Incorporation of labelled thymidine into DNA of different rat brain regions was studied after 30 min of forebrain ischaemia and recirculation periods up to 24 hours. The amount of label incorporated into DNA showed a different pattern in the brain. After 1 hour of recirculation, the incorporation was reduced in the cortex and in the striatum, without any significant change in the hippocampus. After 3 to 9 hours the incorporation remained depressed in the cortex, diminished in the hippocampus, and increased by 2-2.5 fold in the striatum. Later, after 24 hours, the DNA labelling returned to control values in the striatum and in the cortex, but was increased in the hippocampus.
The mesenteric and intestinal blood flow is organized and regulated to support normal intestinal function, and the regulation of blood flow is, in part, determined by intestinal function itself. In the process of the development and adaptation of the intestinal mucosa for the support of the digestive processes and host defense mechanisms, and the muscle layers for propulsion of foodstuffs, a specialized microvascular architecture has evolved in each tissue layer. Compromised mesenteric and intestinal blood flow, which can be common in the elderly, may lead to devastating clinical consequences. This problem, which can be caused by vasospasm at the microvascular level, can cause intestinal ischaemia to any of the layers of the intestinal wall, and can initiate pathological events which promote significant clinical consequences such as diarrhea, abdominal angina and intestinal infarction. The objective of this review is to provide the reader with some general concepts of the mechanisms by which neurohumoral vasoactive substances influence mesenteric and intestinal arterial blood flow in health and disease with focus on transmural transport processes (absorption and secretion). The complex regulatory mechanisms of extrinsic (sympathetic-parasympathetic and endocrine) and intrinsic (enteric nervous system and humoral- endocrine) components are presented. More extensive reviews of platelet function, atherosclerosis, hypertension, diabetes mellitus, the carcinoid syndrome, 5-hydroxytryptamine and nitric oxide regulation of vascular tone are presented in this context. The possible options of pharmacological intervention (e.g. vasodilator agonists and vasoconstrictor antagonists) used for the treatment of abnormal mesenteric and intestinal vascular states are also discussed.
Liver haemodynamics were studied after warm (37 °C) ischaemia of isolated rat livers for periods of 30 s (Group 1), 30 min (Group 2), and 60 min (Group 3) using a constant pressure system with a recirculating blood-free perfusate. Portal flow recovered to basal values within 6 min in livers from Group 1, whereas it was significantly reduced in Group 2 during the initial 15 min and in Group 3 during the first 33 min of reperfusion. Thus, the recovery of liver flow was proportional to the duration of ischaemia. By using the same mode of liver perfusion, the effect of norepinephrine on portal resistance was also studied in normal livers. At the beginning of reperfusion, the values of portal resistance in ischaemic livers were comparable to the values of portal resistance mediated by norepinephrine at concentrations between 10“7 and 10"6 mol/1 in normal livers. The results suggest that vasoconstriction of the hepatovasculature may be a contributing factor to the reperfusion injury of the liver following warm ischaemia.
In the myocardium, the sarcoplasmic reticulum (SR) plays an essential role in the regulation of cytosolic free Ca2 + ion concentration and, hence, in the contraction-relaxation cycle. The aim of this review is to summarize the role of the SR, particularly the main SR Ca2+ transport proteins, Ca2+-ATPase pump and Ca2+ release channel (ryanodine receptor), in contractile impairment during ischaemia and reperfusion. As suggested by most studies, SR dysfunction may contribute to contractile failure during ischaemia. However, SR function is largely restored during reperfusion and minor changes are unlikely to explain the severe postischaemic contractile dysfunction.
Differential pulse voltammetry with a carbon fibre microelectrode (ME) was used in pentobarbital- anaesthetized rats for monitoring the stobadine current (STB.C) on both sides of the blood-brain barrier (BBB) in the arterial bloodstream (BS) and in the corpus striatum (CS). The STB.C exhibited a distinct peak at a polarization voltage 540±30 mV (n=4). The maximum of STB.C in BS attained 2-3 min after the STB administration (2.8 mg/100 g in 1.0 ml saline solution i.a.) was followed by a rapid decrease to about 20 % within next 3 min. The STB readily passed across the BBB: the STB.C peak appeared in the CS in the 3rd minute and continued to rise up to the 30th min. The administration of STB did not prevent a large increase (1347±326 %, n=3) of the catechol-oxidative current (CA.OC) occurring in the CS between the 4th and 5th minute after cardiac arrest. However, a decrease of ME sensitivity to CA.OC in the presence of STB was observed. This fact leads to the speculation whether a similar "quenching" of dopamine by STB could not participate in the protective effects of STB observed in the brain exposed to hypoxia-reoxygenation.
The uptake, reflux and excretion of bromosulfophthalein (BSP) were studied on a model of total warm ischaemia for 30 min (group 1) or 60 min (group 2) followed by reperfusion for 45 min in the isolated perfused rat liver of unfasting rats. In group 1, the BSP hepatic uptake was comparable to control livers (30 s ischaemia plus 45 min reperfusion), but was significantly reduced in group 2. The reflux of BSP from liver to perfusate in group 1 and group 2 resulted in the appearance of secondary concentration time peaks of BSP in the reservoir perfusate. This result suggests that ischaemia-reperfusion induced a qualitative change in BSP pharmacokinetics. Excretion of the dye into bile was significantly impaired in group 2 only. The leakage of lactate dehydrogenase into the perfusate was increased moderately in both group 1 and group 2 in comparison to the controls, suggesting a low degree of liver parenchymal injury. In conclusion, the results of this investigation showed that BSP pharmacokinetics were not only undergoing quantitative changes but also a qualitative change in the model of ischaemia-reperfusion injury of the liver obtained from fed rats and may thus serve as a highly sensitive indicator of liver viability.