Double-blind, randomized, placebo-controlled evaluation of atropine to prevent vasovagal reaction during removal of femoral arterial sheaths.

STUDY OBJECTIVE: To evaluate the efficacy and safety of atropine in preventing vasovagal reactions (VVRs) during removal of femoral arterial sheaths after diagnostic left heart catheterization. DESIGN: Prospective, double-blind, randomized, placebo-controlled study. SETTING: University-affiliated, 450-bed teaching hospital. PATIENTS: One hundred sixty-five patients undergoing left heart catheterization. INTERVENTIONS: Eighty-eight patients were assigned to receive atropine 0.5 mg intravenously and 77 received placebo 5 minutes before sheath removal. MEASUREMENTS AND MAIN RESULTS: The frequency of VVRs was significantly reduced in the atropine group compared with the placebo group, 2.3% and 10.4%, respectively (overall relative risk in the atropine group 0.22, 95% CI 0.12-0.41, p=0.03). Significant decreases in systolic (35.2 +/- 5.8 mm Hg, p<0.001) and diastolic blood pressures (12.6 +/- 12.6 mm Hg, p=0.002) occurred in the 10 patients with VVRs compared with those without VVR. No cardiac arrhythmias occurred after atropine administration. Dry mouth was the only side effect reported with atropine (8/88, 9%). CONCLUSION: Atropine significantly reduced the frequency of VVRs associated with removal of femoral arterial sheaths after diagnostic left heart catheterization. The drug should be studied in a larger series of patients to assess its ability to decrease the morbidity and costs associated with VVR.

Severe acute metabolic alkalosis.

We have presented the case of a 34 year old male patient who was admitted with severe metabolic alkalosis (MA). Peak serum HCO3 was 96 mg/dl and compensatory PCO2 was 95 which, to our knowledge, has never been reported before in a patient with MA. MA was probably generated by consumption of high amount of NaHCO3 and renal impairment and maintained by impaired renal function due to volume depletion hypokalemia and hyochloremia. The patient was successfully treated with IV administration of saline and KCL.

Cortical blindness after cardiac catheterization: effect of rechallenge with dye.

Transient cortical blindness (CB) is a rare complication of dye usage during cardiac catheterization, percutaneous transluminal coronary angioplasty (PTCA) or directed coronary atherectomy (DCA), and is limited to few case reports. In this paper, we are describing three such cases of CB who, upon reexposure to dye during subsequent cardiac catheterization, did not develop CB. To our knowledge, the consequences of reexposure of these patients to dye has not been described in literature.

Heparin-flush associated thrombocytopenia--induced hemorrhage: a case report.

Thrombocytopenia is a well known complication of heparin. It occurs when heparin is used in full therapeutic dose or in subcutaneous mini-doses for prophylaxis. This has also been reported with minuscule dose of heparin used in heparin-flushes to keep vascular access catheters patient. We are reporting for the first time, a case of severe hemorrhage due to thrombocytopenia associated with heparin flushes.

Total inferior vena cava thrombosis following coronary artery bypass surgery.

A 44-yr-old male presented with abdominal and back pain following coronary bypass surgery (CABG). Total inferior vena cava (IVC) thrombosis was then documented by computed tomography as well as IVC contrast cineangiography. Furthermore, the patient developed multiple pulmonary emboli. This presentation with severe abdominal and back pain with lack of early peripheral edema without apparent hepatic or renal dysfunction and with extreme elevation of erythrocyte sedimentation rate seems rather unusual. To our knowledge, such massive IVC thrombosis has not been reported following CABG. Thrombolytic and anticoagulant therapy was utilized with good recovery.

Modification of the hyperthermic response on neuroblastoma cells by cAMP and sodium butyrate.

The role of adenosine 3',5'-cyclic monophosphate (cAMP) and sodium butyrate in modifying the effect of heat on murine neuroblastoma cells (NBP2) in culture was evaluated on the criterion of survival. An elevation of cellular cAMP level by prostaglandin (PG) A2, a stimulator of adenylate cyclase, and 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (R020-1724), an inhibitor of cyclic nucleotide phosphodiesterase, only during heat treatment (43 degrees C and 40 degrees C) was sufficient to enhance the effect of heat. The extent of enhancement (additive versus synergistic) depended upon the cAMP stimulating agent and the experimental condition. When these agents were added after heat treatment for the entire observation period, they produced similar results. PGA2 and R020-1724 are known to increase the intracellular level of cAMP in these cells by three and fivefold, respectively; therefore, the effect of these agents in enhancing the heat-response may be mediated by cAMP-dependent mechanisms. The presence of sodium butyrate during heat treatment alone was ineffective; however, when it was added before or after heat treatment for the entire observation period, the survival of heated cell was markedly reduced.

Vitamin E enhances the chemotherapeutic effects of adriamycin on human prostatic carcinoma cells in vitro.

Vitamin E (tocopherol) enhances the growth inhibitory effects of adriamycin (ADR) on a variety of cancer cells in vitro. The role of vitamin E (d-alpha-tocopheryl) acid succinate in adjuvant chemotherapy with ADR was assessed in DU-145 human prostatic carcinoma cells in culture. Adriamycin produced a dose-dependent growth inhibition of DU-145 cells. The ID50 of DU-145 cells on the criteria: of clonal assay was 13 ng./ml. and of cell count assay was 14 ng./ml. Vitamin E succinate also inhibited the growth of DU-145 human prostatic carcinoma cells in a dose-dependent manner. 4.4 micrograms./ml. and 5.4 micrograms./ml. vitamin E succinate in the culture medium produced inhibition of growth to 50 per cent of control (ID50) in the clonal and the cell count assays respectively. When adriamycin and vitamin E succinate were used in combination, both additive and synergistic effects were observed, depending on the concentration of vitamin E succinate used. Doses of vitamin E succinate greater than its ID50 had a synergistic effect while doses smaller than its ID50 had an additive effect. In either case, the presence of vitamin E succinate caused an enhancement of tumor cell cytotoxicity of adriamycin while decreasing its ID50. Equivalent concentrations of sodium succinate and ethanol used to dissolve vitamin E succinate did not have any effect on DU-145 cells. Thus, it is concluded that the effect of vitamin E succinate is due to vitamin E and not due to succinate or ethanol. These results suggest that vitamin E may have a role in the treatment of human prostatic cancer as an adjuvant agent to adriamycin.

Ethanol. A heat sensitizer on neuroblastoma cells in culture.

The presence of 1% ethanol in culture medium during heat treatment (40 degrees C for 8 hours and 43 degrees C for 15 minutes) was sufficient to enhance the effect of hyperthermia on murine neuroblastoma cells (NBP2) in culture, on the criteria of growth (number of viable cells per dish) and survival (colony formation). However, the metabolites of ethanol, acetaldehyde, and sodium acetate at concentrations of 0.003% and 0.125% in culture medium, respectively, under the same experimental conditions did not modify the effect of heat (40 degrees C) on these cells. The presence of same concentration of ethanol, acetaldehyde, or sodium acetate for 15 minutes or 8 hours at 37 degrees C did not affect the growth or the survival of NB cells in culture. These results suggest that ethanol itself rather than its metabolites is responsible for the enhancement of heat effect on NB cells. When ethanol and its metabolites were allowed to remain in the culture medium for the entire periods of heat treatment and observation, they also enhanced the effects of heat on NB cells; however, acetaldehyde was more effective.

Effects of dl-alpha-tocopheryl succinate in combination with sodium butyrate and cAMP stimulating agent on neuroblastoma cells in culture.

The effect of dl-alpha-tocopheryl (vitamin E) succinate in combination with Prostaglandin A2 (PGA2) and sodium butyrate on mouse neuroblastoma cells (NBP2) in culture, according to the criteria of growth inhibition and morphological differentiation (neurite formation), was studied. Results showed that PGA2 and sodium butyrate inhibited the growth of NB cells in a dose-dependent manner. The combined effects of vitamin E succinate with PGA2 or sodium butyrate, according to the criterion of growth inhibition, were additive. Vitamin E succinate by itself did not induce morphological differentiation, but it enhanced PGA2-induced morphological differentiation. Sodium butyrate alone or in combination with vitamin E succinate did not significantly increase the level of morphological differentiation. Sodium succinate and an equal amount of solvent (ethanol) failed to modify the effect of PGA2 or sodium butyrate. This suggests that the effect of vitamin E succinate in modifying the response of PGA2 and sodium butyrate on NB cells is due to the effect of vitamin E rather than to that of succinate.

Effect of hyperthermia in combination with vitamin E and cyclic AMP on neuroblastoma cells in culture.

The effect of heat in combination with DL-alpha-tocopheryl (vitamin E) succinate and adenosine 3', 5'-cyclic monophosphate (cAMP) stimulating agents on mouse neuroblastoma cells ( NBP2 ) in culture on the criterion of growth inhibition (due to cell death and inhibition of cell division) was studied. Heat (41 degrees-40 degrees) alone inhibited growth; however, the extent of growth inhibition was dependent upon the temperature and the time of heat treatment. Heat (41 degrees-40 degrees) in combination with vitamin E succinate (5 micrograms/ml) produced an additive effect on the criterion of growth inhibition. Vitamin C (100 micrograms/ml) failed to modify the effect of heat. Prostaglandin A2, a stimulator of adenylate cyclase, and 4 - (3-butoxy-4-methoxybenzyl)-2-imidazolidinone ( R020 -1724), an inhibitor of cyclic nucleotide phosphodiesterase, are known to induce irreversible differentiation in mouse neuroblastoma cells in culture. These agents, in combination with heat (40 degrees) produced a synergistic effect on the criterion of growth inhibition. These data suggest that the addition of vitamin E and cAMP stimulating agents may increase the effectiveness of hyperthermia protocol.

Study on the specificity of alpha-tocopheryl (vitamin E) acid succinate effects on melanoma, glioma and neuroblastoma cells in culture.

d- and dl-alpha-tocopheryl succinate inhibited growth and caused morphological changes in mouse melanoma (B-16), mouse neuroblastoma (NBP2), and rat glioma (C-6) cells in culture. To study whether the effects of alpha-tocopheryl (vitamin E) succinate on tumor cells are mediated by antioxidant mechanisms, the effects of lipid-soluble antioxidants, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) were compared with those of vitamin E succinate. Results showed that these antioxidants produced alterations on the growth and morphology of neuroblastoma, melanoma, and glioma cells which are similar to those produced by vitamin E succinate; however, the extent of the effect depended upon the type of antioxidant and the form of tumor cells. These data suggest that the effects of vitamin E succinate on tumor cells may be mediated, in part, by antioxidant mechanisms.