SUMMARY1. The effects of histamine were investigated on mechanical and electrophysiological parameters in isolated electrically driven human ventricular papillary muscles. The effects of cimetidine and propranolol on histamine responses were also investigated.2. The effects ofhistamine were compared with those ofnoradrenaline, isoprenaline, dimaprit, a selective H2-receptor agonist, and a cyclic AMP derivative, 8-(4-chlorphenylthio) cyclic AMP.3. The effects of histamine and dimaprit and the effects of cimetidine on histamine responses were also investigated in guinea-pig right ventricular papillary muscles in order to allow a comparison with human papillary muscles.4. In human papillary muscles, histamine caused concentration-dependent increases in the force of contraction and reductions in both time-to-peak tension and time-to-half-maximal relaxation. Histamine simultaneously caused distinct changes in the action potential configuration with increases in the height and duration of the plateau phase and an increase in the over-all action potential duration.5. Noradrenaline and isoprenaline produced similar responses to histamine, as did 8-(4-chlorphenylthio) cyclic AMP, consistent with the view that the effects of histamine as well as the fi-adrenoceptor agonists on human ventricle, were associated with cyclic AMP mediated increases in calcium-dependent slow inward current.

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This study tests the hypothesis that reperfusion injury is the principal cause of limb loss after acute arterial occlusion and that this injury is avoidable. Of 61 isolated hindlimbs amputated at the level of the hip joint, 17 were controls (group I), 5 were perfused without ischemia to establish the validity of the model (group II), and 15 underwent 4 hours of ischemia at room temperature without reperfusion (group III). Acute embolectomy was simulated in 24 limbs after 4 hours of ischemia; 12 were reperfused with standard Krebs-Henseleit solution at 100 mm Hg (group IV), and 12 were reperfused under controlled conditions (i.e., 37 degrees C, 50 mm Hg) with substrate-enriched modified reperfusate (group V). Leg volume, water content, contractile function, and high-energy phosphate content were assessed and data were expressed as mean +/- SD. Four hours of ischemia caused a profound fall in adenosine triphosphate content (4.0 vs 26.0 mmol/L/gm of protein, p less than or equal to 0.001). Uncontrolled reperfusion resulted in severe reperfusion injury; massive edema developed (83% vs 75%, p less than or equal to 0.01), leg volume increased markedly (21.5% above control, p less than or equal to 0.001), and no contractile function followed electrical stimulation. In contrast, controlled reperfusion resulted in normal water content (76.9% vs 75.0%, NS) and minimal change of leg volume (5.5% +/- 5% of control, NS), replenished adenosine triphosphate completely (24.2 vs 26.4 mmol/L/gm of protein, NS), and restored immediate contractile function in all limbs (24.3% +/- 14% of control). This study shows that 4 hours of room-temperature ischemia (18 degrees C) does not produce irreversible damage of the rat hindlimb because the reperfusion injury that follows uncontrolled reperfusion can be avoided. Immediate recovery of contractile function can be restored if the conditions of reperfusion are controlled by gentle reperfusion pressure (50 mm Hg) at 37 degrees C and if a modified substrate-enriched, hyperosmotic, alkalotic, low-Ca++ reperfusate is administered.

37 patients undergoing coronary revascularization were randomly assigned to three protocols for intraoperative myocardial protection: hypothermic ventricular fibrillation (HF) (n = 13), multi-dose blood cardioplegia (BCP) (n = 12) and single-dose Bretschneider's crystalloid cardioplegia (CCP) (n = 12). As intraoperative markers of ischemic damage myocardial ultrastructure, ATP, and CP contents were determined in left ventricular biopsy specimens taken before and after cardiac arrest. Release of serum enzymes (CK, CK-MB, LDH, SGOT) was determined pre- and postoperatively. Hemodynamic data were assessed before, during, and after operation. The incidence of low cardiac output, positive inotropic support, intraaortic balloon counterpulsation, peri-operative myocardial infarction, rhythm disturbances, and the rate of spontaneous defibrillation was compared between groups. The results show a better preservation of high energy phosphates in the BCP group as compared to the HF and CCP groups. Myocardial ultrastructure showed moderate ischemic damage in the hypothermic fibrillation group; in contrast, only slightly deteriorated cells were seen after cardiac arrest, when cardioplegia was used. The incidence of rhythm disturbances was 25% for HF and 42% for CCP. In contrast, only 17% of new rhythm disturbances were seen in the BCP group. Functional recovery (i.e. CI and SWI) of hearts protected with BCP was generally greater as compared to HF and CCP. Release of MB-creatine-kinase isoenzyme was higher in the HF group as compared to cardioplegia. Clinical outcome in terms of incidence of peri-operative infarction, positive inotropic support and low cardiac output was superior in the BCP group but not significantly different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to investigate the extent of connective tissue of the human right ventricle induced by cardiac pacing electrodes. Between January 1984 and July 1987, 34 consecutive patients with VVI-pacing systems were autopsied in the Department of Pathology at the University of Frankfurt/M. The surrounding tissue of these 34 electrodes (17 Siemens Elema 412 S, five Medtronic 6957, one Medtronic 6959, one Medtronic 4011, three Biotronik D2K, three Biotronik K 10, two Osypka FY 62, one Biotronik N, and one Siemens Elema 588) in the right ventricle were investigated histologically. The tissue was stained with Giemsa and the thickness of the connective tissue layer was measured. Stimulation threshold data at various times were known in four of eight screw-in electrodes, in seven of 17 vitreous carbon electrodes and in two of seven smooth surface electrodes. Electrode surface area, implantation time, age of the patient and cause of death were comparable for all three electrode groups. However, a significant difference was found in the extent of connective tissue between the porous surface and screw-in electrodes (128 +/- 55 vs 397 +/- 269 micron, P less than or equal to 0.01) and porous surface and smooth surface electrodes (128 +/- 55 vs 307 +/- 117 micron, P less than or equal to 0.01). No relation (r = 0.106) was found between the duration of implantation and the extent of connective tissue for the vitreous carbon electrodes (Siemens Elema 412 S).(ABSTRACT TRUNCATED AT 250 WORDS)

Since 1978, 2,365 polyurethane (PU) insulated cardiac pacing leads were implanted transvenously at our institution. To date, there have been no insulation failures in those leads. Thirty-seven PU leads were explanted, mainly for exit block, and 28 of these were investigated using the scanning electron microscope. We found a homogeneous distribution of surface changes in all lead segments in 56% of the 28 examined. These changes were more pronounced at the ligature site; severe surface cracking was noticed in 21%, with the deepest crack being 40 micron (average range of 10-15 micron). There appeared to be no time-dependency of the surface changes as indicated by regression analysis (r = 0.32, p greater than 0.05). The ultimate severity and outcome of this degradation process in the leads reported in this study will only be known in the future after longer use. We conclude that excess stress must be avoided during the implantation procedure and that careful surveillance is necessary.