Fatal occlusion of the left coronary main stem by a fragment from the femoral artery: a previously unreported complication of cardiac catheterization.

A 59-year-old man with grade III angina pectoris and 80% stenosis of the left anterior descending coronary artery developed an acute total occlusion of the artery during percutaneous transluminal coronary angioplasty (PTCA). Attempts at recanalisation and resuscitation were ineffective, and the patient died. The medico-legal autopsy revealed obstruction of left main coronary artery by a ringshaped piece of arterial wall that had been torn out of the femoral artery at the punction site and driven around the tip of the catheter into the orifice of the left coronary artery, filling it. This kind of complication of PTCA has not been described previously.

Regulation of vascular permeability in rat testes by modified human chorionic gonadotrophin.

High-performance liquid (HPL)-anion-exchange chromatography of testicular interstitial fluid (IF) and medium conditioned by polymorphonuclear leucocytes (PMN) revealed two major peaks (at fractions 2-3 and 7-8), which, with human chorionic gonadotrophin (hCG) increased vasopermeability in rat testes measured by the uptake of iodinated hCG and by interstitial fluid volume. When hCG was incubated with the fraction 7-8 peak and subsequently purified on HPLC it significantly increased testicular vasopermeability with a concomitant accumulation of PMNs in the testicular blood vessels and interstitium. The removal of hCG from the purified preparation with anti-hCG Sepharose 4B abolished the vasopermeability effect of the preparation, confirming that hCG itself is modified in such a way as to produce the response. The results suggest that both IF and PMN-conditioned medium contain two components with different charges, which interact with hCG to increase vasopermeability by a PMN-mediated process. The results also indicated that hCG may itself be modified chemotactically, or so that it elicits production of leucoattractant in the testes.

Plasminogen activator is involved in the hCG-induced neutrophil extravasation and vasopermeability increase in the rat testis.

The role of proteolytic enzymes in the hCG-induced increase in testicular vasopermeability and neutrophil extravasation was studied using protease inhibitors. An intra-testicular injection of hCG together with incubation medium conditioned by polymorphonuclear leucocytes (PMNs) caused a significant increase in vasopermeability and a coincident extravasation of PMN's from the postcapillary venules in the rat testis. When p-aminobenzamidine, a serine protease inhibitor which inhibits urokinase-type plasminogen activator, was administered together with hCG in the incubation medium, both the permeability increase and PMN extravasation were prevented. Aprotinin, another serine protease inhibitor, and Eglin C, a specific neutrophil elastase and cathepsin G inhibitor were, however, without effect. None of these inhibitors caused any non-specific vascular effects in the testis at the concentrations used. These results support the concept that the hCG-induced increase in vasopermeability in the rat testis is related to extravasation of PMNs and suggest that urokinase-type plasminogen activator is involved in migration of these cells through the postcapillary venular walls.

Rat testicular interstitial fluid contains mediators of vasopermeability.

An intradermal injection of testicular interstitial fluid (IF) produced a marked increase in vasopermeability in a dose-dependent manner. Likewise bovine follicular fluid caused a smaller but significant response. The effect of IF was associated with accumulation of polymorphonuclear leucocytes (PMNs) inside the dermal venules and with their adherence to the venular endothelium. A minor but significant response was noticed after injecting anterior chamber fluid, but there was no response after an injection of amniotic fluid or serum intracutaneously. Destroying the Leydig cells with ethane dimethanesulphonate did not change the vasopermeability-increasing effect of IF, but after denaturation of IF proteins the effect was diminished by about 50%. Intravenous administration of hCG did not increase the ability of IF to cause the effect. These results suggest that rat testicular interstitial fluid contains mediators of vasopermeability, probably specific for the testis and also follicular fluid. The vasopermeability effect of IF does not seem to depend on the collecting time or on Leydig cells and is at least partly mediated by PMNs which are seen in the dermal venules shortly after an injection of IF.

Interaction of hCG with testicular interstitial fluid produces a leucotactic factor.

An intratesticular injection of hCG (5 ng) mixed with testicular interstitial fluid (IF) increases vascular permeability in the rat testis. The present results show that the permeability increase induced by this treatment is accompanied by a massive accumulation of polymorphonuclear leucocytes (PMNs) in both the testicular postcapillary venules and the interstitium. Depletion of neutrophils in the circulation by treatment with anti-neutrophil serum significantly inhibited the permeability increase induced by this treatment. An intratesticular injection of PMNs (10(7) cells) or hCG alone had no effect on permeability, but a combination of the two caused a significant increase in permeability. The PMNs were found to secrete a component in vitro which, when injected intratesticularly together with hCG, caused a increase and a simultaneous massive accumulation of PMNs in the postcapillary venules and interstitium. This permeability increase was prevented by the serine protease inhibitor p-aminobenzamidine, suggesting an involvement of the plasminogen activator system in the response. The results suggest that hCG interacts with an IF component to produce leucotactic factors that increase permeability indirectly by attracting PMNs to the tissue, and that the IF component may originate in the PMNs.

Luteinising hormones activate a factor(s) in testicular interstitial fluid which increases testicular vascular permeability.

The mechanism by which hCG increases the rat testicular vascular permeability was studied by injecting the testes with hCG (0.1-100 ng) together with testicular interstitial fluid (150 mul) or with the fluid alone (control) and measuring the uptake of i.v. injected [125I]hCG and the interstitial fluid volume in the testes. Both parameters were already increased with 1 ng of hCG and maxima were seen with 2 ng of hCG. The effect of hCG was not inhibited by injection of a 1000-fold excess of deglycosylated hCG together with hCG. No increase was seen after injection of 2 ng of hCG in saline or in rat serum. The response was specific to luteinising hormones since only rLH mimicked the effect of hCG, but deglycosylated hCG, rFSH or rat prolactin did not. Denaturation of the fluid or addition of serine protease inhibitor (p-aminobenzamidine) to the fluid prevented the effect of hCG. Treatment of the hCG-activated fluid with anti-hCG gamma-globulin Sepharose did not abolish the permeability effect of the fluid. This, and the finding that hCG is not catabolised during incubation in the fluid, suggests that hCG itself is not transformed to a vasoactive compound in the fluid. These results strongly suggest that luteinising hormones activate a factor(s) in rat testicular fluid which mediates their permeability effect. The putative factor(s) seems to be heat-sensitive with a molecular weight of over 10 000 Da.

The hCG-induced increase in hormone uptake and interstitial fluid volume in the rat testis is not mediated by steroids, prostaglandins or protein synthesis.

The possible mediation by steroids, prostaglandins or protein synthesis on the hCG-induced increase in hormone uptake and interstial fluid volume in the rat testis in vivo was studied following a single iv injection of hCG. A high dose of hCG increased its own uptake in the testis and this uptake coincided with an increase in capillary permeability and accumulation of interstial fluid. The possible role of steroids, prostaglandins and protein synthesis in these changes was studied in vivo using aminoglutethimide, indomethacin and cycloheximide, respectively, as inhibitors. However, none of these prevented the hCG-induced changes in uptake and interstial fluid volume, which suggests that they do not mediate this phenomenon.

The effect of varying doses of hCG on the in vivo uptake by rat testis and serum testosterone response.

The in vivo uptake of human chorionic gonadotropin (hCG) in the rat testes and mode of the early testosterone response were studied after a single intravenous injection of varying doses of hCG. The uptake of hCG by the testes was parallel up to 6 h with all hormone doses, decreased thereafter to low level by 24 h with low hormone doses but continued to increase up to 24 h with the highest dose of hCG. The clearance rate of hCG from the blood was independent of the hormone dose used. Serum testosterone peaked gradually earlier when the hCG dose increased, and the highest hCG dose caused a slightly biphasic response with maxima at 1 and 12 h, the former peak being more pronounced. These results suggest that the in vivo uptake of hCG in the testes is modulated by the hormone dose used and that the mode of early serum testosterone response to varying hCG doses is dose dependent.

Immunocytochemical localization of receptor human chorionic gonadotropin complexes in rat leydig cells.

Localization of receptor-bound human chorionic gonadotropin (hCG) in rat testis was studied by the peroxidase-antiperoxidase (PAP) complex method. The rats were injected with a single intravenous dose (1000 IU) of hCG. Three, 6, 12, and 24 hr after injection the testes were removed for localization of the hormone. The hormone localized to the periphery of the Leydig cells at all observation points. The intensity of the staining varied between the cells, suggesting that the number of receptors or the accessibility of the receptors to the circulating hormone varies from one cell to another. The staining surrounded the Leydig cells unevenly, but no progressive patching or capping was found. This observation suggests that hCG binds preferentially to the cell surface areas directed toward the capillaries. Compatible results were obtained with anti-hCG serum and with antisera against the hCG subunits. These results are consistent with previous observations that the luteinizing hormone (hCG) receptors accessible to the circulating hormone are located at the surface of the Leydig cells.

Localization of receptor-human chorionic gonadotropin complex to the surface of the luteal and interstitial glandular cells in the pseudopregnant rat ovaries with the peroxidase-antiperoxidase (PAP) complex method.

Receptor-bound hCG was localized in pseudopregnant rat ovarian cells at semiultrastructural level with the peroxidase-antiperoxidase (PAP) complex method. The animals received 2, 6, 12 or 24 h prior to killing a single intravenous injection of hCG and the hormone was localized in the 5-micrometer paraffin sections and in the 1-micrometer epon sections using the pre-embedding technique. The peroxidase staining localized to the periphery of the luteal and interstitial glandular cells. No significant staining occurred in the intracellular structures of the cells during the 24-h observation period. However, the appearance of staining in the subplasmalemmal structures can not be excluded. These results are compatible with the previous observations that the receptor-hCG complexes are primarily formed at the surface of the luteal and interstitial glandular cells.