, although involved in the control of vascular tone, these receptor systems are unlikely to be involved in the process of particle-induced vasoconstriction. Arguments are presented that 5 HT and its receptors may play a critical role and the hypothesis is advanced that particle-induced focal endothelial injury may be the primary lesion in a complex sequence of events leading to induction of transient vasoconstriction.
Animals↗
Streptokinase treatment of thrombosed mitral valve prosthesis monitored by Doppler ultrasound.
A case of prosthetic mitral valve thrombosis treated with streptokinase is described. The diagnosis was made and the treatment was monitored using Doppler ultrasound. Doppler may be superior to other non invasive methods for this application because of its ability to grade the dysfunction more accurately and avoid bleeding complications associated with cardiac catheterization.
Adult↗
The management of spontaneous oesophageal perforation by thoracoscopy and irrigation.
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Esophageal Diseases↗
Increased myosin orientation during muscle contraction: a measure of cardiac contractility.
Myosin form birefringence has been studied in cryostat sections of left ventricular myocardium from the dog and human. The muscle in such sections has been shown to demonstrate the sliding filament phenomenon. The sarcomere length of canine myocardium agreed with that found in comparable electron micrographs. Unexpectedly, it was found that glycerol, normally used as an inert and optically ideal mountant, caused profound change in myosin birefringence. This apparently invalidates results obtained with this mountant. The absolute birefringence found in these sections, whether mounted in glycerol or in an ATP-calcium buffer, corresponded to values found by other workers with skeletal muscle and isolated myosin. However, the birefringent properties (optical path difference: o.p.d.) of well functioning muscle was found to be low, the o.p.d. increasing when exposed to ATP and calcium. Poorly functioning muscle could be distinguished from well functioning muscle on the basis of its higher 'in air' o.p.d. This difference correlated well with physiological assessments of myocardial function or with clinical assessments of cardiac failure. Evidence is presented indicating that changes in apparent birefringence, caused by ATP-calcium or by anoxia, are due to altered orientation of the myosin micelles and can be inhibited by agents that inhibit myosin ATPase activity.
Adenosine Triphosphate↗