Effects of almitrine in decompensated chronic respiratory insufficiency.
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Biomedical subjects
Publications and source records attributed to P Mols.
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PURPOSE: The aim of this prospective study was to evaluate the relative value of CT and (99m)Tc-DMSA scintigraphy in the diagnosis of acute pyelonephritis (APN) in adult patients suspected of having urinary tract infection. METHOD: The study was conducted in 36 patients presenting with symptoms suggestive of urinary tract infection. Plain B-mode sonography, CT with contrast medium, and (99m)Tc-DMSA scintigraphy of the kidneys were performed in all patients. Both CT and (99m)Tc-DMSA scintigraphy were performed within 72 h after admission. RESULTS: Twelve patients with clinical and biological signs of urinary tract infection had no CT or (99m)Tc-DMSA scintigraphy abnormalities. Among these patients, lower urinary tract infection was found in 10 patients and 2 patients had ureteral obstruction. In the 24 remaining patients, the diagnosis of APN was made. Among these patients, a correlation was found between CT and (99m)Tc-DMSA scintigraphy in 11 cases. In two cases, both examinations were normal, and in nine cases, both were abnormal. In 11 cases of the 13 remaining patients, abnormal CT was found with normal (99m)Tc-DMSA scintigraphy, whereas the 2 last cases had normal CT and abnormal (99m)Tc-DMSA scintigraphy results. In two cases, bilateral lesions found on CT manifested as unilateral abnormalities on (99m)Tc-DMSA scintigraphy images. CONCLUSION: The diagnosis of APN in adult patients is based on clinical presentation and biological findings. Few studies have compared (99m)Tc-DMSA scintigraphy with CT in the detection of parenchymal involvement in APN. We conclude that CT is more accurate than (99m)Tc-DMSA scintigraphy in the detection of APN lesions in adult patients.
Central and regional hemodynamic studies were performed before and after administration of nitrendipine, a recently introduced calcium-channel blocker, in 10 normotensive patients with chronic obstructive pulmonary disease. None of them had a mean pulmonary artery pressure higher than 20 mm Hg. Ninety minutes after oral intake of 20 mg nitrendipine, cardiac output increased by 22%, heart rate increased by 12%, mean arterial pressure decreased by 7%, and pulmonary artery pressures as well as filling pressures of the heart did not change. Venous admixture and alveolar to arterial PO2 gradients increased by 54% and 22%, respectively. Hepatic blood flow increased by 33%. Renal blood flow remained unchanged and glomerular filtration rate decreased by 11%. Thus, in normotensive patients, nitrendipine administration induces systemic vasodilatation with an apparently reflex increase in cardiac output. These effects are accompanied by a deterioration in pulmonary gas exchange, increase in hepatic perfusion, no change in renal perfusion, and possibly a slight deterioration in renal function.
OBJECTIVE: To determine the safety and possible efficacy of diaspirin cross-linked hemoglobin (DCLHb) in the treatment of patients in Class II-IV hemorrhagic, hypovolemic shock. DESIGN: Multicenter, randomized, normal saline-controlled, dose-escalation study. SETTING: Eleven hospitals in the U.S. and Belgium. SUBJECTS: One hundred and thirty-nine (139) hospitalized patients with Class II-IV hemorrhagic, hypovolemic shock within the previous 4 hours who still were requiring therapy for shock. INTERVENTIONS: Beginning with the lowest dose, patients were randomized to receive 50, 100, or 200 mL of either 10% DCLHb or normal saline infused intravenously over 15 minutes. Following infusion of either treatment, further fluid resuscitation could be given, as necessary, to maintain perfusion. Vital signs, laboratory assessments, blood and fluid administration, complications, and adverse events were recorded at various times from the end of infusion through 72 hours after infusion. RESULTS: A total of 29 (13 DCLHb- and 16 saline-treated) patients died during the study period. Adverse events were experienced by 61% of patients in the DCLHb group and 53% of patients in the saline group; serious adverse events occurred in 28% of DCLHb-treated patients and 30% of saline-treated patients. The incidence of prospectively defined, clinical complications, including renal insufficiency and renal failure, was similar between the treatment groups except for the occurrence of dysrhythmias/conduction disorders, which occurred significantly more frequently in the saline-treated patients than the DCLHb-treated patients (p = 0.041). At the highest dose level (200 mL), statistically significant between-group differences were observed with greater increases in serum amylase, LDH, the isoenzymes LD1,2,4 and 5, and CK-MB in the DCLHb group compared to the control group; none were of clinical significance. The volume of blood administered did not differ between the groups. Overall 24- and 72-hour survival rates were similar between treatment groups, although the hospital discharge rate was slightly higher in the DCLHb-treated patients (80%) compared with the saline-treated patients (74%). CONCLUSION: Administration of 50 to 200 mL of DCLHb to patients in hemorrhagic, hypovolemic shock was not associated with evidence of end organ toxicity or significant adverse events. Further studies involving larger doses and, perhaps, earlier administration of DCLHb are warranted.
Pulmonary haemodynamics and blood gas tensions were investigated in eight healthy volunteers, breathing room air and at the 15th min of an acute inspiratory hypoxia (fraction of inspired oxygen, (FIO2), 0.125) before and after administration of ibuprofen, a cyclooxygenase inhibitor, and of dazoxiben, a thromboxane A2 (TxA2) synthetase inhibitor; both drugs either with or without an infusion of prostaglandin E1. Hypoxia decreased arterial oxygen tension (PaO2) to below 50 mmHg in every subject and increased pulmonary vascular resistance by an average of 100-150% from baseline values. Acute and chronic dazoxiben or ibuprofen administration markedly reduced serum thromboxane B2 (TxB2), the stable metabolite of TxA2, but had no effect on pulmonary haemodynamics and blood gas tensions in both normoxic and hypoxic conditions. Prostaglandin E1 given in addition to ibuprofen or to dazoxiben did not inhibit hypoxia-induced increases in pulmonary vascular resistance. The stability of this hypoxic pressor response on repetition of an acute hypoxic exposure was established in six additional healthy subjects. Although obtained on a small number of subjects, these results do not suggest that products of the cyclooxygenase pathway of arachidonic acid metabolism play an important role in modulating normoxic or hypoxic pulmonary vascular tone in man.
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