Images in clinical medicine. Stab wounds to the heart: a useful radiological sign.
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Biomedical subjects
Publications and source records attributed to C Saldanha.
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Sodium fluorescein angiography is a widely used routine ophthalmological diagnostic procedure which enables the study of chorioretinal microcirculation and consists of the injection of sodium fluorescein into the systemic bloodstream. The aim of the present study was to evaluate whether or not fluorescein interferes with erythrocyte properties during the angiographic procedure. In a group of 37 patients, 26 with non-insulin-dependent diabetes mellitus (DM) with and without retinopathy, and 11 without diabetes mellitus (non-DM) although affected by other ophthalmological diseases, all undergoing routine angiography, blood samples were drawn before (T0) and 30 min (T30) after fluorescein injection. The erythrocyte aggregation index (EAI), membrane lipid fluidity and erythrocyte acetylcholinesterase activity were determined in both groups. After fluorescein injection there was no statistical change in EAI and erythrocyte membrane fluidity in either group. Erythrocyte acetylcholinesterase activity, a marker of membrane protein integrity, decreased significantly (p < 0.01) in the DM group. Membrane lipid fluidity did not change with fluorescein injection, however (i) in the DM group erythrocyte membranes became more rigid than in the non-DM (DPH: p < 0.01); (ii) EAI and membrane lipid fluidity became significantly correlated (r = 0.6263, p < 0.05) in non-DM patients at T30. In conclusion, fluorescein administration for angiographic procedures seems to interact with erythrocyte membrane, namely, in diabetic patients, which may interfere with the blood flow in the microcirculation.
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The effects of single- and multi-dose cardioplegia on post-ischaemic vascular function and contractile activity were compared in 69 blood-perfused neonatal pig hearts, as were the protective properties of two different cardioplegic solutions. Hearts (n = 6 or 9 per group) from neonatal (3-5 days old) pigs were excised, arrested with a 2 min infusion (at 15 degrees C) of St Thomas' Hospital cardioplegic solution number 1 (STH1) or number 2 (STH2), and then maintained in a state of hypothermic (15 degrees C) ischaemia for 6 or 8 h. Hearts in the multi-dose groups received cardioplegia every hour (2 min at 15 degrees C). At the end of ischaemia all hearts were reperfused (60 +/- 2 mmHg perfusion pressure) for 40 min with blood from a support pig. Systolic and diastolic functions were assessed with an intraventricular balloon, and endothelial and smooth muscle functions by measuring the response to infusions of defined concentrations of acetylcholine (8, 16 and 32 micrograms/min) and glyceryl trinitrate (40, 80 and 160 micrograms/min). Hearts (n = 9) not subjected to ischaemia were perfused for the same duration to act as aerobic controls. At the end of the perfusion period, hearts were frozen and taken for metabolite analysis. After 8 h ischaemia, the recovery of left ventricular developed pressure was greatest in the multi-dose STH1 and single-dose STH2 groups (113 +/- 6 and 117 +/- 6 mmHg, respectively, v 128 +/- 9 mmHg in aerobic controls, at an end-diastolic pressure of between 3 and 9 mmHg; P = N.S.) and the poorest in the single-dose STH1 group (92 +/- 5 mmHg; P < 0.05 v controls). The recovery of diastolic function was greatest in the multi-dose STH2 group and again poorest in the single-dose STH1 group (left ventricular end-diastolic pressure 1 +/- 2 and 30 +/- 10 mmHg, at a ventricular volume of 3.0 ml, v -1 +/- 1 mmHg in aerobic controls). Vascular responses to acetylcholine and glyceryl trinitrate and the myocardial high-energy phosphates content were better preserved in multi-dose groups and with STH2. Inter-group differences were less when the duration of ischaemia was reduced to 6 h. In conclusion, the neonatal pig heart was best preserved with multi-dose cardioplegia and STH2 was more efficacious than STH1. However, not all indices were optimally protected by multi-dose STH2. Thus, the best protection of systolic function was obtained with multidose STH1 and this was followed by single-dose STH2. Diastolic function was best preserved with multi-dose STH2 as were vascular function and high-energy phosphates.
Although cardioplegic solutions successfully protect myocardial contractile cells against ischemic injury, their effect on the vasculature remains controversial. To address this we used a vascular bed preparation (isolated rat mesentery) that permits the study of vascular function without the coincident changes in contractile status that affect vascular tone (and hence the assessment of vascular function in isolated hearts). Smooth muscle cell contraction was assessed by measurement of the vasoconstrictor response to phenylephrine, and relaxation was assessed by measurement of the vasodilator responses to sodium nitroprusside and the endothelium-dependent relaxant adenosine triphosphate. After characterization of basal vascular function, mesenteries were subjected to normothermic ischemia for 60, 90, 120, 150, and 180 minutes (n = 12 for each time period; 6 preparations were subjected to ischemia alone and 6 to ischemia preceded by a 3-minute infusion of the St. Thomas' Hospital cardioplegic solution). The tissue was then reperfused for 20 minutes and vascular function reassessed. Ischemia alone caused progressive time-dependent deterioration in vasoconstrictor responses (99% +/- 13%, 90% +/- 10%, 63% +/- 6%, 51% +/- 10%, and 27% +/- 4%), endothelium-independent vasodilation (93% +/- 3%, 86% +/- 2%, 78% +/- 5%, 61% +/- 5%, and 38% +/- 9%), and endothelium-dependent vasodilation (93% +/- 3%, 96% +/- 2%, 94% +/- 2%, 87% +/- 7%, and 62% +/- 11%). There were similar time-dependent deteriorations in mesenteries subjected to ischemia coupled with cardioplegic solution that were not significantly different from any of the ischemia-alone groups when matched for ischemic times. Thus, for example, after 180 minutes of ischemia alone, the vasoconstrictor response was 18% +/- 3%, endothelium-independent vasodilation was 44% +/- 7%, and endothelium-dependent vasodilation was 40% +/- 9%. The results demonstrate that under the conditions of this experiment, the St. Thomas' Hospital cardioplegic solution neither protects nor injures the vasculature during an episode of ischemia and reperfusion. However, in studies with 150 minutes of normothermic ischemia, multiple infusions of cardioplegic solution (given every 30 minutes during ischemia) resulted in protection of smooth muscle and endothelial function. Thus, after multiple infusions, vasoconstriction to phenylephrine was 74% +/- 4%, vasodilation to nitroprusside was 81% +/- 6%, and vasodilation to adenosine triphosphate was 89% +/- 5%. In conclusion, when the St. Thomas' Hospital cardioplegic solution is used as a single infusion and coupled with ischemia, the solution fails to protect smooth muscle and endothelial function against ischemic injury, but some protection is obtained when the solution is infused intermittently throughout the ischemic period.
Ischemia and reperfusion may result in injury to one or more of the cellular components of the heart. In addition to damaging myocytes and their contractile capability, ischemia and reperfusion may inflict early and severe injury on the vasculature which, in turn, may further jeopardize the survival of the myocytes. While ischemia is known to cause progressive injury to endothelium and vascular smooth muscle it now appears that reperfusion can inflict additional, possibly severe, injury on the microcirculation which may compromise the return of normal coronary perfusion. This post-ischemic/reperfusion microvascular incompetence ranges from a transient exacerbation of the increase in vascular resistance initiated during ischemia, to a sustained loss of competent capillaries and eventually to the "no reflow" phenomenon which is characterized by the total inability of the affected tissue to be reperfused. Whereas "no reflow" may be of little importance if it occurs in already infarcted tissue, post-ischemic microvascular incompetence in potentially salvable myocardium could be of considerable significance. Evidence is presented that the vascular endothelium, and its ability to regulate coronary vascular tone, play a central and early role in the pathogenesis of myocardial injury. Mechanisms underlying microvascular injury have been identified and pharmacological strategies now exist for the effective manipulation of this injury--a prospect that is of considerable importance in the light of the widespread use of thrombolytic procedures for the reperfusion of the human myocardium.
The aim of this work was to evaluate a possible correlation between erythrocyte acetylcholinesterase activity (AChE) and membrane fluidity expressed by fluorescence polarization of--1,6--diphenyl 1,3,5--hexatriene (DPH). Blood samples of 34 Alzheimer's patients (18F and 16M) were obtained and haemoglobin concentration, haematocrit, plasma (butyrylcholinesterase, BuChE) and erythrocyte (AChE) esterase activities and fluorescence polarization after introduction of DPH in erythrocyte membrane have been determined. Results were compared with values obtained from blood samples of 34 apparently healthy volunteers with the same age variation (53-82 years). There was no correlation between AChE activity and fluorescence polarization in the control group nor in the patients' group. There was a significant negative correlation (r = -0.82; p < 0.001) between mean corpuscular hemoglobin concentration (MCHG) and erythrocyte acetylcholinesterase activity in Alzheimer's patients. This correlation suggests that any variation of internal globular viscosity (or MCHG) may indirectly affect AChE enzymatic activity and consequently contribute to the loss of interrelation between AChE activity and membrane lipid fluidity, verified in the present work. A biological marker for Alzheimer's disease diagnosis remains to be discovered.
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Using the isolated, Langendorff-perfused rat heart (n = 8 per group), we have studied the effects of 5-hydroxytryptamine and papaverine on coronary flow before and after a 30-minute infusion of hypothermic (20 degrees C), nonoxygenated cardioplegic solution containing potassium in a concentration of either 25 or 40 mmol/L. Before infusion of the 25 mmol/L potassium cardioplegic solution, both 5-hydroxytryptamine (1 x 10(-7) mol/L) and papaverine (5 x 10(-6) mol/L) caused similar increases in flow (+21.2% +/- 1.6% and +22.8% +/- 1.6%, respectively). After cardioplegia, the vasodilatory response to 5-hydroxytryptamine was completely lost and a slight vasoconstriction was observed (-0.2% +/- 1.2%). However, there was no significant change in the response to papaverine, which maintained a +23.7% +/- 1.4% vasodilation. With the cardioplegic solution containing a 40 mmol/L concentration of potassium, the initial responses to 5-hydroxytryptamine and papaverine were again similar (+21.5% +/- 2.5% and +24.1% +/- 3.0%, respectively). After cardioplegia, 5-hydroxytryptamine caused a significant vasoconstriction (-4.3% +/- 1.1%), whereas the response to papaverine was again maintained (+19.1% +/- 2.3%). The results of this study support the concept that hyperkalemic crystalloid cardioplegic solutions cause vascular damage possibly involving the endothelium or its function, which may adversely affect vascular responsiveness.
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Two selected cases of retinal vasculitis, apparently of unknown aetiology, are reported; one case without any systemic or laboratory manifestation and the second case with a clinical picture similar to VKH syndrome and immunodepression. Both cases showed abnormal haematological parameters related to blood viscosity in the early and acute phases which could be manipulated by therapy. Reduction or near normalisation of these haemorrheological parameters coincided with clinical and angiographic improvement. The second case with severe immunodepression was found to be retrovirus HIV-2 positive.
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.
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The authors report the results obtained in the necropsic study of nine cases of the so-called acute, visceral form of Hodgkin's disease (HD). Most of the patients (six men and three women, ranging from 42 to 74 years of age) lacked peripheral lymphadenopathies and had fever, weight loss, abnormality of hepatic function, and pancytopenia. Mixed cellularity was diagnosed in two, diffuse fibrosis in four, and reticular subtype of lymphocyte depletion in three cases. Despite the predominant infradiaphragmatic involvement, supradiaphragmatic lymph nodes were involved in six and tonsils in three cases. Spleen and bone marrow were involved in eight cases and the liver was involved in seven cases. In four cases there were also lesions in other extralymphoid organs. The involvement of the bone marrow was widespread and showed concurrent myelofibrosis and/or other signs of hematopoietic disturbance. There was a close relationship between the presence of vascular invasion (seven cases) and the extent of HD spread. It is concluded that despite its peculiarity, this form of HD fits the classic model of unicentric origin, lymphogenic contiguous spread, and hematogeneous dissemination, and should not be identified with any particular histologic type of HD.
Selected medical students for undergraduate medical courses in Portugal exhibit each year substantial deficiencies in chemistry. The group of students admitted to the Faculty of Medicine of Lisbon in 1989/1990 were selected by admission criteria apparently more restrictive than before. The aim of this study was to evaluate the quality of the theoretical knowledge in chemistry showed by those students before learning biochemistry. Eight-four of the admitted students were invited to participate in the study, by replying to an anonymous questionnaire on chemistry. A second questionnaire to identify a variety of personal/social factors was completed by the same students some days later. The results obtained have confirmed a clearly insufficient chemical background, in spite of the high scores achieved by those students in chemistry and other science subjects on the application. The majority of the students here studied declared financial security, live with their families, study at home, and report scarce outside distractions. It may be concluded that the new admission criteria to the faculties of medicine do not select students with better academic performances on chemistry than before. Otherwise, the sociocultural characteristics of the entrants do not fulfill the expectations that could contrast them clearly with average groups of students.
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Joint pain and tenderness increased significantly during metyrapone tests in 21 patients with rheumatoid arthritis who had never received corticosteroid therapy and who had no evidence of endocrine disease. This observation implies that the normal circulating plasma corticol exerts an anti-inflammatory effect.