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At least 19 recordsLinked to original sources

PubMed1989

Long-term prognosis of patients with silent ischemia, symptomatic ischemia and without ischemia after acute myocardial infarction.

The prognosis of 55 patients with silent ischemia (group I: asymptomatic ST segment depression of greater than or equal to 0.1 mV on symptom-limited ergometer exercise) was compared with that of 25 patients with angina and ST depression (group II), 22 patients with angina but without ST depression (group III) and 94 patients without angina and without ST depression (group IV) on ergometer testing in the first post-infarction month. Patients for whom PTCA or coronary artery bypass graft surgery was planned for the next months following discharge were excluded. Groups were well matched in terms of age, sex, diabetes, non-Q-wave infarctions and global left ventricular function, but groups I and II had more inferior wall infarctions (76% and 68% respectively) than groups III and IV (18% and 34%, p less than 0.0001). After a mean follow-up time of between 26 and 33 months 11% in group I, 16% in group II, 14% in group III, but only 6% in group IV had died from cardiac disease or reinfarcted (p = 0.06). Using Cox's model, the Killip index, presence of non-Q-wave infarction, maximal ST depression on ergometer exercise and global left ventricular ejection fraction were found to be important prognostic variables affecting reinfarction-free survival, whilst angina was not. Results suggest that the presence or absence of angina as an isolated symptom is not of prognostic important after acute myocardial infarction, in comparison with objectively determinable parameters.

Angina Pectoris↗

PubMed1985

Different effects of thiopental in severe hypoxia, total ischemia, and low-flow ischemia in rat heart muscle.

The effect of thiopental (100 mg X 1(-1] during total ischemia, low-flow ischemia, and severe hypoxia with maintained flow was investigated in the isolated perfused rat heart. During total ischemia the rate of decline of tissue creatine phosphate and adenosine triphosphate was no different in thiopental-treated and untreated hearts. The development of ultrastructural damage during total ischemia, the release of creatine kinase on reperfusion, and the exacerbation of ultrastructural damage after reperfusion were unaffected by thiopental. When thiopental was added to the perfusate during hypoxia and during low-flow ischemia at a normal pH(7.4), creatine kinase release during reoxygenation and during reperfusion was significantly less (P less than 0.005 and P less than 0.05, respectively) than in the untreated groups. After low-flow ischemia at a low pH (6.5), creatine kinase release was no different in thiopental-treated and untreated hearts. Thus, thiopental afforded protection of the myocardium in hypoxia and low-flow ischemia at pH 7.4 but not in total ischemia and low-flow ischemia at pH 6.5. The data are consistent with the hypothesis that during total ischemia and low-flow ischemia at pH 6.5, acidosis favors the entry of thiopental into the cell, causing inhibition of mitochondrial function and reduction of ATP production. During hypoxic perfusion and low-flow ischemia at pH 7.4, when the decrease in pH is less, the cardiodepressant effect of thiopental may offset any deleterious effect of the drug on intracellular organelles such as mitochondria.

Adenosine Triphosphate↗

PubMed1986

[Experimental study on reversibility of cerebral ischemia--residual blood flow and duration of ischemia].

This experimental study was designed to estimate the flow thresholds and the time thresholds for reversibility of cerebral ischemia. We used a "canine model of completely ischemic brain regulated with a perfusion method", in which the cerebral blood flow (CBF) could be controlled. The residual blood flow was reduced to 10%, 20%, 30% or 40% of normal CBF, and the recirculation was started after 1, 2, 3 or 4 hours of ischemia. CBF was measured by a laser doppler flow meter. EEG and somatosensory evoked potential (SEP) was monitored and used as a parameter expressing the brain function. In the 10% and 20% ischemia group, functional recovery could not be obtained even if reperfusion was started at 1 hour after the onset of ischemia. On the other hand, in the 30% ischemia group, nearly complete recovery of EEG and SEP could be seen when reperfusion was done at 1 hour from the onset of ischemia. But recirculation after 2 hours of ischemia did not lead to significant functional recovery. In the 40% ischemia group, reperfusion within 3 hours of ischemia allowed full recovery of ischemic brain. On the contrary, reperfusion after 4 hours of ischemia showed a gradual deterioration of EEG and SEP. Accordingly, it was clearly demonstrated that the reversibility of ischemic brain was critically correlated to severity and duration of cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Patients with symptomatic ischemia have larger thallium perfusion abnormalities and more adverse prognosis than patients with silent ischemia.

OBJECTIVE: To evaluate the mechanism for silent ischemia and the effect on prognosis. DESIGN: To test the hypothesis that patients with silent (compared with symptomatic) ischemia have less severe ischemia and a more favorable prognosis, the authors prospectively evaluated 152 consecutive patients with a positive exercise electrocardiogram with exercise thallium scintigraphy and followed them for two years. SETTING: Tertiary care university-based hospital. RESULTS: Asymptomatic patients during the exercise test had a greater exercise duration (9.4 +/- 3.1 versus 6.3 +/- 2.5 mins, P < 0.01), maximal heart rate (155 +/- 20 versus 136 +/- 20 beats/min, P < 0.01), systolic blood pressure (184 +/- 21 versus 176 +/- 23 mmHg, P < 0.05) and double product than patients who were symptomatic with chest pain. Although there was no difference in the magnitude of ST depression, time to ST depression was greater in the asymptomatic (5.6 +/- 2.7 mins), compared with symptomatic (4.6 +/- 2.6 mins), group (P < 0.01). Thallium ischemic score was smaller during asymptomatic ischemia (2.1 +/- 2.7) compared with symptomatic ischemia (3.9 +/- 3.1, P < 0.01). These findings were also demonstrated in a subgroup of 107 patients with both a positive exercise electrocardiogram and positive thallium scan. The patients with asymptomatic ischemia had a two-year cardiac event rate of 5.1% compared with 13.8% in the symptomatic patients (P = 0.065). CONCLUSIONS: Patients with asymptomatic ischemia have less severe myocardial ischemia and a better prognosis than patients with symptomatic myocardial ischemia during exercise testing.

Angina Pectoris↗

PubMedDate not supplied

Forebrain ischemia in the rat. Relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery.

The relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery was studied in a rat model giving reversible subtotal forebrain ischemia. Ischemia was induced by bilateral carotid artery clamping and controlled hemorrhage to a mean arterial pressure of 50 mm Hg in animals artificially ventilated under 70% N2O. After variable lengths of time, the clamps were removed and the drawn blood was reinfused. In some animals, the ganglion blocker Arfonad was given (group A+) on induction of ischemia to facilitate hypotension. There was a strict dose-response relationship between duration of ischemia and mortality. Mortality was higher among animals not given Arfonad (group A-; 37% after 10 min of ischemia and 100% after 13 min) than in group A+ (about 20% after 12-13 min of ischemia, 50% after 15 min and 80% after 19 min). In group A+ more than half of the animals died later than 24 h after ischemia. All of them were hyperexcitable and 12% died during witnessed epileptic fits. Group A- animals regularly died within the first 24 h, with no indication of central nervous system involvement. Less blood had to be drawn to attain hypotension (mean arterial pressure 50 mm Hg) in group A+ (1.5 +/- 0.3 ml/100 g b.w.) than in group A- (2.5 +/- 0.2 ml/100 g b.w.). Group A+ also had less "washout" acidosis 5 min after reinfusion of the shed blood than group A- (15 min of ischemia: pH 7.24 +/- 0.07 v 6.96 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Role of oxygen-derived free radicals in gastric mucosal injury induced by ischemia or ischemia-reperfusion in rats.

Oxygen-derived free radicals have been implicated as possible mediators in the development of tissue injury induced by ischemia and reperfusion. Clamping of the celiac artery in rats reduced the gastric mucosal blood flow to 10% of that measured before the clamping. The area of gastric erosions and thiobarbituric acid (TBA) reactants in gastric mucosa were significantly increased 60 and 90 min after clamping. These changes were inhibited by treatment with SOD and catalase. Thirty and 60 min after reoxygenation. produced by removal of the clamps following 30 min of ischemia, gastric mucosal injury and the increase in TBA reactants were markedly aggravated compared with those induced by ischemia alone. SOD and catalase significantly inhibited these changes. The serum alpha-tocopherol/cholesterol ratio, an index of in vivo lipid peroxidation, was significantly decreased after long periods of ischemia (60 and 90 min), or after 30 and 60 min of reperfusion following 30 min of ischemia. These results indicated that active oxygen species and lipid peroxidation may play a role in the pathogenesis of gastric mucosal injury induced by both ischemia alone and ischemia-reperfusion. Although, allopurinol inhibited the formation of gastric mucosal injury and the increase in TBA reactants in gastric mucosa, the depletion of polymorphonuclear leukocytes (PMN) counts induced by an injection of anti-rat PMN antibody did not inhibit these changes. As compared with the hypoxanthine-xanthine oxidase system. PMN seem to play a relatively small part in the formation of gastric mucosal injury induced by ischemia-reperfusion.

Allopurinol↗

PubMed1985

[Effects of cerebral protective agents in experimental cerebral ischemia. Relationship between the degree of ischemia and EEG].

We have previously demonstrated that the preischemic administration of perfluorochemicals (PFC) in combination with 20% mannitol, vitamin E and dexamethasone is effective in protecting the brain from cerebral ischemia. This experimental study was designed to evaluate the effect and limitation of the post-ischemic administration of those 4 agents on cerebral ischemia. We used "Canine model of complete ischemic brain regulated with a perfusion method." Using this model we were able to control the amount of blood flow to the left cerebral hemisphere by using an infusion pump. Infusion blood volume was reduced to 30%, 40% or 50% of the normal state, then the combined treatment was started 1,2,3,4,5 or 6 hours after the onset of ischemia in each ischemic group. By monitoring the EEG for 8 hours of ischemic period, we were able to evaluate the effect of the drugs on cerebral ischemia. In untreated groups, electrical activity deteriorated gradually. In the 30% ischemia group, the EEG became isoelectric within 1 hour following ischemia. In half of the 40% ischemia group, the EEG became isoelectric but in the other half low voltage slow wave were seen to last for 6-8 hours. In the 50% group, the EEG deteriorated gradually but did not disappear within 8 hours. The effectiveness of the treatment was judged by the degree of the recovery of electrical activity. The effectiveness of the treatment appeared to depend on the severity and the duration of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Effects of glyburide on ischemia-induced changes in extracellular potassium and local myocardial activation: a potential new approach to the management of ischemia-induced malignant ventricular arrhythmias.

The increase in extracellular potassium [K+]o levels during the early phase of myocardial ischemia may result in part from activation of adenosine triphosphate-sensitive K+ channels. Glyburide, a second-generation hypoglycemic sulfonylurea, is a potent blocker of these channels. We studied the effects of glyburide on [K+]o and on intramyocardial conduction delay during a 10-minute occlusion of the left anterior descending artery in the dog. K(+)-sensitive electrodes and bipolar plunge electrodes were introduced to record, respectively, [K+]o and local electrograms from close sites in midmyocardial regions in normal, border, and ischemic zones. Recordings were obtained before (control ischemia [CI]) and 20 minutes after intravenous administration of 0.15 mg/kg of glyburide (glyburide plus ischemia [G + I]). During G + I the extent of the increase in [K+]o was less compared to that during CI, and the difference was statistically significant during the first 7 minutes of ischemia in the ischemic zone and during the first 4 minutes of ischemia in the border zone. On the other hand, the degree of local intramyocardial conduction delay was significantly reduced during G + I compared to CI during the entire 10 minutes of ischemia in both the ischemic and border zones. In summary, our results have shown that glyburide significantly reduced the rise of [K+]o and intramyocardial delay during the early phase of acute ischemia and could thus attenuate the electrophysiologic consequences of ischemia that underlie the initial phase of malignant tachyarrhythmias. Although the effects of glyburide may result in part from a direct action of the drug on cardiac adenosine triphosphate-sensitive K+ channels, other metabolic antiischemic effects cannot be ruled out.

Animals↗

PubMed1990

Comparison of propranolol, diltiazem, and nifedipine in the treatment of ambulatory ischemia in patients with stable angina. Differential effects on ambulatory ischemia, exercise performance, and anginal symptoms. The ASIS Study Group.

Episodes of transient myocardial ischemia during ambulatory activities are common in patients with stable coronary artery disease and who are often asymptomatic. Selection of therapy for episodes of asymptomatic ischemia is limited by a lack of direct comparative studies. To determine the most effective monotherapy for patients with stable angina and a high frequency of asymptomatic ischemic episodes, propranolol-LA (mean daily dose, 293 mg), diltiazem-SR (mean daily dose, 350 mg), nifedipine (mean daily dose, 79 mg) were each compared with placebo, each for 2 weeks, in a randomized, double-blinded, crossover trial. Entry criteria were a positive exercise treadmill test during placebo therapy characterized by 1.0 mm or more ST segment depression and angina pectoris, and six or more episodes of transient ST segment depression of 1.0 mm or more on a 48-hour ambulatory electrocardiogram. One hundred ninety-four patients were screened, 63 were eligible and received randomized therapy, of which 56 patients completed at least two of the four treatment periods and were included in an intent-to-treat analysis. Fifty patients completed all four treatment phases and were included in the protocol-completed analysis. Anti-ischemia efficacy was assessed by 48-hour ambulatory electrocardiographic monitoring, exercise treadmill tests, and anginal diaries. Ninety-four percent of all episodes of ambulatory ischemia were asymptomatic. Compared with placebo, only propranolol was associated with a marked reduction in all manifestations of asymptomatic ischemia during ambulatory electrocardiographic monitoring (2.3 versus 1.0 episodes/24 hr; mean duration of ischemia per 24 hours, 43.6 versus 5.7 minutes; both p less than 0.0001). Diltiazem's reduction of the frequency of episodes compared with placebo (2.3 versus 1.9 episodes/24 hr) was associated with a trend (p = 0.08) in the protocol-completed analysis and with a significant reduction in the intent-to-treat analysis (p = 0.03). Nifedipine had no significant effect on any measured variable of ambulatory ischemia. The dosages of medication used may have been excessive for some patients, and a more beneficial effect may have been evident at a lower dose. In contrast to the marked effects of the active agents on ambulatory asymptomatic ischemia, the effects on exercise performance and angina pectoris were slight. The active agents modestly improved treadmill exercise duration time until 1 mm ST segment depression (3%), and only propranolol and diltiazem had significant effects. Only diltiazem significantly prolonged the total exercise time. Anginal frequency was significantly decreased by both propranolol and diltiazem.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris↗

PubMed1992

Modifying pulmonary ischemia-reperfusion injury by altering ventilatory strategies during ischemia.

We used an intact in vivo canine model of pulmonary ischemia-reperfusion (IR) injury to evaluate the differential effects of alveolar hypoxia and ventilation during 2 h of unilateral warm lung ischemia. Serial measurements of regional pulmonary blood flow, extravascular density (EVD), and transcapillary protein flux were made after reperfusion with the quantitative imaging technique of positron emission tomography. Twenty-seven animals were divided into five experimental groups: VENT O2 (n = 5) in which the left lung was ventilated with 40% O2 during ischemia, STATIC O2 (n = 4) in which the left lung was statically inflated with 40% O2 during ischemia, VENT N2 (n = 5) in which the left lung was ventilated with 100% N2 during ischemia, VENT N2/CO2 (n = 5) in which the left lung was ventilated with 95% N2-5% CO2 during ischemia, and STATIC N2 (n = 8) in which the left lung was statically inflated with 100% N2 during ischemia. These groups were compared with a control group (CONT, = 3) that was studied previously. Protein flux was significantly increased in the previous ischemic lung only for the STATIC N2 group [median 175 x 10(-4) min-1 (range 53-1,217) for the STATIC N2 group vs. 50 x 10(-4) min-1 (range 40-56) for the CONT group] 0.25 h after reperfusion and did not change over 3 h. EVD also increased but not significantly. Protein flux and EVD in the other groups were not different from CONT.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMedDate not supplied

Reperfusion after cerebral ischemia: influence of duration of ischemia.

The influence of the duration of ischemia on the pattern of cerebral blood flow in recirculation was studied in anesthetised rats. Severe incomplete cerebral ischemia (mean ischemic flow = 5.8 +/- 0.4 ml/100 g/min) was produced by four-vessel occlusion and recirculation permitted after 15, 30 or 60 minutes ischemia. All three groups showed an immediate hyperemia followed by hypoperfusion. Hyperemia was maximal following 15 minutes ischemia and least pronounced following 60 minutes ischemia (p = 0.0249). Hypoperfusion started most quickly following 15 minutes ischemia and was delayed following 60 minutes ischemia (p less than 0.001). In established hypoperfusion there was no difference in flow between the three groups. The possible mechanisms of these changes in flow are discussed.

Animals↗

PubMed1991

The relative contributions of myocardial wall thickness and ischemia to ultrasonic myocardial integrated backscatter during experimental ischemia.

The purpose of this study was to assess the empirical relationship between myocardial integrated backscatter (IB) and myocardial wall thickness (WT) in normal myocardium. A second object was to estimate the additional contribution to acute ischemic integrated backscatter levels given this relationship. Myocardial IB measurements and simultaneous myocardial WT measurements were made in 16 open-chested pigs with intact coronary circulation (normal myocardium) and 10 min after the flow in the left anterior descending coronary artery had been reduced to 20% of its baseline value (ischemic myocardium). Measurements were made 50 times during one cardiac cycle and averaged over 10 cardiac cycles. IB and WT measurements were normalized with respect to the nonischemic end-diastolic values. The relationship between IB and WT in normal myocardium was estimated in every individual pig by simple linear regression. Estimates of IB during ischemia were calculated on the basis of this relationship and the ischemic WT measurements. Differences of the estimator and the actual measurement made during ischemia depict the actual contribution of the state of acute ischemia, without the influence of WT. The slope of the relationship between IB and WT during normal myocardial contraction ranged from -0.16 to 0.03 dB/% (mean = -0.036 dB/%, SD = 0.06 dB/%). The additional contribution of ischemia ranged from -3.84 to 5.56 dB (mean = 0.31 dB, SD = 2.72 dB). It was concluded that the average contribution of ischemia to IB measurements is insignificant if the IB dependency on WT is removed from the data and that the higher level of ischemic IB measurements can be explained by the decrease in wall thickness during ischemia and not by the ischemia itself.

Animals↗

PubMedDate not supplied

Mechanisms of myocardial ischemia induced by epinephrine: comparison with exercise-induced ischemia.

The role of epinephrine in eliciting myocardial ischemia was examined in patients with coronary artery disease. Objective signs of ischemia and factors increasing myocardial oxygen consumption were compared during epinephrine infusion and supine bicycle exercise. Both epinephrine and exercise produced myocardial ischemia as evidenced by ST segment depression and angina. However, the mechanisms of myocardial ischemia induced by epinephrine were significantly different from those of exercise. Exercise-induced myocardial ischemia was marked predominantly by increased heart rate and rate-pressure product with a minor contribution of end-diastolic volume, while epinephrine-induced ischemia was characterized by a marked increase in contractility and a less pronounced increase in heart rate and rate-pressure product. These findings indicate that ischemia produced by epinephrine, as may occur during states of emotional distress, has a mechanism distinct from that due to physical exertion.

Arousal↗

PubMed1990

Myocardial ischemia following surgery: preliminary findings. Study of Perioperative Ischemia (SPI) Research Group.

Humoral changes, changes in hemodynamics, and the incidence of ischemia appear to be highest during the postbypass-postoperative period. Preliminary data also suggest that postbypass ischemia detected by transesophageal echocardiography may be predictive of outcome. Our previous experience with postoperative hypertension following coronary artery surgery has led us to increase analgesic medication of patients during and following anesthetic emergence. Patterns of postoperative ischemia observed in patients undergoing noncardiac and cardiac surgery suggest that extension of anesthesia to the postoperative period may be beneficial with respect to suppression of ischemia. It appears that by maintaining a continuous infusion of a high dose of narcotic, postoperative myocardial ischemia can be modified. The implication is that by blunting activation of the sympathetic nervous system in the postoperative period, and preventing the resultant endocrine, metabolic, and hemodynamic changes, the imbalance of myocardial oxygen supply and demand can be shifted away from ischemia. Further investigation is needed to confirm these data, and to address the effects of modification of postoperative myocardial ischemia on eventual postoperative cardiac outcomes.

Cardiac Surgical Procedures↗

PubMed1992

Predictors of postoperative myocardial ischemia in patients undergoing noncardiac surgery. The Study of Perioperative Ischemia Research Group.

OBJECTIVE: To identify predictors of postoperative myocardial ischemia in patients scheduled to undergo major noncardiac surgery. DESIGN: Historical, clinical, laboratory, and physiological data were obtained prospectively before and during surgery to identify potential univariate predictors of postoperative myocardial ischemia, which then were entered into multivariate logistic models. Continuous two-lead electrocardiograms before, during, and after surgery were used to identify episodes of myocardial ischemia. SETTING: Department of Veterans Affairs tertiary care hospital. PATIENTS: A consecutive sample of 474 men at high risk for or with coronary artery disease who were scheduled to undergo major noncardiac surgery (95% compliance rate). MAIN OUTCOME MEASURE: Significant variables identified by multivariate logistic models that are associated with postoperative myocardial ischemia. RESULTS: Five major preoperative predictors of postoperative myocardial ischemia were identified: (1) left ventricular hypertrophy by electrocardiogram; (2) history of hypertension; (3) diabetes mellitus; (4) definite coronary artery disease; and (5) use of digoxin. The risk of postoperative myocardial ischemia increased progressively with the number of predictors present: in 22% of patients with no predictors, in 31% with one predictor, in 46% with two predictors, in 70% with three predictors, and in 77% with four predictors. CONCLUSION: Patients subgroups who are at high risk for developing postoperative myocardial ischemia and who might benefit the most from intensive Holter monitoring in the postoperative period now can be identified preoperatively.

Aged↗

PubMed1989

Deterioration of baroreflex by transient global cerebral ischemia: its correlation with the degree of ischemia or post-ischemic hypoperfusion in the medulla oblongata.

In a canine model of transient global cerebral ischemia, the correlation between the decrease in baroreflex sensitivity (BRS) following 5-min ischemia and the degree of ischemia or post-ischemic hypoperfusion was investigated. Although the medulla oblongata and the cerebral cortex suffered a similar degree of ischemia, the extent of post-ischemic decrease in BRS was inversely correlated with the residual blood flow during ischemia in the medulla, but not with that in the cerebral cortex. A similar degree of post-ischemic hypoperfusion occurred in the medulla and the cerebral cortex. However, the extent of decrease in BRS was not correlated with the degree of hypoperfusion, and the cortical EEG was not significantly affected. These results suggest that the decrease in BRS may be due to the functional damage in the medulla and that the selective decrease in BRS without concomitant impairment of the EEG cannot be ascribed to the regional difference in the degree of ischemia or post-ischemic hypoperfusion.

Animals↗

PubMed1989

[Neurofunctional disturbances as related to cortical ischemia and white matter ischemia].

We evaluated regional cerebral blood flow (rCBF) by means of hydrogen clearance method as well as [14C]-iodoantipyrine autoradiographic method, cortical auditory evoked potentials (AEP), somatosensory evoked potentials (SEP) induced by forelimb (median nerve) stimulation (SEP-F), and SEP induced by hindlimb (tibial nerve) stimulation (SEP-H) in cats after occlusion of the left middle cerebral artery (MCA) under alpha-chloralose anesthesia. According to the degree of ischemia, the experimental animals were divided into two groups. One was the critical ischemia which was defined as permanent total suppression of AEP, and low residual blood flow in the auditory cortex. And the other was the non-critical ischemia which included transient suppression and spontaneous recovery of the cortical sensory evoked potentials, and high residual blood flow (greater than 15 ml/100 g/min). In one cat with transient suppression of three kinds of sensory evoked potentials, the [14C]-iodoantipyrine (IAP) autoradiograph revealed only a limited ischemic area of subcortical white matter. In the critical ischemia group, ischemia of the primary sensory cortex ranged from the mostly affected primary auditory cortex (supplied by the MCA) to the least affected hindlimb projection area within primary somatosensory cortex (supplied by the ACA). The forelimb projection area of the primary somatosensory cortex (supplied by both ACA and MCA) showed a mild or moderate reduction of rCBF after occlusion. The [14C]-IAP autoradiograph showed severe reduction of the white matter including the somatosensory pathway in the wide range. However, rCBF in the thalamus and hindlimb projection area within somatosensory cortex was almost intact in the cat with ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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↗