[Conservative principles in the therapy of subarachnoid hemorrhage].
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Antifibrinolytic Agents↗
Biomedical subjects
R Ritz
Publications and source records attributed to R Ritz.
[Long-term course over three years in a patient with unstable angina pectoris].
The long-term follow up in 48 patients with unstable angina pectoris was analyzed retrospectively. All patients were hospitalized in a coronary care unit during the acute phase and responded favourably to a medical regimen consisting of nitrates in 45 patients, betablockers in 23, calcium channel blocking agents in 22 and i.v. nitroglycerin in 12. 30 patients (group 1) responded promptly to oral medication with one or a combination of two drugs, whereas in 18 patients a combination of at least three drugs or intravenous nitroglycerin were necessary. After 42 +/- 6 months 21 patients remained asymptomatic, with 8 still on antianginal therapy. In 27 patients (56%) complications had occurred. These complications were severe limiting angina pectoris in 16, of whom 11 were treated surgically after 3.5 +/- 3 months, and myocardial infarction in 11 patients after 16 +/- 9 months, of whom 4 patients died. Complications occurred in 10 of the 30 patients in group 1 and in 16 of the 18 patients in group 2 (33% vs. 89%, p less than 0.01). This study confirms that the long-term course in patients with unstable angina is often complicated by severe angina pectoris or myocardial infarction. The late response to initial therapy and the need for the combination of more than two antianginal drugs or of i.v. medications identifies a subgroup of patients with a high complication rate.
Adrenergic beta-Antagonists↗
[Amino acid uptake and release by colorectal cancer in man].
Little information is available regarding the amino acid exchange by human tumors. To characterize this exchange in vivo, 21 patients with resectable colorectal carcinomas were studied during curative operations. Concerning the amino acid uptake and release by peripheral tissues, 20 non-cancer patients served as controls. Both groups of subjects were well-nourished, as indicated by anthropometric and biochemical variables. In the cancer patients, we cannulated a peripheral artery and vein as well as a central tumor-draining vein and the portal vein. Plasma concentrations and concentration differences were determined in mumol/l and in percentages of the total amino acid amounts. Peripheral glutamate uptake per liter plasma was reduced in the cancer patients (p = 0.02). In these patients, the central tumor-draining vein contained less glutamine (p = 0.002) and more glutamate (p = 0.002) than the peripheral vein. Glutamine uptake by the tumor occurred more often than glutamine release, while glutamate had a negative balance across the tumor in all but three cases. The qualitative differences between the peripheral tissues and the tumors with respect to glutamine and glutamate exchange reached high levels of significance (p = 0.002 for both of the amino acids). In addition, the tumors released more glycine, ornithine, and tyrosine than the periphery. As to glutamine and glutamate metabolism, there was a significant difference between the tumors and the portal-drained organs (p greater than or equal to 0.05). The discussion of the results emphasizes the contributions made by the periphery and the tumor to the plasma amino pattern. The role of glutamine as a potential high importance energy source for neoplastic tissues is delineated.
Aged↗
Effects of intravenous aspirin on prostaglandin synthesis and kidney function in intensive care patients.
The effects of intravenous acetylsalicylic acid (1.0 g bolus) on renal function and prostaglandin synthesis were evaluated in a prospective, controlled study in eight patients in an intensive care unit. Four of these patients had congestive heart failure. Administration of acetylsalicylic acid caused significant antidiuresis (-56%), antinatriuresis (-82%), renin suppression (-26%) and decreased GFR (-41%). All of these changes were completely reversible within 1-2 hours and tended to be more pronounced in the patients with congestive heart failure. Urinary excretion of prostaglandin E2 was depressed profoundly (-93%) and did not return to more than 45% of control 6 h after the administration of acetylsalicylic acid. We conclude that intravenous acetylsalicylic acid affects kidney function in a manner similar to other prostaglandin synthesis inhibitors. Its effects are, however, short-lived. The inhibition of urinary PGE2 excretion outlasts GFR depression, antidiuresis, antinatriuresis and renin suppression by several hours.
Aged↗
[Fibrinolysis therapy in massive lung embolism. Experiences in 10 patients 1982-1984].
Between October 1982 and July 1984 systemic thrombolysis was carried out in 10 patients (5 males and 5 females aged 19 to 66 years) with massive pulmonary embolism (PE). Mean thrombolytic treatment duration was 77 hours. The main fibrinolytic agent used (9 cases) was streptokinase. Sequential treatment with streptokinase and urokinase was given to 2 patients and urokinase alone to one. 5 patients received porcine plasmin additionally, and one patient BRL 26921 (streptokinase-plasminogen complex) and human plasminogen. Pulmonary arterial pressures were recorded serially. Pulmonary angiograms were obtained before, occasionally during and after thrombolysis. Pulmonary arterial pressures (systolic: p less than 0.01, diastolic: p less than 0.05, mean: p less than 0.01, paired t-test, two tailed) and pulmonary angiograms (p less than 0.001, paired t-test, two tailed) all showed significant improvement. Thrombolytic treatment had to be discontinued in two patients due to side effects. Patients with the most recent PE showed the best response. Patients with recurrent PE and preexisting pulmonary hypertension showed no improvement. In PE without deep vein thrombosis (DVT), treatment duration of up to three days seems to be appropriate. In PE with concomitant DVT the treatment should be prolonged to achieve complete lysis of thrombi.
Adult↗
Moxalactam in nosocomial infections with Serratia marcescens.
Ten critically ill patients presenting with nosocomial infection caused by Serratia marcescens (SM) not responding to prior chemotherapy were treated in an open study with Moxalactam (MOX) alone [6] or in combination with an aminoglycoside [4]. In initial disc diffusion tests, all isolates of SM were highly susceptible to MOX. Clinically, three patients were cured and four improved. Three patients died: one from SM pneumonia, one from gangrenous cholecystitis and another from ARDS. Bacteriologically, SM were eliminated from blood cultures in all seven patients with septicemia but were recovered post mortem from the lung of one patient. In three cases with localized infection, SM were eliminated once and persisted twice. Selection of resistant SM was observed in three patients but became clinically relevant in one case only. Resistant SM strains also showed reduced susceptibility to other cephalosporins and aminoglycosides. Emergence of enterococci occurred four times, in two cases with clinical consequences. MOX is a useful drug for the treatment of SM infections, but a definite risk of selecting multiresistant SM strains and of enterococcal overgrowth must be kept in mind.
Adult↗
Prejunctional alpha 2-adrenoceptors and norepinephrine release in the forearm of normal humans.
To investigate the prejunctional alpha 2-adrenoceptor-mediated autoinhibitory feedback for norepinephrine (NE) release, we measured the response of forearm blood flow (FAF, mercury in silastic strain gauge plethysmography) and changes of the forearm venous-arterial NE difference (delta VA-NE, deep forearm vein, brachial artery norepinephrine concentration) induced by six intrabrachial artery 5-min infusions of clonidine in 13 normal volunteers. NE spillover into the forearm circulation was estimated as the product of delta VA-NE and FAF after three clonidine infusions. Clonidine caused dose-dependent decreases in FAF with a maximum reduction of FAF after the highest dose of clonidine of 32 +/- 8%, (N = 7, p less than 0.01) indicating postjunctional alpha-adrenergic stimulation. delta VA-NE increased slightly yet calculated norepinephrine spillover remained statistically unchanged after clonidine. The results suggest that auto-inhibitory feedback control of neuronal transmitter release via prejunctional alpha 2-adrenoceptors may not to an important degree modulate norepinephrine release in the forearm vasculature of healthy subjects.
Adult↗
Exercise and resting blood pressure and heart rate changes 24 h after dosing in patients with essential hypertension receiving 16/260 oxprenolol Oros once daily.
Nineteen patients receiving oxprenolol slow-release (SR) 160 mg (three patients) or 320 mg (16 patients) once daily for mild to moderate hypertension were treated with oxprenolol Oros 16/260 once daily for 3 weeks following a 2 week placebo wash-out period. Repeated dosing with both Oros and SR oxprenolol preparations, in comparison with placebo, significantly reduced supine systolic and diastolic blood pressures, and pulse rate at 24 h after dosing. Single Oros doses also significantly reduced pulse rate and diastolic, but not systolic, blood pressure at 24 h. The reduction in supine systolic blood pressure was greater during repeated dosing with oxprenolol SR than after a single dose of the Oros preparation. Control of supine diastolic blood pressure (less than or equal to 90 mm Hg) at 24 h after dosing was achieved in 13 out of 18 patients with oxprenolol SR (two out of three patients given 160 mg, and 11 out of 15 given 320 mg). Similar control was achieved in 11 out of 18 patients after a single dose of oxprenolol Oros, and in 13 out of 17 patients treated for 3 weeks. The mean percentage reduction in exercise heart rate (EHR) compared to placebo, at 24 h after dosing, was 16% following Oros treatment for 3 weeks, and 12% following SR administration. After a single dose of oxprenolol Oros EHR, was reduced by 9% at 24 h compared to placebo. At 3 weeks the Oros formulation was significantly better than the SR tablet at reducing EHR. Oxprenolol Oros 16/260 was effective over 24 h and well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Influence of moderately elevated levels of carboxyhemoglobin on the course of acute ischemic heart disease.
The purpose of this prospective study in 66 patients with acute ischemic heart disease was to analyze the possible effects of moderately elevated levels of carboxyhemoglobin (COHb) on the early course of this disease. Thirty-one patients presented with a level of COHb less than or equal to 2% and 35 with a level of greater than 2%. In the group with elevated COHb, more patients developed transmural infarction, but the difference was not significant (p = 0.123). Patients with transmural infarction had higher maximum CPK values (p less than 0.01), when COHb levels were greater than 2%. During the first 6 h after admission to hospital, these patients needed an antiarrhythmic treatment significantly more frequently (p = 0.003). Differences in rhythm disorders were still present at a time when nicotine, due to its short biological half-life, was already eliminated. We conclude that a moderately elevated level of COHb is not just a marker for recent smoking but may aggravate the course of acute ischemic heart disease.
Arrhythmias, Cardiac↗
Hormonal modulation of intracellular free calcium in platelets from normotensive and hypertensive subjects.
Sensitivity to adrenaline-antagonism of the inhibitory effect of PGI2 on thrombin-induced increase in [Ca2+]i was measured in platelets from normotensive and untreated hypertensive subjects. Platelets from hypertensive subjects exhibited an increased sensitivity to adrenaline. This effect was more pronounced in younger patients with hypertension, and suggests an increased adenylate cyclase sensitivity in the early hypertension. The data also indicate that a mechanism linked to calcium-influx plays an important role in older hypertensives. This may explain the greater efficacy of calcium entry blockers in older hypertensive patients with essential hypertension.
Blood Platelets↗
[Incidence and course of complex ventricular arrhythmias in myocardial infarct as a function of infarct size, heart function and persistent ischemia].
Incidence and course of complex ventricular ectopic activity (VEA) after myocardial infarction was prospectively evaluated in 217 patients in relation to infarct size, location, ventricular function and signs of persistent ischemia. Complex VEA (Lown greater than III) was found acutely in 138 patients (63.6%) and at hospital discharge in 42 (19.3%). Of 79 patients with VEA Lown less than or equal to III in the first 24 hours, 93.7% remained VEA-free at follow-up. Patients with persistent complex VEA differed from those who became VEA-free only in left and right ventricular ejection fraction, whereas all the other infarct related factors had no influence on the course of VEA.
Aged↗
[A frequent problem in the laboratory control of heparinization: contamination of blood specimens with exogenous heparin].
If blood for monitoring of heparin therapy is collected through indwelling catheters it may be contaminated by exogenous heparin. A prospective study comparing thrombin times in plasma obtained by venipuncture and by collection through heparin perfused catheters showed that 26 out of 77 catheter samples were contaminated. In 16 of these 26 cases, overestimation of the heparin effect would have led to incorrect dosage recommendations. It is concluded that blood for laboratory monitoring of heparin treatment should be collected by venipuncture.
Blood Coagulation Tests↗
[Prolonged coma caused by diazepam sedation in ventilated patients. Diagnostic and therapeutic use of the benzodiazepine antagonist Ro 15-1788].
Repeated administration of diazepam in two ventilated patients had caused drug cumulation and coma over several days. In both cases central nervous depression could be demonstrated by the benzodiazepin antagonist Ro 15-1788 which induced reversal of coma. Estimation of plasma concentrations in a 70-year-old female patient 150 hours after the last administration showed a diazepam concentration of 437 ng/ml and a desmethyl-diazepam concentration of 483 ng/ml. The calculated elimination half-life of these substances were 109 and 403 hours. In the second case benzodiazepin could be demonstrated in urine for 10 days after withdrawal of medication. These observations suggest that diazepam is not a suitable drug for prolonged sedation in artificially ventilated patients. The benzodiazepin antagonist Ro 15-1788 represents a valuable diagnostic aid in ascertained or suspect cases of benzodiazepin intoxications. It can also be used therapeutically for reversal of central nervous depression.
Aged↗
Clinical experience with computerized ICU-monitoring.
Computer monitoring in an intensive (ICU) and in a coronary (CCU) care unit is discussed. It can handle much data simultaneously, it can calculate complex results. Trends in parameters can be watched. On-line measurements with alarm signals in emergency situations can be made.
Computers↗
Plasma prekallikrein, factor XII, antithrombin III, C1(-)-inhibitor and alpha 2-macroglobulin in critically ill patients with suspected disseminated intravascular coagulation (DIC).
In nine patients with suspected disseminated intravascular coagulation (DIC) and five controls, the following analyses were performed on admission and 7-29 hours later: Routine coagulation studies (fibrinogen, platelet count, fibrin(ogen) degradation products, ethanol gelation, reptilase time, Factor V) providing a semiquantitative DIC score, prekallikrein (PK), Factor XII, antithrombin III (AT-III), C1(-)-inhibitor and alpha 2-macroglobulin. Significant correlations were found: PK or AT III with the DIC-score, PK with AT-III and Factor XII, AT-III with Factor XII. The changes (expressed as a percentage of normal plasma) of PK and AT-III from the first to the second evaluation were nearly identical. The two patients with rapidly fatal irreversible shock showed the highest DIC score and a pronounced decrease of PK and AT-III, whereas in reversible shock stable or increasing PK and AT-III values were found. The other variables showed an overlap between reversible and irreversible shock. DIC in these shock patients, accompanied by a decrease in PK, probably was mediated via Factor XII activation. PK and AT-III might be of prognostic value in patients with (septic) shock.
Aged↗
Measuring gas leakage from bronchopleural fistulas during high-frequency jet ventilation.
A simple volumetric system can be used to measure leakage from bronchopleural fistulas even when inspiratory volumes are unknown or when constant suction is required.
Bronchial Fistula↗
Parallel reduction of calcium-influx-dependent vasoconstriction and platelet-free calcium concentration with calcium entry and beta-adrenoceptor blockade.
In essential hypertension, calcium-influx-dependent vasoconstriction is enhanced, and free calcium concentration in platelets is elevated. To investigate calcium-influx-dependent vasoconstriction as related to platelet calcium concentration blood pressure, forearm blood flow (FAF) and free calcium concentration in platelets were measured in five patients with essential hypertension before and after a 6-week treatment with nitrendipine or acebutolol. Starting from comparable basal values, the increase in FAF (ml/min/100 ml tissue) to intraarterially infused nitrendipine (20 micrograms/100 ml tissue) was 40.7 +/- 6.1 before and 30.7 +/- 12.3 after chronic nitrendipine treatment (p less than 0.05) and 41.6 +/- 6.2 before and 34.6 +/- 14.9 after chronic acebutolol treatment. The "nonspecific" vasodilator response to intraarterial sodium nitroprusside or to postischaemic reperfusion were similar before and during treatment. Platelet-free calcium concentration fell on nitrendipine (p less than 0.05) and on acebutolol (p less than 0.01) treatment. Antihypertensive treatment with calcium entry as well as beta-adrenoceptor blockade resulted in a reduction of calcium-influx-dependent vasoconstriction and a fall in free calcium concentration in platelets. Thus, increased calcium platelets may reflect increased calcium in vascular smooth muscle cells and arteriolar tone.
Acebutolol↗
Free calcium response to adrenaline in platelets of normal and hypertensive (untreated and treated) subjects.
That adrenaline is involved in the pathophysiology of essential hypertension (EHT) is suggested by the observed elevation of plasma adrenaline concentration in some patients. Adrenaline, by stimulating the alpha-2 adrenoceptor, causes vasoconstriction in the smooth muscle cell and initiates shape change and aggregation in platelets. Therefore, the effect of adrenaline on intracellular free calcium concentration ([Ca2+]i) in the platelets of hypertensive subjects was investigated as a model for vascular smooth muscle. Platelets from untreated patients with EHT had an elevated [Ca2+]i and incubation with adrenaline for 30 min caused a greater increase in [Ca2+]i in treated patients with EHT than in normotensive controls. This long-term effect of adrenaline was possibly linked to a defective calcium extrusion mechanism in hypertension. No immediate effect was observed on [Ca2+]i by PGI2 and adrenaline, while both modulated [Ca2+]i if the platelets were stimulated with thrombin. PGI2 prevented the thrombin-induced increase in [Ca2+]i and adrenaline antagonized the effect of PGI2. Platelets from untreated patients with EHT exhibited an increased sensitivity to thrombin and adrenaline when compared to normotensive and treated hypertensive subjects. It is suggested that these supersensitivities are related to the elevated [Ca2+]i in untreated hypertensive patients.
Adolescent↗