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At least 19 recordsLinked to original sources
PubMed1978

Diffuse cerebral ischemia in the cat: I. Local blood flow during severe ischemia and recirculation.

The effects of severe cerebral ischemia on postischemic brain perfusion were examined in a series of pentobarbital-anesthetized cats. Ischemia of 15 or 30 minutes' duration was produced by occlusion of both common carotid arteries and the basilar artery and was coupled with mild systemic hypotension. A 90-minute period of normotensive postischemic recirculation was permitted in some animals. In 9 of 10 animals studied at the end of the ischemic insult and not allowed to recover, blood flow in the cerebral hemispheres was greatly reduced, with minimal flow (0.01 to 0.11 ml gm-1 min-1) persisting only in scattered perisulcal regions in 4 animals. Following 15 minutes of ischemia, blood flow was restored uniformly during recirculation, though at subnormal levels (31 to 35% of control). In contrast, 30 minutes of prior ischemia led to marked heterogeneities of local cerebral perfusion during recirculation, with multiple zones of persistent severe ischemia. Thus, while recirculation was suboptimal following both 15 and 30 minutes of ischemia, the 30-minute insult led to focal postischemic perfusion abnormalities that were sufficiently severe to make the possibility of functional recovery appear unlikely.

Animals↗
PubMedDate not supplied

Effects of phenobarbital in cerebral ischemia. Part I: cerebral energy metabolism during pronounced incomplete ischemia.

Changes in cerebral cortex concentrations of high-energy phosphates, glycolytic metabolites, citric acid cycle intermediates, associated amino acids, and ammonia, were studied after 5, 15 and 30 min of incomplete ischemia in rats anesthetized with 70% N2O or 150 mg.kg-1 of phenobartibal. Previous results have shown that with this type of ischemia (bilateral carotid artery occlusion combined with reduction in blood pressure to 50 mm Hg) cortical blood flow is reduced to below 10% of nitrous oxide values, whether animals are anesthetized with 70% N2O or 150 mg.kg-1 of phenobarbital. In animals under 70% N2O, changes in tissue concentrations of phosphocreatine, ATP, ADP and AMP were similar to those previously obtained in complete ischemia. However, some glucose remained in the tissue, and the lactate concentrations gradually rose to reach excessive values. Changes occuring in glycolytic and citric acid cycle intermediates were similar to those seen in complete ischemia but, after 30 min, there was some reduction in the pool size of amino acids. In those animals given phenobarbital and which lost all EEG activity during ischemia, changes in cerebral metabolites were virtually identical to those observed in nitrous oxide-anesthetized animals. However, some animals exposed to 5 or 15 min of ischemia had some remaining EEG activity. In these, cerebral energy state was significantly less deranged, and levels of glycogen, glucose and pyruvate were higher.

Adenosine Diphosphate↗
PubMed1979

Diffuse cerebral ischemia in the cat: III. Neuropathological sequelae of severe ischemia.

The neuropathological consequences of sever diffuse cerebral ischemia were investigated in an animal model in which postischemic alterations of regional brain blood flow and energy metabolism had been previously characterized. Pentobarbital-anesthetized cats received either 15 or 30 minutes of ischemia produced by basilar artery and bilateral carotid artery occlusions plus mild hypotension; this was followed by 60 to 90 minutes of normotensive recirculation. The brains were perfusion-fixed for light microscopy. Both insult durations resulted in unequivocal ischemic cell change affecting neurons of the cerebral neocortex, striatum, thalamus, and hippocampus and portions of the rostral brainstem. Animals with 30 minutes of prior ischemia differed from those with 15 minutes of ischemia in showing a more apparent regional accentuation of ischemic change in the parasagittal cortical gyri--the sites of previously documented focal postischemic heterogeneities of blood flow and metabolism. In other respects, however, the overall distribution and spectrum of severity of the ischemic alterations were similar for the two insult durations. These data support the view that significant permanent neuronal injury may result from a period of cerebral ischemia as brief as 15 minutes.

Animals↗
PubMed1977

Evolution of regional ischemia distal to a proximal coronary stenosis: self-propagation of ischemia.

The temporal evolution of myocardial ischemia was studied in open chest dogs at constant preload, afterload and heart rate. In one group of animals, a variable circumflex arterial stenosis was used to maintain constant distal circumflex arterial hypotension (40 to 50 mm Hg). During a 3 hour period of stenosis, flow in the subendocardial fourth of the ischemic ventricular wall decreased from 0.22 to 0.09 ml/g per min (P less than 0.02), whereas subepicardial flow was not significantly changed. Local vascular resistance, therefore, doubled in the most ischemic area of myocardium. In a second group of animals in which proximal coronary stenosis was held constant and pressure varied, an ischemia-mediated increase in local vascular resistance was also demonstrated. In addition, a reciprocal relation was observed between changes in flow in the left anterior descending coronary region and changes in collateral flow to the region of the circumflex artery. A coronary steal mechanism and an ischemia-mediated resistance increase may be two means by which ischemia is self-propagating.

Animals↗
PubMed1978

Diffuse cerebral ischemia in the cat: II. Regional metabolites during severe ischemia and recirculation.

Metabolite levels were measured in seven brain regions in cats after 15 or 30 minutes of a severe ischemic insult and after a 90-minute period of recirculation following 15 or 30 minutes of ischemia. Brain levels of phosphocreatine were depleted after a 15- or 30-minute insult, and lactate levels were extremely high at both times. The adenosine triphosphate (ATP) content in many brain areas and the presence of microregions of low reduced nicotinamine-adenine dinucleotide in the brains of the animals that had 15 minutes of ischemia suggested that the ischemia, though severe, was not complete. Recirculation following a 15-minute insult restored brain levels of ATP and phosphocreatine to 70 to 100% of control values in all regions analyzed. In contrast, metabolic recovery from a 30-minute insult was regionally heterogeneous. Thus, there was persistent depression of ATP and phosphocreatine and elevation of lactate, which was localized in discrete cortical foci near the longitudinal midline. The factors governing the localization of metabolic failure must have become manifest during the recirculation period since the ischemic insult itself caused similar metabolic perturbations in all cortical regions.

Adenosine Triphosphate↗
PubMed1979

Biochemical and morphological correlates of acute experimental myocardial ischemia in the dog. IV. Energy mechanisms during very early ischemia.

Tissue energy metabolism was examined in posterior (ischemic) and anterior ("control") regions of canine ventricles after 5 and 10 minutes of left circumflex coronary artery occlusion. When compared to identical regions of normal hearts, the following changes were found: (1) decreases in glycogen and phosphorylase activity in the anterior and posterior regions, (2) depressed state 3 rates of oxygen consumption of isolated mitochondria in both anterior and posterior regions, (3) shifts in optimum substrate concentrations for palmityl-CoA (+ carnitine) oxidation by mitochondria in the anterior and posterior regions, and (4) decreases in the apparent zero order and first order rates of mitochondrial palmitylcarnitine production. These changes correlated with a marked decrease in developed tension in the posterior regions. Depression in tension development in the posterior regions of the heart still was present after 30--60 minutes of reperfusion following a 10-minute period of occlusion. Glycogen content in the reperfused areas was significantly decreased after 60 minutes of reperfusion when compared to normal areas and to control hearts perfused for 70 minutes. After reperfusion, mitochondrial function appeared to return toward "normal." However, the slow restoration of contraction of the ischemic area suggests that cellular mechanisms operative in vivo to restore pump function still might be abnormal.

Acyl Coenzyme A↗
PubMedDate not supplied

Brain blood flow and metabolism after global ischemia and post-insult thiopental therapy in monkeys.

We measured total and regional cerebral blood flow (CBF, rCBF) and cerebral metabolic rate (CMR) of oxygen (O2), glucose (G), and lactate (L) levels for 4 h after 16 min global brain ischemia in rhesus monkeys with and without post-insult thiopental therapy. Eleven monkeys weighing 4-5 kg anesthetized with 1 percent halothane, 66 percent nitrous oxide and 33 percent oxygen, were subjected to 16 min global brain ischemia by a combination of trimethaphan hypotension (to a mean arterial pressure of 50 torr) and a high pressure (1500 torr) neck tourniquet. Post-ischemia, 7 monkeys were untreated (controls) and 4 received thiopental 90 mg/kg infused intravenously over 60 min, beginning at 5 min post-ischemia. Total CBF and rCBF were measured by continuous monitoring of cerebral venous (torcula) and parietal-occipital (external scintillation) 133Xe activity, respectively, after intra-innominate artery injection of 500 micronCi 133Xe in saline. In control monkeys, hyperemia in rCBF, but not in total CBF was observed at 6-7 min post-ischemia, whereas both total CBF and rCBF increased in thiopental treated monkeys. The hyperemia in thiopental treated monkeys coincided with an increase in CMRG without a proportional increase in CMRO2 or lactate levels. Indeed, CMRO2 was depressed in the first 30 min post-ischemia. At 30 min post-ischemia, CMRO2 rose to twofold greater than pre-ischemia in control monkeys, but only to pre-ischemic levels in thiopental treated monkeys. The data suggest that thiopental therapy improves distribution of brain blood flow and brain glucose uptake early post-ischemia and depresses CMRO2 later post-ischemia.

Animals↗
PubMed1976

Mechanical and surgical interventions for the reduction of myocardial ischemia.

To reduce myocardial ischemia effectively, mechanical or surgical interventions must achieve either augmentation in coronary blood flow, a reduction in myocardial oxygen demand, or a combination of both. Coronary bypass graft procedures can achieve an immediate augmentation in coronary blood flow distally through the involved vessel and thereby improve myocardial perfusion and oxygen delivery and thus have the potential for reversing myocardial ischemia both acutely and for the long term. Although myocardial revascularization may resolve the ventricular functional alterations associated with acute myocardial ischemia it remains uncertain whether revascularization can reverse ischemic myocardial cellular injury and in what time framework, as related to reversible vs. irreversible ischemic cellular changes. Mechanical circulatory assistance (MCA) using diastolic counterpulsation effectively reduces myocardial ischemia by the physiologic mechanisms of 1) decrease in left ventricular after-load and left ventricular wall tension, 2) improvement is cardiac output by diastolic counterpulsation and 3) augmentation of coronary blood flow by diastolic pressure augmentation. The most effective indication for either MCA or myocardial revascularization is for interruption of myocardial ischemia prior to the development of infarction. Clinical sudies have demonstrated that acute myocardial ischemia can be effectively interrupted by intraaortic balloon pumping (IABP) including reversal of left ventricular dysfunction associated with acute myocardial ischemia. In most instances, cessation of IABP resulted in recurrence of myocardial ischemia indicating the need for urgent revascularization surgery. In the management of medically refractory myocardial ischemia. IABP has been effective in complete suppression of ischemia in 80 percent and resulted in marked improvement in all, allowing safe revascularization surgery with an operative mortality in the range of 5% and perioperative myocardial infarction incidence of 2%. In patients with acute myocardial infarction and cardiogenic shock (AMI-CS), IABP can resolve CS in 75 percent. The combination of IABP and surgery has resulted in survival approaching 45 percent indicative of a significant improvement in salvage in this group of patients where expected mortality approaches 100 percent.

Assisted Circulation↗
PubMed1977

Peripheral nerve injury and recovery after temporary ischemia.

Nerve (NCV) and motor (MNCV) conduction velocities of the rat sciatic nerve were examined between 1 and 90 days after ischemia for 1, 2, 3, 4 or 6 h. The results were compared to light and electron microscopy of the nerve. Slight diminution in the MNCV was observed 1 day after 1-2 h ischemia, whereas 3-6 h ischemia resulted in a complete conduction block. Diminution in the NCV occurred first after ischemia for 2 h and a complete block was seen after 4 and 6 h ischemia. Reduced NCV and MNCV were seen between 4 and 18 days only in the animals subjected to ischemia of longer duration of 3-6 h. Both the NCV and MNCV were nearly normalized at the 90th day. Ischemia of 4 and 6 h resulted in denervation of some of the muscle fibers, seen as spontaneous fibrillation at the 4th and 18th day. Electron microscopy and histometric studies showed degeneration of myelinated fibers increasingly after longer durations of ischemia; ischemia for 2 h caused a degeneration of about 5%, 3 h of about 35%, 4 h about 45%, and 6 h about 75% of the fibers. Myelinated fibers of different sizes were equally damaged. In the teased fiber preparations normal and myelin sheaths undergoing Wallerian-like degeneration was seen. Regeneration occurred, but even at the 90th day there was a tendency of the myelin/axon ratio towards values less than control values.

Animals↗
PubMed1979

Incomplete versus complete cerebral ischemia: improved outcome with a minimal blood flow.

It has been reported that incomplete cerebral ischemia with cerebral blood flow less than 10% of control may be more damaging than an equal period of complete ischemia. In this study, the effects of severe, incomplete cerebral ischemia on neurological outcome and cerebral metabolism were studied in dogs anesthetized with nitrous oxide. The results were compared with those of a previous study concerned with the effects of complete ischemia. Dogs could sustain only 8 to 9 minutes of complete ischemia with return of normal neurological function, whereas maintenance of a cerebral blood flow rate less than 10% of control extended this limit to 10 6o 12 minutes. Following a 10-minute exposure, only dogs undergoing incomplete ischemia regained a normal cerebral oxygen consumption within 90 minutes; similarly, animals subjected to incomplete ischemia enjoyed a faster return of EEG activity than dogs exposed to complete ischemia of the same duration. Cerebral metabolite levels did not prove to be a good index of return of neurological function. Within periods of cerebral ischemia in which meaningful neurological recovery might be expected, we conclude that some blood flow is better than no flow.

Animals↗
PubMed1978

Quantitation of particles in the freeze-fractured nuclear membrane after renal ischemia.

Changes in the number and sizes of membrane-associated particles have been quantitated in the protoplasmic (P) and exoplasmic (E) fracture faces of the outer membrane of nuclei isolated from the inner cortex following renal ischemia and reflow in the rat. No changes were observed in the inner nuclear membrane. After 20-min ischemia, the number of particles in both fracture faces decreased. With reflow, the total number of particles decreased after both 20- and 60-min ischemia. The partition coefficient (Kp = CPF/CEF) increased from 10 to 11 and 17 at 20- and 60-min ischemia then fell below control values to a Kp of 7 after 120 min. After reflow, Kp steadily decreased except after 20-min ischemia followed by 240-min reflow when Kp began to rise. The sizes of particles were predominantly 60 A in the P face of control outer membranes but became larger after ischemia. After 20- and 60-min ischemia with reflow, the size distribution became more normal. The shifts in particle numbers and sizes seem to indicate modifications within the membrane resulting from ischemia.

Animals↗
PubMed1978

Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality.

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.

Animals↗