Vena cava filters: a synopsis of complications and related topics.

Deep venous thrombosis and pulmonary embolism constitute common preventable causes of morbidity and mortality. The incidence of venous thromboembolism (VTE) continues to increase. Standard anticoagulation therapy may reduce the risk of fatal PE by 75% and that of recurrent VTE by over 90%. For patients who are not candidates for anticoagulation, a vena cava filter (VCF) may be beneficial. Despite a good overall safety record, significant complications related to VCF are occasionally seen. This review discusses both procedural and non-procedural complications associated with VCF placement and use. We will also discuss VCF use in the settings of pregnancy, malignancy, and the clinical need for more than one filter.

Spontaneous renal artery dissection: three cases and clinical algorithms.

Spontaneous renal artery dissection (SRAD) is rare. Clinical manifestations vary from minimal symptoms to life-threatening hypertension. We analysed three cases from our institution and conducted a literature review in order to design diagnostic and treatment algorithms for SRAD.

Ragweed sensitization alters pulmonary vascular responses to bronchoprovocation in beagle dogs.

In ragweed (RW)-sensitized beagle dogs, we tested the hypothesis that reactivity of the pulmonary vasculature was enhanced with aerosolized histamine (Hist) and RW. Seven dogs were neonatally sensitized with repeated intraperitoneal RW injections, and 12 dogs were controls (Con). The dogs were anesthetized with intravenous chloralose, mechanically ventilated, and instrumented with femoral arterial and pulmonary artery catheters. Specific lung compliance (CLsp), specific lung conductance (Gsp), systemic vascular resistance index, and pulmonary vascular resistance index (PVRI) were measured before and after bronchoprovocation with Hist and RW. After Hist inhalation (5 breaths of 30 mg/ml), both Con and RW dogs had significant (P < 0.05) decreases in CLsp (-51 +/- 4 and -53 +/- 5%, respectively) and Gsp (-65 +/- 5 and -69 +/- 3%, respectively), but only RW-sensitized dogs had a significant increase in PVRI (38 +/- 10%). After RW inhalation (60 breaths of 0.8 mg/ml), only RW-sensitized dogs had significant increases (62 +/- 20%) in PVRI and decreases in Gsp (-77 +/- 4%) and CLsp (-65 +/- 7%). We conclude that, compared with Con, RW-sensitized beagle dogs have increased pulmonary vasoconstrictive responses with Hist or RW inhalation.

The effect of tris(2-chloroethyl)amine on human hemoglobin.

The reaction of tris(2-chloroethyl)amine (TCEA) with purified hemoglobin and its effect on properties of hemoglobin was studied using 14C-labeled TCEA. Hemoglobin remained soluble after binding as much as 4 TCEA per heme. In concentrations which did not denature hemoglobin TCEA reacted only with a small proportion of the free SH groups; blockade of the SH groups with PMB did not noticeably affect the binding of TCEA to hemoglobin. Hydrolysis by trypsin or chymotrypsin of hemoglobin which had reacted with TCEA yielded radioactive peptides besides not radioactive peptides and radioactive compounds not reacting with ninhydrin. The reaction with TCEA caused a change in electrophoretic mobility of hemoglobin and prevented its complete disintegration by PMB into subunits. After reaction with TCEA the affinity of hemoglobin for oxygen was strongly increased and the heme-heme interaction strongly diminished. The Bohr effect and the effect of 2,3-diphosphoglycerate on oxygen affinity remained unchanged. The effect of TCEA on the properties of hemoglobin points to specificity in its reaction with functional groups of hemoglobin.

Effects of 4-dimethylaminophenol, Co2EDTA, or NaNO2 on cerebral blood flow and sinus blood homeostasis of dogs in connection with acute cyanide poisoning.

The effects of the cyanide antidotes DMAP, Co2EDTA, and NaNO2 on cerebral blood flow (CBF) and cerebral blood gases were investigated in connection with acute poisoning of dogs by cyanide. The substances were injected intravenously. Local CBF as measured with thermocouples in the cingulum increased by 100-200% after a non-lethal dose of KCN (1 mg/kg) and by 50% after injection of NaNO2 (15 mg/kg), that oxidized some 20% of the total hemoglobin to ferrihemoglobin. Co2EDTA (10 mg/kg) induced a decrease in local CBF of 30% and in brain temperature of 0.5 degree C. The temperature diminished also after poisoning by KCN, but it rose by 0.15 degree C after the administration of NaNO2. Local CBF and sinus sagittalis blood flow increased by 60-160% for about 15 min, and the brain temperature decreased by 0.4-0.5 degree C when DMAP (3.25 mg/kg) or Co2EDTA (15 mg/kg) was injected 1 min after poisoning by cyanide (4 mg/kg), a dose that always caused respiratory arrest. Immediately after injection of DMAP the brain temperature rose transiently by 0.1-0.2 degree C. Co2EDTA did not exert such an effect. In the sinus sagittalis blood of artificially ventilated animals pCO2 decreased rapidly by 10-20 mmHg after poisoning and approached the initial level after treatment with DMAP or Co2EDTA. The highest value of pO2 was about 80 mmHg and 50 mmHg after injection of DMAP and Co2EDTA, respectively; thereafter pO2 declined to 20 mmHg or 40 mmHg at 20 min. The lactate concentration increased by 60-70% without tendency to return to normal.

Interactions of the chelating agent 2,3-dimercaptopropane-1-sulfonate with red blood cells in vitro. I. Evidence for carrier mediated transport.

Uptake of the water soluble 1,2-dimercaptopropanol (BAL) derivative 2,3-dimercapto-1-sulfonate (DMPS) into human red blood cells was found in vitro and the mode of penetration studied in detail. The compound entered erythrocytes in a concentration dependent manner. In contrast to sealed ghosts where inside and outside concentrations reached the same value, DMPS accumulated in intact erythrocytes. Since no binding of DMPS could be detected, the reason for accumulation was assumed to be a conversion of DMPS into chelates or metabolites which penetrated the membrane in a slower rate. A facilitated transport of DMPS mediated by the anion carrier protein was concluded on the basis of the following similarities with the anion transport: inhibition of [14C]DMPS-uptake by N-ethylmaleimide (NEM), tetrathionate (90%), sulfate (50%), 5,5'-dithio bis(2-nitrobenzoic acid) (DTNB) (25%); inhibition of uptake and efflux by 4,4'-diisothiocyano-2,2'-stilbene disulfonate (DIDS) (80%), dipyridamole (55%); temperature dependency (activation energy 24 Kcal/mol); pH-dependency (pH optimum about 6.9); counter-transport; activation of uptake by preincubation with DMPS (transmembrane effect).

Interactions of the chelating agent 2,3-dimercaptopropane-1-sulfonate with red blood cells in vitro. II. Effects on metalloproteins.

The implications of the carrier mediated uptake of 2,3-dimercaptopropane-1-sulfonate (DMPS) (D.B. Wildenauer et al., Chem.-Biol. Interact., 42 (1982) 165) on cytoplasmic components of human red blood cells have been investigated in vitro. The water-soluble chelating agent caused a mobilization of metals (zinc and copper) from metalloproteins which resulted in a permeation of the membrane. Furthermore, a cytoplasmic protein was found to be attached to the membrane after DMPS treatment of red blood cells. The protein was isolated and identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), amino acid analysis and finger-printing as carbonic anhydrase. The enzyme could be solubilized from the membrane by addition of beta-mercaptoethanol, suggesting an involvement of sulfhydryl-groups. In a reconstitution experiment, DMPS-treated human carbonic anhydrase could be attached to inside-out vesicles which were prepared from human erythrocytes. In contrast, bovine carbonic anhydrase, which is known to lack sulfhydryl-groups, failed to bind to the same vesicles. Moreover, attachment of carbonic anhydrase to the membrane did not occur when intact bovine erythrocytes were treated with DMPS. It is suggested that zinc-depletion of carbonic anhydrase causes the liberation of a sulfhydryl-group of the enzyme. This is followed by a disulfide formation with a component of the membrane which results in the observed membrane attachment.

[Antidotes in acute poisonings]. / Antidote bei akuten Vergiftungen.

Inhalation of dexamethazone (Auxiloson) prohibits a toxic edema of the lungs after poisoning with irritants. Poisoning with methanol is to be treated with ethanol trisbuffer and tetrahydrofolic acid (Folsan). "Solvents" should be "bound" in paraffinum liquidum in order to prohibit their absorption. Poisoning with organophosphates is to be treated with high doses of atropine and with the reactivator obidoxime (Toxogonin). Cyanide poisoningis are to be treated with 4-dimethylamino-phenol (DMAP) and sodium thiosulfate. In methemoglobin-poisoning the reduction of ferrihemoglobin is accelerated when toluidine-blue is applied intravenously.

Therapeutic effects of the bis-pyridinium salts HGG-12, HGG-42, and atropine, benactyzine in organophosphate poisoning of dogs.

Therapeutic properties of various combinations of the bispyridinium salts HGG-12 and HGG-42 against soman and sarin poisoning were investigated in male beagles. Best therapeutic efficiency was shown by HGG-42 in a dosage of 30 muMol/kg. Also good effects were produced by the combination of both oximes in a low dosage of 3 muMol/kg for each one. In soman poisoning no significant reactivation of cholinesterase in serum or erythrocytes was observed.

Therapeutic effects of HS-3, HS-6, benactyzine, and atropine in soman poisoning of dogs.

Investigations into the therapeutic properties of various combinations of the bispyridinium salts HS-3 and HS-6 and the cholinolytics atropine and benactyzine against soman poisoning in unanesthetized male beagles were performed. In our investigations we observed that: 1. The most effective protection against soman poisoning was attained if both oximes were applied early i.m. 6 min after intoxication together with the cholinolytics. 2. On the basis of clinical symptoms HS-6 proved to have a more intensive therapeutic effect than HS-3 upon early application. 3. If HS-3 was applied early after s.c. intoxication with low concentrations of soman (up to 3 LD50), a significant protection or reactivation effect on serium cholinesterase was measured. 4. When HS-3 was applied at the beginning of convulsions--generally 28 min after s.c. intoxication--it also raised the rate of surviving animals. 5. The maximal blood levels for HS-3 and HS-6 were measured 20-30 min after i.m. injection; the half-life values of HS-3 and HS-6 in plasma were 45-60 min.

Effects of 4-dimethylaminophenol in rat kidneys, isolated rat kidney tubules and hepatocytes.

1. Addition of 4-dimethylaminophenol (DMAP) to suspensions of isolated rat kidney tubules increased extracellular lactate dehydrogenase (LDH) at concn. which did not markedly affect gluconeogenesis. ATP content was also decreased by DMAP but this did not occur until the membrane became permeable to LDH. There was no similar leakage of the mitochondrial enzyme glutamate dehydrogenase. 2. After i.v. injection of DMAP to rats in doses which did not inhibit gluconeogenesis, kidney glutathione was decreased and the urinary LDH was increased. DMAP was irreversibly bound to tissue in rat, with the highest binding in the kidney. The highest binding occurs in those tissues in which DMAP causes necrosis. 3. In isolated rat hepatocytes, DMAP caused toxic effects which were similar but less extensive than occur on addition of DMAP to kidney tubules. The formation of acid-soluble metabolites was higher in isolated rat hepatocytes (20 nmol/mg protein) than in rat kidney tubules (4 nmol/mg protein). DMAP-glucuronide and DMAP-sulphate comprised the major acid-soluble metabolites in both preparations; conjugates of DMAP with glutathione or cysteine were also found.