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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased microvascular permeability, which occurs in conditions such as the adult respiratory distress syndrome and diabetes mellitus, is related to physicochemical alterations in the microvascular barrier. We postulate that, in part, capillary pericytes affect microvascular permeability via production of a vasoactive cytokine, viz, vascular endothelial growth factor (VEGF), also known as vascular permeability factor. The goal of the present study was to evaluate the effects of phorbol myristate acetate (PMA), a substance known to produce nonhydrostatic pulmonary edema in intact animals, on VEGF gene expression in pericyte cultures. Microvascular pericytes were isolated from bovine retinas using magnetic microspheres coated with 3G5 monoclonal antibody. Pericyte identity was confirmed both morphologically and by immunostaining for alpha-smooth muscle actin and 3G5 ganglioside. The cultured pericytes were stimulated with N(omega)-nitro-L-arginine methyl ester (L-NAME, 1 x 10(-4) mmol/L), angiotensin II (1 x 10(-6) mmol/L), and PMA (5 x 10(-8) mmol/L), selected because of their ability to upregulate VEGF mRNA expressions in other cell types. Northern blot analysis was performed using [32P]dCTP labeled human VEGF cDNA (Genentech). Lane-loading differences were normalized using mouse GAPDH control cDNA probe. VEGF mRNA expression was upregulated by PMA (10(-9) to 10(-6) mol/L) in a dose-dependent manner, whereas neither L-NAME nor angiotensin II affected VEGF mRNA expression in pericytes. These results support the hypothesis that pericytes increase permeability of the endothelial barrier through increased VEGF production.
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PMID:Vascular endothelial growth factor mRNA in pericytes is upregulated by phorbol myristate acetate. 945 54

Coronary artery disease (CAD), arterial hypertension, chronic bronchitis and diabetes mellitus are the most frequently encountered diseases complicating the clinical course of the vascular patient. Clinical signs of cardiac or pulmonary disease are often absent in patients with decreased functional capacity due to claudication. For instance, clinical evidence of coronary artery disease was found in 36% of patients scheduled for different vascular surgical procedures, whereas coronary angiography revealed significant stenoses in as many as 53-68%. Patients with chronic hypertensive disease, coronary artery disease and increased impedance to left ventricular ejection due to atherosclerosis frequently develop impairment of left ventricular (LV) function. Even without clinical or radiological evidence, approximately 20-35% of vascular patients have a LV ejection fraction below 50% indicating impaired systolic LV function. The incidence of diabetes mellitus in vascular surgical patients is around 18%. When requiring insulin treatment, diabetes is an independent risk factor for postoperative ischemic events and congestive heart failure. Those with autonomic neuropathy are often asymptomatic as regards coronary artery disease. Coronary artery disease is responsible for over 50% of the immediate, medium- and long-term mortality and morbidity. Unstable myocardial ischemia, acute myocardial infarction which is detected by troponin I and ischemic pulmonary edema are the most common immediate postoperative cardiac complications. A large number of recent studies, using long-term ECG recording techniques, have allowed more accurate estimation of the incidence and time course of perioperative myocardial ischemia in vascular surgical patients. The highest incidence of ischemia when compared to daily life activities has been noted during the first two days after surgery but has been reported to remain elevated even 3-5 days after surgery. Interestingly, the incidence of intraoperative ischemia is lower than that observed during daily life. Knowledge of the etiology of perioperative myocardial infarction is essential if one is to improve cardiac outcome after vascular surgery. Many studies have addressed this important field in patients undergoing vascular surgery. They have documented a relationship between perioperative myocardial ischemia and postoperative myocardial infarction. Although postoperative myocardial infarctions are in most cases limited to endocardium (non Q wave infarction) they significantly reduce life expectancy of the vascular surgical patients. The reduction of cardiac risk following general surgery should focus on methods by which the incidence of myocardial ischemia, particularly during the postoperative period, could be reduced. These methods include intensive intraoperative analgesia or preventive administration of cardiovascular treatment which limit postoperative stress: alpha-2 agonists or betablocking agents. There are, at present, no studies which convincingly confirm an overall decreased mortality if coronary bypass surgery is performed prior to peripheral vascular surgery. Although it has been demonstrated that the mortality of the peripheral procedure is reduced to approximately one half, the mortality of a coronary bypass procedure in vascular surgical patients is five to eight times that recorded in a coronary artery bypass population without peripheral vascular disease. It remains to be shown if the use of coronary angioplasty prior to peripheral vascular surgery can provide a more satisfactory overall outcome. Several non-invasive techniques have been suggested to improve the identification of high-risk patients undergoing vascular surgery. These tests include exercise ECG, ambulatory ECG, dipyridamolethallium scintigraphy and determination of left ventricular ejection fraction by gated radionuclide imaging. (ABSTRACT TRUNCATED)
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PMID:[Physiopathologic introduction to anesthesia and resuscitation of the vascular patient]. 955 51

A 74 year old patient with diabetes mellitus was hospitalized because of nausea, recurrent vomiting and increasing fatigue. Shortly before admittance the patient had diarrhea. He also reported a recent onset of aversion against meat consumption. Clinical investigation revealed a possible right-sided paraumbilical abdominal tumor, normal bowel sounds, a vascular bruit and a normal white blood count with increased band forms. During hospitalisation the general condition of the patient deteriorated rapidly with fever and increasing numbers of immature granulocytes. The patient finally died under the symptoms of a paralytic ileus with hypotonia and hypoglycemia. Autopsy revealed a fist-sized stenosing tumor in the cecum with the histology of a mainly well differentiated, cylindrocellular adenocarcinoma. As immediate cause of death a bilateral paracentral lung embolism with pulmonary edema was found, the latter probably as immediate consequence of preterminal heart failure.
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PMID:[Intestinal paralysis in long-term diabetes mellitus]. 965 91

In view of the relative risk of intracranial haemorrhage and major bleeding with thrombolytic therapy, it is important to identify as early as possible the low risk patient who may not have a net clinical benefit from thrombolysis in the setting of acute myocardial infarction. An analysis of 5434 hospital-treated patients with myocardial infarction in the Perth MONICA study showed that age below 60 and absence of previous infarction or diabetes, shock, pulmonary oedema, cardiac arrest and Q-wave or left bundle branch block on the initial ECG identified a large group of patients with a 28 day mortality of only 1%, and one year mortality of only 2%. Identification of baseline risk in this way helps refine the risk-benefit equation for thrombolytic therapy, and may help avoid unnecessary use of thrombolysis in those unlikely to benefit.
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PMID:Refining the risk-benefit equation for thrombolysis: how to identify the low risk patient before administering thrombolytic therapy. 977 33

We treated two cases of diabetes mellitus who developed acute pulmonary edema following accidental aspiration of sweetened water for emergency treatment, when they had fallen into hypoglycemic coma following an overdose of injectable insulin. Although they showed hypoxemia and radiological examinations revealed pulmonary edema, they improved by giving only oxygen and antibiotics in a few days. The osmotic pressure of the sweetened water in each case was approximately 2,600 mOsm and 1,900 mOsm. We suppose that the pathogenesis of the pulmonary edema was due to the sweetened water causing water within the pulmonary vessels to permeate into the alveoli.
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PMID:Acute pulmonary edema caused by accidental aspiration of sweetened water in two cases of diabetes mellitus. 986 63

The acute complications of diabetic ketoacidosis in children and adolescents are well recognized but not completely understood. Clinical studies have focused primarily on brain edema. We have investigated the prevalence and course of interstitial pulmonary edema in patients with severe diabetic ketoacidosis all of whom had uneventful clinical courses. High resolution computed tomography scans of the lungs were analyzed by determining the Hounsfield attenuation level and then converting to physical density values. All seven patients had evidence of interstitial pulmonary edema on the first scan, which was performed within 1 h of hydration and prior to receiving insulin; six of the seven patients had increased pulmonary density 6-8 h into treatment, and all had complete resolution of the interstitial changes at discharge. Our study suggests that subclinical interstitial pulmonary edema may be a frequent occurrence in children and adolescents with severe diabetic ketoacidosis and may very well be present prior to treatment. The study also supports the philosophy of cautious rehydration and the close monitoring of children and adolescents with diabetic ketoacidosis until a more complete understanding of this pathophysiologic event is achieved.
J Diabetes Complications
PMID:Interstitial pulmonary edema in children and adolescents with diabetic ketoacidosis. 987 65

Compression stockings are a safe, noninvasive treatment for patients with symptomatic orthostatic hypotension due to autonomic nervous system dysfunction. In this report, we describe a 75-year-old man who had development of pulmonary edema approximately 45 minutes after placement of compression stockings on the first postoperative day following a carotid endarterectomy. No sudden changes were noted on an electrocardiogram or echocardiogram or in the cardiac isoenzymes associated with the pulmonary edema. The patient had a history of coronary artery disease, diabetes mellitus-induced autonomic nervous system dysfunction, and recent surgery near the carotid baroreceptor. All these factors may have limited his ability to compensate for a rapid increase in central blood volume. The temporal relationship of the patient's respiratory distress to the placement of the compression stockings, in the absence of laboratory findings of primary cardiac dysfunction, make stocking-related fluid shift the likely precipitating event in the formation of acute pulmonary edema. This case suggests that compression stockings should be used with caution in patients with limited cardiac reserve.
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PMID:Acute pulmonary edema associated with placement of waist-high, custom-fit compression stockings. 1048 2

The aim of the present study is to separate the most important in-hospital and long term outcome risk factors in patients with myocardial infarction. We analysed 251 women and 630 men hospitalised for acute myocardial infarction between 1992-96. We compared history data, in-hospital course and long term observation within 2-6 years in a group of patients who died versus group of patients who survived. The most important risk factors of in-hospital death were: cardiogenic shock--with mortality rate--6.2, pulmonary oedema--2.8, ventricular fibrillation--2.7, third degree A-V block--2.5, supraventricular arrhythmia (atrial flutter, atrial fibrillation--2.4, previous myocardial infarction--2.4, diabetes--2.0, disturbances of intraventricular conduction--1.8. The most important risk factors of long term outcome were: congestive heart failure--III, IV class of NYHA at discharge--mortality rate--3.0, ejection fraction < 40%--2.7, disturbances of intraventricular conduction--2.2, in-hospital cardiogenic shock and/or oedema pulmonum--2.0, prior myocardial infarction--1.9, diabetes--1.7, in-hospital ventricular fibrillation--1.6, supraventricular arrhythmia--1.6. Better predictors of survival we can obtain using multivariate analysis. This analysis allows to separate groups of patient with good, mean and poor prognosis which finally simplify choice of efficient kind of therapy.
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PMID:[Risk factors for in-hospital course and long-term outcome in myocardial infarction]. 1078 91

The histotoxic effects of chronic cyanide insult on heart, lung and pancreatic tissues, and some corroborative enzyme and metabolite changes were studied in New Zealand White rabbits using colorimetric, enzymatic and histochemical methods. Two groups of rabbits were fed for 10 months on either pure growers mash or grower mash +702 ppm inorganic cyanide. There were no significant differences in time-course profiles of serum amylase and fasting blood glucose between the cyanide-fed group and control. Pancreatic islet and heart histologies showed no pathological changes, and there were no significant differences in both serum and heart aspartate transaminase activities between the two groups. However, there were significant decreases (P<0.01) in alkaline phosphatase activity in the lungs of the cyanide-fed group, with corresponding significant (P<0.05) increases in the serum activity of the enzyme. Histological examination of lung tissue of the cyanide-treated rabbits revealed focal areas of pulmonary oedema and necrosis. These results suggest the existence of variabilities in tissue susceptibilities to the toxic effect of chronic cyanide exposure. It would appear that chronic cyanide exposure may not predispose to diabetes in the presence of adequate protein intake.
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PMID:Differential effects of chronic cyanide intoxication on heart, lung and pancreatic tissues. 1082 6

The use of perinatal steroid therapy, first introduced in 1972 is effective in precocious maturation of human lungs. Antenatal corticosteroid therapy results in reduction of fetal mortality, respiratory distress syndrome, intraventricular hemorrhage in preterm babies. These benefits extend to a broad range of gestational age. They comprise the interval between 24 and 34 weeks of human pregnancy and are not limited by the infant's gender or race. The beneficial effects of corticosteroids are the best pronounced after more than 24 hours from the beginning of the treatment. Noteworthy is that therapy less than 24 hours of duration may also improve outcomes. In the presence of premature rupture of membranes, or better with intact membranes, antenatal corticosteroids reduce frequency of RDS, IVH and finally mortality and morbidity. Review of meta-analyses based on randomized trials supports general option that premature infants whose mothers received corticosteroids before delivery are less likely to develop RDS and its complications. Recent data showed that benefits derived from ANS are additive to those of surfactant therapy, rendering the latter more effective. Followup of children up to 12 years of age indicate that ANS do not impair physical growth or psychomotor development. Short-term adverse effects including maternal infection, maternal pulmonary edema were not clearly demonstrated. Pulmonary edema has not been reported when ANS were used alone (i.e. not in combination with betamimetic tocolytics). No long-term unwanted effects on maternal adrenal function have been observed. There is no serious maternal risk resulting from immunosuppressive effect of corticosteroid therapy on maternal immune system. Although glucocorticoid therapy is likely to provoke insulin resistance, and thereby deterioration in diabetic control, and potentially causes cortisol resistance in the fetal lung, the results of scarce randomized trials are not conclusive. In any rate strict control of maternal diabetes mellitus reduces incidence of RDS. Current available data are not indicative of higher risk of fetal mortality in association with maternal hypertensive disease and ANS. In conclusion, most randomized trials of ANS has provided a positive evidence of efficacy and safety of this highly cost effective therapy in most common clinical situations. However, further trials and more precise estimates are justified on ANS treatment specifically related to blood glucose control and evidence concerning the promotion of fetal lung maturity in babies of women with diabetes mellitus. Although benefits of the corticosteroid therapy are beyond any doubts, more experience is needed to assess the effect of ANS on maternal and/or fetal infection in presence of premature rupture of membranes. And finally, further assessments are required on antenatal corticosteroids with dose regimens in patients with multifetal gestation, more common after wide use of techniques of the assisted human reproduction.
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PMID:[Intrauterine stimulation for fetal respiratory system maturation; benefits and risks]. 1114 22


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