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Biomedical subjects

R Cardinal

Publications and source records attributed to R Cardinal.

88 records · Page 5Linked to original sources
PubMed1977

Comparison of the Hoesch and the Watson-Schwartz tests for urinary porphobilinogen.

A comparison of the Hoesch and the Watson-Schwartz tests shows that the latter, although slightly more complicated, generally yields more concise results and is superior in sensitivity and specificity for porphobilinogen. The recommendation of the Hoesch test for use as a "bedside screening" method seems unrealistic. Before the diagnosis of an "inducible" porphyria is made, a positive Hoesch test requires that indoles, indoleacetic acid, methyldopa, end-stage alcoholic malnutrition, and phenazopyridine HCl be excluded, to avoid misinterpretation.

Chromatography, Thin Layer↗
PubMed1976

Hematin treatment of acute porphyria. Early remission of an almost fatal relapse.

Intravenous infusions of hematin in a young woman with acute porphyria in profound relapse was followed within 48 hours by remission of symptoms and rapid recovery. From a state of severe central and peripheral nervous-system involvement, the patient recovered so completely that she was able to leave the hospital in less than a month, with only a residual weakness of her arms. Serial studies of serum and urinary levles of porphyrin precursors and serum level of hematin provided highly important information about the effect of hematin on acute porphyria.

Acute Disease↗
PubMed1976

The activities of uroporphyrinogen synthetase and cosynthetase in congenital erythropoietic porphyria (CEP).

Normal or increased amounts of series III porphyrins with greater amounts of series I were observed on incubation of PBG in hemolysates of congenital erythropoietic porphyria vs. normal erythrocytes, human or bovine. Correlation with reticulocyte percentage was poor, in the aggregate a general trend toward increased values of both isomers I and III was noted with increasing reticulocytes. When the percent of type III was low the net amount was increased as compared with normal. Hemolysates of non-porphyric, reticulocyte-rich red cells (hemolytic or posthemorrhagic anemia) formed only minute amounts of type I porphyrin but at the same time no more, or even less type III than the porphyric hemolysates, although representing red cells of greater reticulocyte content. No evidence of deficient heme synthesis was observed in porphyric hemolysates incubayed with [14C]-porphobilinogen or 59Fe. Other studies of porphyric hemolysates incubated with and without added mouse spleen synthetase failed to reveal evidence of an absolute UPG-III cosynthetase (Co-S) deficiency. The large increases of type I porphyrin with normal or increased formation of type III, both in the disease and in the hemolysates, are believed due to a primary increase of ALA-S or UPG-S activity rather than a decrease of Co-S. Possible mutations which might be responsible for this increase are considered.

Adult↗
PubMed1975

Effects of hematin in hepatic porphyria. Further studies.

The present study was carried out in five cases of hepatic porphyria, including three of acute intermittent porphyria, one of variegate porphyria, and one of porphyria cutanea tarda in clinical remission. In two cases of acute intermittent porphyria (in relapse), a marked lowering effect on serum and urine porphobilinogen and delta-aminolevulinic acic was observed, together with prompt and gratifying clinical improvement. In a third case, in chemical remission but with longstanding psychoneurosis, no significant effects were noted, nor were any observed in the case of porphyria cutanea tarda. Although clinical improvements occurred in the case of variegate porphyria, the results were inconclusive for reasons given. Hematin was generally well tolerated. Preliminary reference is made to a transitory renal injury, without sequelae, where an excess of hematin was given in relation to time. Limits of tolerance are proposed. In the light of these observations the basic mechanism of the acute attack is diccussed.

Adult↗
PubMed1974

Repression by hematin of porphyrin biosynthesis in erythrocyte precursors in congenital erythropoietic porphyria.

Hematin administered intravenously in a patient with congenital erythropoietic porphyria evidently entered erythrocyte precursors in the bone marrow, producing the well-known negative feedback repression of porphyrin biosynthesis with marked decline of porphyrin concentrations in urine, circulating plasma, and erythrocytes. A delay in the major segment of this effect corresponded roughly with the sum of the average transit times through the maturation compartments of the erythrocyte precursors. This delay was considerably longer than previously observed in the decline of porphyrin precursors after administration of hematin in patients with hepatic porphyria. The effect of hematin was compared with that of packed erythrocyte transfusions given at regular intervals in the same patient over a period of 2.5 years. In general, administration of hematin results in a reduction of porphyrin formation of the same order of magnitude, but of shorter duration, possibly in relation to the relatively small amounts of hematin infused.

Adult↗
PubMed1971

Repression of the overproduction of porphyrin precursors in acute intermittent porphyria by intravenous infusions of hematin.

In a patient with a severe attack of acute intermittent porphyria, hematin given intravenously caused marked diminution of serum delta-aminolevulinic acid and porphobilinogen. The decline of aminolevulinate was more rapid than that of porphobilinoge. After 2 days of hematin administration, about 5 days were required for delta-aminolevulinic acid, and 11 days for porphobilinogen to return to the concentrations that were detected before treatment. Urinary excretion of both compounds also decreased after hematin administration. Considerable amounts of porphobilinogen were also found in the cerebrospinal fluid of the patient.

Adult↗
PubMedDate not supplied

Relationship between an arrhythmogenic action of lidocaine and its effects on excitation patterns in acutely ischemic porcine myocardium.

To investigate the relationship between the effects of lidocaine on excitation patterns and its effects on the incidence of arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine, at a dose of either 2.5, 5.0, or 10.0 mg/kg i.v., in 29 open-chest anesthetized pigs. Sixty-three unipolar electrograms and a surface lead electrocardiogram were continuously recorded during atrial pacing and spontaneous ventricular arrhythmias. Ventricular fibrillation (VF) occurred only in four of a total of 45 control occlusions. VF occurred in two of five pigs following injection of lidocaine 2.5 mg/kg, in 15 or 17 pigs following injection of a 5 mg/kg dose, and in all three preparations following injection of a 10 mg/kg dose. Just prior to VF during occlusions preceded by injections of lidocaine 5 mg/kg, activation time of ischemic myocardium in atrial-paced beats was delayed by only 30 +/- 17 ms beyond preocclusion values, compared with 18 +/- 11 ms at a similar time during control occlusions and 33 +/- 18 ms at the end of control occlusions (mean +/- SD; n = 8). As ventricular tachycardia (VT) developed in the presence of lidocaine, conduction was further slowed or blocked in ischemic areas, and slowed in nonischemic regions; at the transition from VT to VF, excitation patterns displayed circus movement involving nonischemic regions.

Animals↗
PubMedDate not supplied

Continuous ST segment recording during thrombolysis in acute myocardial infarction: a report on orthogonal ECG monitoring.

BACKGROUND: A noninvasive, real time method is needed to identify failures of thrombolysis and evaluate new treatments in acute myocardial infarction (MI). OBJECTIVE: To study XYZ monitored ST segment evolution during thrombolysis in acute MI and to examine the correlation of ST parameters to outcome. DESIGN: Thirty-five patients receiving tissue plasminogen activator (tPA) (n = 18) or streptokinase (SK) (n = 17) for acute MI were monitored by vector-cardiography during the first 12 h of thrombolytic therapy. Computer constructed ST vector magnitude (ST-VM) trends were analyzed for 0.5 or greater decline from the initial ST amplitude (IA) lasting for 10 mins or longer (ST response) and for ST re-elevation 0.75 IA or more following ST decline. The degree of ST response, time from treatment onset and ST-VM re-elevation were correlated to peak creatine phosphokinase (CPK), left ventricular ejection fraction (EF) and final ST-VM. RESULTS: The presence of an ST response correlated with a lower peak CPK (2691 +/- 1625 versus 4057 +/- 1622 U/L, P = 0.043) and tended to higher EF (0.48 +/- 0.11 versus 0.36 +/- 0.09, P = 0.057). The ST responder group had fewer patients with ST re-elevation than the group of nonresponders (13 of 30 versus five of five patients, P = 0.041). Moreover, ST response before 120 mins was associated with lower peak CPK (2089 +/- 1299 versus 3367 +/- 177 U/L, P = 0.02) and better EF (0.54 +/- 0.06 versus 0.41 +/- 0.12, P = 0.02) compared with later or no ST response. The degree of ST response correlated significantly with a lower ST-VM during the last hour (r = -0.744, P = 0.001). ST trends showed no significant differences between treatment groups (tPA versus SK). The tPA group, however, tended to an overall earlier ST response (117 +/- 75 versus 163 +/- 64 mins, P = 0.13). CONCLUSIONS: Early ST-VM trends are closely associated with electrocardiographic and clinical outcome and may provide a basis for clinical management, therapeutic comparisons and better insight into thrombolysis in MI.

Aged↗