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Biomedical subjects

T M Frank

Publications and source records attributed to T M Frank.

6 recordsLinked to original sources

Temporal resolution in mesopelagic crustaceans.

Mesopelagic crustaceans occupy a dim-light environment that is similar to that of nocturnal insects. In a light-limited environment, the requirement for greater sensitivity may result in slower photoreceptor transduction and increased summation time. This should be reflected by a lower temporal resolution, as indicated by a lower critical flicker fusion frequency (CFF). Therefore, one would predict that the CFFs of mesopelagic organisms would be relatively low compared with those of their shallow-water relatives, just as nocturnal insects tend to have lower CFFs than diurnal insects. Using an electrophysiological apparatus that was adapted for shipboard use, the dark-adapted CFFs of a variety of species of mesopelagic crustaceans were determined using the electroretinogram. The parameter examined was the maximum CFF--the point at which further increases in irradiance no longer result in a faster flicker fusion frequency. The results summarized here indicate that there is a trend towards lower CFFs with increasing habitat depth, with some interesting exceptions.

Adaptation, Physiological↗

Interaction of adenosine and prostacyclin in coronary flow regulation after myocardial ischemia.

The role of adenosine and prostacyclin in post-ischemic vasodilation was investigated using a model of sequential perfusion of two isolated hearts. Two guinea pig hearts were sequentially perfused (10 ml/min) without (control, n = 4) or with preceding 10-min ischemia (n = 6) of Heart I. Under control conditions no hemodynamic changes were observed in Heart II during sequential perfusion. After 10 min of ischemia of Heart I coronary perfusion pressure decreased by 23% in Heart II at the onset of sequential perfusion. Adenosine A1 and A2 receptor antagonists 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (2 microM) and 3,7-dimethyl-1-propargylxanthine (DMPX) (20 microM) infused simultaneously inhibited this decrease in coronary perfusion pressure by 74%, whereas indomethacin (5 microM) had no effect. DPCPX, DMPX and indomethacin in combination induced a significant increase in coronary perfusion pressure. Adenosine release (HPLC) into the coronary effluent after ischemia was significantly enhanced in the presence of indomethacin. These results suggest that after myocardial ischemia prostacyclin has an inhibitory effect on adenosine release.

Adenosine↗

Influence of polymorphonuclear leukocytes and plasma on coronary vasomotion after ischemia.

BACKGROUND: The role of plasma and neutrophils in endothelial dysfunction following myocardial ischemia was investigated. METHODS: Isolated rabbit hearts were perfused at constant pressure with a modified Krebs-Henseleit solution. After a 30-minute global ischemia the hearts were perfused at the onset of reperfusion for 10 minutes with either NaCl (group I, n = 6), autologous plasma alone (group II, n = 5), autologous polymorphonuclear leukocytes alone (PMN, group III, n = 6), or PMN and plasma in combination (group IV, n = 5). Before and after ischemia the effects of intracoronary endothelial dependent and independent vasodilation by acetylcholine (1 x 10(-7)mol/L) and glycerol trinitrate (1 x 10(-6) mol/L) were investigated. RESULTS: A similar increase in coronary flow was induced in groups I, II, and III by acetylcholine and glycerol trinitrate before and after ischemia. In contrast, in group IV the endothelial dependent vasodilation was significantly depressed (p < 0.05). In groups II and IV a moderate but significant reduction in the recovery of the left ventricular pressure was observed after ischemia and reperfusion. CONCLUSIONS: These results suggest that after myocardial ischemia, plasma is required for neutrophil-mediated endothelial dysfunction.

Animals↗

Release of a stable cardiodepressant mediator after myocardial ischaemia during reperfusion.

OBJECTIVE: The aim of this study was to investigate whether cardiodepressant mediators are released after myocardial ischaemia during reperfusion. METHODS: Using a double heart model, the effect of the reoxygenated coronary effluent of an isolated guinea pig heart on a sequentially perfused second heart was studied under control conditions and after 10 min ischaemia of the first heart. Investigation of the modulating role of known autacoids took place by using free radical scavengers, an NO synthase inhibitor and adenosine receptor antagonists. In order to identify the chemical nature of cardiac metabolites, the coronary effluent was also subjected to different chemical treatment modes. RESULTS: No haemodynamic changes were observed during sequential perfusion under control conditions. After 10 min of global ischaemia in heart I, a marked decrease in LVP (-22%), LVdP/dtmax (-43%), LVdP/dtmin (-41%) and coronary perfusion pressure (-25%) was measured in heart II during sequential perfusion. The negative inotropic effect was rapid in onset and reversible within 5 min; free radicals, nitric oxide and adenosine were not involved. Storage of the coronary effluent of the first heart up to 24 h, heating, or protease treatment did not modify its cardiodepressant effects on the second sequentially perfused heart. CONCLUSIONS: These results suggest the release--from an isolated heart after ischaemia during reperfusion--of a cardiodepressant mediator which induces a potent reversible negative inotropic effect on a sequentially perfused heart. The mediator is stable and in all probability not a protein.

Adenosine Deaminase↗

Excitation of Limulus photoreceptors by hydrolysis-resistant analogs of cGMP and cAMP.

cGMP was proposed to be the agent which directly opens the light-sensitive channel in Limulus ventral photoreceptors. However, the light-sensitive rhabdomeral-lobe (R-lobe) is not uniformly responsive to cGMP injection; that is, there are 'hot spots' of sensitivity. A potent phosphodiesterase which rapidly hydrolyses cGMP was suggested to explain the existence of these 'hot spots'. To test this idea we injected ventral photoreceptors with hydrolysis-resistant cyclic nucleotide analogues. Whereas there can be a lack of a response to cGMP injection into the R-lobe, we find a reproducible depolarization upon R-lobe injection of hydrolysis-resistant cGMP analogues. Furthermore, the depolarization resulting from the injection of cGMP analogues does not require a rise in intracellular Ca2+, as it is not blocked by the Ca2+ buffer, BAPTA. Surprisingly, R-lobe injection of a hydrolysis-resistant cAMP analogue also depolarized ventral photoreceptors. Further work will be needed to resolve the role of cGMP in Limulus visual transduction.

Animals↗

The role of the inositol phosphate cascade in visual excitation of invertebrate microvillar photoreceptors.

The identity of the transmitter(s) involved in visual transduction in invertebrate microvillar photoreceptors remains unresolved. In this study, the role of inositol 1,4,5-trisphosphate (IP3) was examined in Limulus ventral photoreceptors by studying the effects on the light response of heparin and neomycin, agents that inhibit the production or action of IP3. Both heparin and neomycin reduce responses to brief flashes of light and the transient component of responses to steps of light, and also inhibit IP3-induced calcium release, indicating that IP3 plays a direct role in invertebrate visual excitation. The effects of BAPTA, a calcium buffer, were also examined and shown to be consistent with a role for IP3-mediated calcium release in visual excitation. However, all three agents fail to block the plateau component of the response to a step of light, indicating that a single pathway involving IP3 and calcium cannot solely be responsible for visual excitation in invertebrates. We suggest that the inositol phosphate cascade and a second parallel process that is not dependent on IP3 are involved in the production of the light response.

Animals↗