These results show that glimepiride maintains myocardial preconditioning, while glibenclamide might be able to prevent it.

We investigated the morphologic structure and fluid content of atherosclerotic specimens of fresh human postmortem artery segments before and after application of a pressure of 5 atmospheres simulated by a weight of 5 kg per 1 cm2. After applying pressure in nonorganized atheromata, we noticed a marked reduction in thickness while in fibrotic atheromata we observed only smaller differences in thickness. Reduction in fluid content was significantly more pronounced in nonorganized atheromatous tissue. Reduction in thickness was closely related to reduction in weight (i e, fluid content). The time of pressure application necessary to achieve the optimal result averaged 60 sec. The conclusions drawn from these experiments were incorporated into clinical application of coronary angioplasty. Prolonged balloon inflation was applied to the last 400 out of a total of 600 coronary angioplasty procedures, performed between October 1977 and October 1983. Stenoses not sufficiently responsive to balloon inflation periods of 5-10 sec were exposed to periods of 60 sec (30-120 sec). The number of "non dilatable" stenoses was 15% with the standard short pressure procedure, but only 5% with the prolonged pressure application. No serious complications related to prolonged pressure application were observed. Thus, from experimental data and clinical experience the application of longer pressure periods appears justified and beneficial.

Cardiac transplantation entails surgical disruption of the sympathetic nerve fibres from their somata, resulting in sympathetic denervation. In order to investigate the occurrence of sympathetic re-innervation, neurotransmitter scintigraphy using the norepinephrine analogue iodine-123 metaiodobenzylguanidine (MIBG) was performed in 15 patients 2-69 months after transplantation. In addition, norepinephrine content and immunohistochemical reactions of antibodies to Schwann cell-associated S100 protein, to neuron-specific enolase (NSE) and to norepinephrine were examined in 34 endomyocardial biopsies of 29 patients 1-88 months after transplantation. Anterobasal 123I-MIBG uptake indicating partial sympathetic re-innervation could be shown in 40% of the scintigraphically investigated patients 37-69 months after transplantation. In immunohistochemical studies 83% of the patients investigated 1-72 months after transplantation showed nerve fibres in their biopsies but not positive reaction to norepinephrine. Significant norepinephrine content indicating re-innervation could not be detected in any biopsy. It was concluded that in spite of the lack of norepinephrine content there seemed to be immunohistological and scintigraphic evidence of sympathetic re-innervation. An explanation for this contradictory finding may be the reduced or missing norepinephrine storage ability compared to the restored uptake ability of regenerated sympathetic nerve fibres.

No abstract

Summary:It is known from experiments that angiotensinconverting enzyme inhibitors can limit infarct size. In a prospective. randomized, placebo-controlled double-blind study, 22 patients were given 1.5-2.0 mg captoprilh I.V., while 24 patients were given placebo. Medication was started between 2 and I8 h from the onset of infarction. The two groups were matched for age, infarct location, and time of intervention. With the exception of one patient in either group, all were concurrently given nitroglycerin. The necrosis parameters were provided by the quantitative measurement of the QRS complex. The Q wave decreased with captopril treatment (-0.003 mV), but increased with placebo (+0.14 mV, p < 0.05). The number of ventricular premature beats at 24 h from the start of treatment was 2 5 h with placebo, and 9/h with captopril (p < 0.02). Ventricular fibrillation occurred seven times in the placebo group, but did not occur in the captopril group. The creatine kinase infarct weight was 59 gram-equivalents (gEq) with placrebo, and 45 gEq with captopril (p = NS). Mean arterial pressure was reduced by 12 mmHg with captopril treatment. The results show a beneficial effect of captopril on infarct size and electrical instability, over and above the effect of standard management with nitroglycerin and thrombolysis.