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Biomedical subjects

C Punzengruber

Publications and source records attributed to C Punzengruber.

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

[Atypical clinical course of thoracic aortic dissection with subacute pericardial hemorrhage].

A case of dissecting aortic aneurysm is reported which occurred without significant pain but was complicated by a subacute pericardial bleeding leading to a large pericardial effusion. The patient was hospitalized because of clinical signs of cardiac tamponade which could be alleviated by pericardiocentesis. Neither 2D-echocardiography nor a portable x-ray of the chest disclosed evidence of aortic dissection. After a symptom-free interval of several hours the patient died because of recurring intractable pericardial tamponade. The differential diagnosis of a large hemorrhagic pericardial effusion should include rupture of a dissecting aortic aneurysm even when typical symptoms are lacking.

Acute Disease↗
PubMed1987

[Peripheral and right atrial plasma levels of atrial natriuretic peptide and their relation to mean atrial pressure].

Atrial myocytes produce natriuretic and vasodilating peptides. Animal experiments have shown that atrial natriuretic peptide (ANP) is released after stretching the atria and drained via the coronary vein effluent. In this study ANP-plasma levels were measured in 14 patients. Blood samples were simultaneously collected from the right atrial cavum and from an antecubital vein. In the right atrial samples, ANP-plasma concentrations were significantly higher than in samples drawn from a peripheral vein (140.3 +/- 114.8 pg/ml vs 96.9 +/- 69.2 pg/ml; p less than 0.05), but a significant linear correlation was found between both values (r = 0.88; p less than 0.001). In patients with elevated atrial pressures significantly higher ANP-levels could be detected than in patients with normal atrial pressures (204 +/- 115 pg/ml vs 55.3 +/- 18.5 pg/ml; p less than 0.05). Mean right atrial pressure correlated to ANP-levels in right atrial blood (r = 0.79; p less than 0.001) as well as to ANP-levels in peripheral blood (r = 0.68; p less than 0.01). These results indicate that higher ANP plasma levels can be measured in samples drawn from a site close to ANP production. On the other hand, atrial pressure might influence the amount of circulating ANP.

Adolescent↗
PubMed1986

Bicyclo-prostaglandin E2 metabolite in congestive heart failure and relation to vasoconstrictor neurohumoral principles.

Vasodilator prostaglandins may play a role in maintaining circulatory homeostasis in patients with congestive heart failure (CHF). Plasma levels of bicyclo-prostaglandin E2 metabolite (PGEm), a chemically stabilized degradation product of the vasodilator prostaglandin E2, were determined in 45 patients with chronic CHF (New York Heart Association class II, III or IV). Mean circulating levels of bicyclo-PGEm were significantly elevated in patients with functional class III (72 +/- 8 pg/ml) or IV CHF (77 +/- 10 pg/ml) compared with control subjects (49 +/- 3 pg/ml) and patients with functional class II CHF (49 +/- 4 pg/ml). Bicyclo-PGEm concentrations correlated with plasma renin activity (r = 0.68, p less than 0.001) and plasma angiotensin II (r = 0.56, p less than 0.001) and plasma noradrenalin levels (r = 0.34, p less than 0.05). An inverse correlation was found between serum sodium concentrations and levels of bicyclo-PGEm (r = 0.46, p less than 0.01) as well as plasma renin activity (r = 0.66, p less than 0.001). Thus, prostaglandin E2 levels in plasma are increased in patients with severe CHF.

Adult↗
PubMed1986

Left ventricular function in well-controlled insulin-dependent (type I) diabetics--an echophonocardiographic study.

A high prevalence of left ventricular dysfunction in insulin-dependent (type-I) diabetics has been reported. However, the exact influence of metabolic control and/or the coexistence of early diabetic microangiopathy is unknown. Thus, we assessed left ventricular function by echophonocardiography in 50 type-I diabetics (mean age 26 +/- 7.9 years), who showed a fairly good metabolic long-term control (mean hemoglobin A1: 8.8%) after the introduction to intensified insulin therapy in comparison with 50 age- and sex-matched controls. Type-I diabetics did not differ from controls in their left ventricular internal diameters, mean wall thickness, ratio of pre-ejection period to left ventricular ejection time and systolic shortening fraction. Isovolumetric relaxation period reflecting an early diastolic event was slightly but significantly prolonged in diabetic subjects, independent of metabolic control status or existence of early microangiopathy. Isovolumetric relaxation period showed a statistically significant correlation to age in type-I diabetics, but not in controls. Possibly, the diabetic status--although well-controlled, but not normalized--may biochemically alter the myocardium and might influence its diastolic properties.

Adult↗
PubMed1986

Platelet sensitivity to prostacyclin in smokers and non-smokers.

Platelet activating effect of cigarette smoking appears to be important in the development of atherosclerosis. We previously demonstrated a reduced sensitivity of platelets to exogenous prostacyclin (PGI2) in vitro from patients with proven atherosclerotic disease, indicating a possible role of altered platelet function in the development of atherosclerosis. We now hypothesize that cigarette smoking might be an important cause of altered platelet sensitivity to PGI2 observed in patients with atherosclerosis. To test this hypothesis, the response of platelets to exogenous PGI2 was tested in chronic smokers and non-smokers, prior to and after smoking two cigarettes (active smoking) and prior to and after exposure to a tobacco smoke-contaminated atmosphere (passive smoking). This study indicates that platelets of chronic smokers are less sensitive to exogenous PGI2 than platelets of non-smokers. In addition, active as well as passive smoking decreases platelet sensitivity to PGI2 in non-smokers, whereas chronic smokers exhibit no further decline. We conclude that decreased platelet sensitivity to PGI2 might be an important contributing factor to the altered platelet function observed in patients with atherosclerosis.

Adult↗
PubMed1986

Thyroid hormones and pericardial effusion may influence plasma levels of atrial natriuretic peptide (ANP) in humans.

Fluid and electrolyte homeostasis is impaired in patients suffering from hypothyroidism and myxedema because myxedema induces retention of salt and water. We have measured plasma levels of human atrial natriuretic peptide (hANP) in 8 female patients who had been totally thyroidectomized because of thyroid carcinoma. Estimations of the hormone were done 4 weeks after diagnostic withdrawal (searching for iodine retaining metastases) and after 2 weeks and 4 weeks of reinitiation of thyroid suppressive therapy by L-thyroxine. hANP levels, although within the normal range (10-80 ng/l) throughout the study, were positively linked to the amount of pericardial effusion (determined by echocardiography), which was highest initially and decreased or vanished with duration of L-thyroxine therapy. Additionally, a positive correlation between thyroid hormone levels and hANP was obtained when the counteracting effect of pericardial effusion was allowed for by partial correlation analysis. Our findings might facilitate explanation of mild polyuria in hyperthyroidism and impaired water excretion in hypothyroidism.

Adult↗
PubMed1986

[Hemodynamic effects of nitroglycerin following acute inhibition of prostaglandin synthesis].

The mechanism of action by which nitrates produce vasodilation has not been fully clarified so far. Experimental studies indicate a possible relationship to the prostaglandin system. This study describes the consequences of acute prostaglandin synthesis inhibition on the hemodynamic effects of nitroglycerin in patients with stable angina pectoris. Intravenous application of 1 g acetylsalicylic acid was associated with a small but significant blunting of the pressure decline in the pulmonary and systemic circulation following the sublingual administration of 0.8 mg nitroglycerin. Premedication with 75 mg indomethacin i.m. was followed by a decrease in pressure decline in the pulmonary artery during intravenous nitroglycerin infusion. Significant inhibition of prostaglandin synthesis was shown by a substantial decline in plasma levels of circulating prostaglandin metabolites in both experiments. These results indicate that the mechanism of action of nitroglycerin may be partially mediated by vasodilatory prostaglandins.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Vasodepressor syncopes in metastasizing laryngeal cancer. Combination therapy using an AV sequential pacemaker and ephedrine].

Syncope due to hypersensitivity of carotid sinus developed in a patient with laryngeal carcinoma. After implantation of a ventricular demand pacemaker a marked vasodepressor component became evident leading to further episodes of fainting. Only after implantation of an AV-sequential pacemaker and additional oral medication with ephedrine syncopes could be prevented.

Carcinoma, Squamous Cell↗
PubMed1985

Severe hyperprolactinaemia is associated with decreased insulin binding in vitro and insulin resistance in vivo.

We studied insulin receptor binding and carbohydrate metabolism in 10 patients with severe hyperprolactinaemia and compared the findings with those obtained in 20 healthy control subjects. Insulin binding to monocytes and erythrocytes was significantly decreased in the patients with an excess of prolactin. Scatchard analysis of binding data indicated that a decrease in the number of receptors rather than in receptor affinity seems to be the prevailing cause of lowered binding in hyperprolactinaemic patients. Furthermore, patients with severe hyperprolactinaemia demonstrated significantly elevated blood glucose levels following oral or intravenous glucose load despite having significantly increased insulin levels after glucose administration. The infusion of insulin induced a delayed hypoglycaemic effect and a decreased inhibition of endogenous insulin secretion, as indicated by the suppression of C-peptide in the hyperprolactinaemic patients. The present data indicate that severe hyperprolactinaemia is associated with an insulin-resistant state, which seems to be caused, at least in part, by a down-regulation of insulin receptors.

Adult↗
PubMed1985

Effects of pressure-controlled intermittent coronary sinus occlusion on regional ischemic myocardial function.

Pressure-controlled intermittent coronary sinus occlusion has been reported to reduce infarct size in dogs with coronary artery occlusion, possibly because of increased ischemic zone perfusion and washout of toxic metabolites. The influence of this intervention on regional myocardial function was investigated in open and closed chest dogs. In six open chest dogs with severe stenosis of the left anterior descending coronary artery and subsequent total occlusion, a 10 minute application of intermittent coronary sinus occlusion increased ischemic myocardial segment shortening from 5.5 +/- 1.2 to 8.2 +/- 2.6% (NS) and from -0.1 +/- 2.1 to 2.3 +/- 1.2% (NS), respectively. In eight closed chest anesthetized dogs, intermittent coronary sinus occlusion was applied for 2.5 hours between 30 minutes and 3 hours of intravascular balloon occlusion of the proximal left anterior descending coronary artery. Standardized two-dimensional echocardiographic measurements of left ventricular function were performed to derive systolic sectional and segmental fractional area changes in five short-axis cross sections of the left ventricle. Fractional area change in all the severely ischemic segments (less than 5% systolic wall thickening) was -4.0 +/- 4.7% at 30 minutes after occlusion, and increased with subsequent 60 and 150 minutes of treatment to 13.1 +/- 3.3 and 7.0 +/- 3.3%, respectively (p less than 0.05). At the most extensively involved low papillary muscle level of the ventricle, regional ischemic fractional area change was increased by intermittent coronary sinus occlusion between 30 and 180 minutes of coronary occlusion from -0.4 +/- 0.1 to 14.4 +/- 4% (p less than 0.05), whereas a further deterioration was noted in untreated dogs with coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

[Diastolic compression of the right atrium and right ventricle as an echocardiographic sign of pericardial tamponade. Case report].

A 33 years old female patient requiring regular hemodialysis for chronic renal failure exhibited a severe hypotensive episode. 2-dimensional echocardiography enabled rapid recognition of the underlying cause. 2-dimensional echocardiography revealed a large pericardial effusion and from the apical window a marked diastolic compression of the right atrium and the right ventricle was noted. These findings have been previously described to be specific for cardiac tamponade. After removal of 400 ml of fluid by pericardiocentesis the clinical symptoms rapidly improved and in the 2-dimensional echocardiography diastolic compression of the right sided heart chambers was not longer evident, although a substantial amount of pericardial fluid was still present. This case report underlines the clinical usefulness of 2-dimensional echocardiography for the diagnosis of cardiac tamponade.

Adult↗
PubMed1984

Retrograde coronary venous contrast echocardiography: assessment of shunting and delineation of regional myocardium in the normal and ischemic canine heart.

Coronary venous injections of sonicated Renografin-76 were performed in seven closed chest dogs during two-dimensional echocardiography to study the ability of this new technique to opacify regional myocardium before and after occlusion of the left anterior descending coronary artery. The balloon of a 4F double lumen catheter was inflated in the great cardiac vein for each contrast injection to prevent backflow through the coronary sinus into the right atrium. Retrograde injections before coronary artery occlusion generally resulted in patchy myocardial contrast uptake. Injections after coronary occlusion always resulted in confluent and transmural myocardial opacification which occupied 42.8 +/- 8.6% (range 26 to 54) (mean +/- standard deviation) of the myocardial circumference. Retrograde opacification always extended into adjacent myocardium beyond the ischemic zone, which was assessed in echocardiograms with antegrade contrast injections into the left main coronary artery and which measured 30 +/- 6.3% of the ventricular circumference. Shunting from the coronary venous system to cardiac chambers was evaluated in a parasternal four chamber view and was graded on a scale of 0 to 4+. Contrast appearance was equally intense in the right atrium and right ventricle (3.5 +/- 0.6+, range 2+ to 4+), less intense in the left ventricular cavity (1.5 +/- 0.6+, range 1+ to 3+) and absent in the left atrium. Postmortem anatomic validation with retrograde great cardiac vein injections of indocyanine green corroborated and in vivo contrast appearance in chambers. Retrograde coronary venous contrast echocardiography appears capable of providing in vivo information about the extent and location of myocardial zones that can be reached by retrograde infusions of therapeutic agents and about the ability of these agents to reach ischemic myocardium. In addition, this new method allows for in vivo evaluation of shunts between coronary veins and cardiac chambers, which may influence the efficacy of retrograde interventions.

Animals↗
PubMed1983

Endogenous prostaglandin E2 metabolite levels, renin-angiotensin system and catecholamines versus acute hemodynamic response to captopril in chronic congestive heart failure.

Hemodynamic and hormonal responses to captopril were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25-mg dose, stroke volume (SV) increased from 53 +/- 7 to 63 +/- 9 ml (p less than 0.05), while pulmonary wedge pressure (PWP) decreased from 20 +/- 2 to 14 +/- 2 mm Hg (p less than 0.01). The hemodynamic changes were associated with increases in plasma renin activity (PRA; p less than 0.05) and in plasma levels of a novel bicyclo-prostaglandin E2 metabolite (bicyclo-PGE-m; p less than 0.01), whereas norepinephrine (NE) showed a falling tendency. In general, basal hemodynamic and basal hormonal levels did not correlate. Captopril-induced changes in mean artery pressure (MAP) and mean pulmonary artery pressure (mPAP) were positively correlated to pre-captopril PRA (r = 0.74, p less than 0.01; r = 0.64, p less than 0.05) and to changes in PRA (r = 0.85, p less than 0.01; r = 0.80, p less than 0.01) with a similar trend for angiotensin II (AII); decreases of systemic vascular resistance were more pronounced in patients with higher control NE levels (r = 0.62, p less than 0.05), the reduction of NE levels being highest in patients with higher basal concentrations (p less than 0.001); the captopril-induced decreases of mPAP and PWP were inversely related to basal bicyclo-PGE-m levels (r = 0.60, p less than 0.05; r = 0.61, p less than 0.05), and changes in mPAP were closely related to basal ratios of AII/bicyclo-PGE-m (r = 0.67, p less than 0.01). Thus, captopril exerts its acute beneficial hemodynamic effect by inhibiting the generation of AII, associated with toning down of sympathetic stimulation and increased production of vasodilating prostaglandins, such as PGE2. The relation between AII and PGE2-counteracting substances-might determine the hemodynamic response to captopril in the patients.

Adult↗
PubMed1982

[Molsidomine, a coronary drug with platelet-aggregating inhibitory activity].

The influence of molsidomin (4 mg i.v.) on platelet function, on the plasma concentrations of 6-oxo-PGF1 alpha, the stable metabolite of prostaglandin I2, and thromboxane B2, the stable metabolite of thromboxine A2 was determined in ten patients with coronary heart disease. Prostaglandin I2 is generated in the vessel wall and is a potent vasodilator and inhibitor of platelet aggregation, whereas thromboxane A2 is a vasoconstrictor and a proaggregatory substance. In addition, in-vitro tests were performed, too. 60 min after bolus injection a decrease of systolic and diastolic blood pressure was observed, whereas heart rate remained nearly constant. Platelet aggregation decreased significantly; the addition of PGI2 in vitro had an additive effect. The plasma concentrations of 6-oxo-PGF1 alpha increased after 60 minutes, whereas thromboxane B2 concentrations remained unchanged. In vitro, SIN1, a metabolite of molsidomin generated in the liver, led to a dose-dependent inhibition of ADP-induced platelet aggregation, whereas molsidomin was nearly inactive. Thus molsidomin shows an inhibition of platelet function besides the known antianginal properties. The vasodilatatory and platelet inhibiting effects of this compound may be due partly to a stimulation of the prostaglandin I2 synthesis in the vessel wall.

Angina Pectoris↗