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Biomedical subjects

K A Reimer

Publications and source records attributed to K A Reimer.

At least 73 records · Page 4Linked to original sources
PubMed1988

Myocardial neutrophil accumulation during reperfusion after reversible or irreversible ischemic injury.

Recent studies suggest that polymorphonuclear leukocytes (PMNs) may cause additional myocyte injury during reperfusion of ischemic myocardium. The present study was done to investigate whether PMNs accumulate in myocardium during early reperfusion after reversible or irreversible ischemic injury. Open-chest anesthetized dogs underwent circumflex coronary occlusions for 12 min (n = 5), 40 min (n = 8), or 90 min (n = 8), followed by 1 h of reperfusion. Autologous PMNs were radiolabeled with 111In and reinjected to quantitate myocardial PMN influx during reflow. 125I-labeled albumin was injected simultaneously to correct for 111In associated with plasma proteins in myocardial tissue. The number of PMNs was determined in the inner, middle, and outer one-third of nonischemic and ischemic-reperfused myocardium. In the 12-min group, 40% fewer PMNs were present in the reperfused than in the nonischemic control tissue. In contrast, in both the 40- and 90-min groups, PMN accumulation was two- to sixfold greater in the ischemic-reperfused than nonischemic myocardium, with a transmural gradient of PMN influx increasing from the outer to inner layers. Collateral blood flow, measured with radioactive microspheres, was not significantly different among the three groups. The failure of PMNs to accumulate during reperfusion after 12 min of ischemia does not support the hypothesis that PMNs contribute to postischemic dysfunction of reversibly injured myocytes. Whether PMNs caused cell death during early reperfusion after longer ischemic episodes remains unknown; however, the rapidity of PMN accumulation in the zones of predicted infarction is consistent with this possibility.

Animals↗
PubMed1988

Quantitative analysis of right and left ventricular infarction in the presence of postinfarction ventricular septal defect.

To quantitate the amount of right and left ventricular infarction in patients dying with postinfarction ventricular septal defect (PIVSD), hearts from 54 patients with anterior or inferior myocardial infarction were studied at autopsy. Fifteen hearts had myocardial infarction with PIVSD and 39 hearts had infarction without PIVSD and were used as a comparison group. All infarcts were sized histologically and the percent of each ventricle infarcted was quantitated by computer-assisted planimetry. The pathologic substrate for PIVSD was diffuse coronary artery disease with acute thrombosis resulting in transmural confluent infarction. Within the PIVSD group, there was significantly more left ventricle involved in anterior infarctions than in inferior infarctions (p less than .04). Conversely, there was more right ventricular infarction in inferiorly located myocardial infarctions with resulting PIVSD (p = .059). When infarctions resulting in PIVSD were compared with infarctions not resulting in PIVSD, the PIVSD group was characterized by larger left and right ventricular infarcts irrespective of infarct location (p less than .003). The incidence of right ventricular infarction was 100% in the PIVSD group (p less than .0001). Twelve of the 15 patients with PIVSD (80%) developed cardiogenic shock within 48 hr of septal rupture. The high incidence of shock and the rapid deterioration may have been secondary to right ventricular infarction in these patients. Therefore, infarcts resulting in PIVSD and subsequent death are characterized by a high incidence of right ventricular infarction. Significantly more infarction of the right ventricle is seen in either anterior or inferior infarctions resulting in PIVSD compared with infarctions not resulting in PIVSD. PIVSD complicating inferior infarctions is associated with the greatest amount of right ventricular infarction.

Aged↗
PubMed1988

Therapy to reduce free radicals during early reperfusion does not limit the size of myocardial infarcts caused by 90 minutes of ischemia in dogs.

It has been postulated that oxygen-centered free radicals are produced in significant quantities upon reperfusion of ischemic myocardium and could cause the death of myocytes that are still reversibly injured at the end of ischemia ("reperfusion injury"). However, we have shown previously that anti-free radical therapies including superoxide dismutase (SOD) and inhibitors of xanthine oxidase did not limit infarct size after 40 minutes of ischemia and 4 days of reperfusion in dogs. To test whether 40 minutes of ischemia is too brief a period to produce the prerequisite conditions for free radical-mediated necrosis upon reperfusion, we studied infarcts produced by 90 minutes of ischemia followed by reperfusion. Dogs in an SOD-catalase group received a 60-minute infusion of SOD (15,000 units/kg) and catalase (55,000 units/kg) beginning 25 minutes before and ending 35 minutes after reperfusion. A second group of dogs received a single injection of the xanthine oxidase inhibitor oxypurinol (20 mg/kg) 25 minutes before reperfusion. Infarct size was assessed histologically relative to the size of the area at risk and to collateral blood flow to the ischemic region. Infarct size as a percentage of the area at risk was similar in the control group (40.7 +/- 5.5%, n = 11), the SOD-catalase group (38.0 +/- 6.4%; n = 8), and the oxypurinol-treated group (41.4 +/- 6.1%; n = 7) [p = not significant (NS) by analysis of variance]. In controls, there was an inverse relation between infarct size and collateral blood flow; neither of the treatments altered this relation (p = NS by analysis of covariance).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Comparison of patients with acute anterior or posterior myocardial infarcts with and without complete heart block.

The differences between myocardial infarct (MI) size, amount, and type of conduction fiber injury and outcome in patients with acute anterior or posterior (inferior) MI with or without complete heart block (CHB) were compared. In patients with acute anterior MIs with CHB the infarcts were larger, CHB was more persistent, necrosis involved the more anterior portions of the conduction system, and the terminal event was cardiogenic shock; whereas in the smaller acute posterior MIs with CHB, the CHB was usually transient, necrosis involved the more posterior portions of the conduction system, and terminal arrhythmias were the main cause of death. This is the first quantitative study that documents the larger size of anterior infarcts with complete heart block in comparison with posterior infarcts with complete heart block.

Heart Block↗
PubMed1987

Failure of superoxide dismutase to limit size of myocardial infarction after 40 minutes of ischemia and 4 days of reperfusion in dogs.

Reactive oxygen species such as the superoxide anion (.O2-) have recently been implicated as important agents involved in causing cell death in the setting of myocardial ischemia and reperfusion. When superoxide anion is involved in ischemic injury the administration of superoxide dismutase (SOD) may limit infarct size by reducing the level of superoxide anions in the myocardium. The study described herein was done to determine whether SOD could limit myocardial infarct size when infarcts were produced in dogs by a 40 min occlusion of the circumflex coronary artery followed by 4 days of reperfusion. The animals in the SOD treatment group received a 1 hr intra-atrial infusion of SOD, at a rate of 250 U/kg/min starting 15 min after occlusion and ending 35 min after reperfusion; control dogs received a saline infusion over the same time frame. Infarct size was determined histologically and expressed as a percentage of the anatomic area at risk (AAR). Infarct size was similar in the two groups, averaging 26.2 +/- 2.5% in the control group (n = 10) and 21.1 +/- 4.8% in the SOD group (n = 11) (p = .40). Hemodynamic variables were not statistically different in the two groups during the occlusion. The transmural mean collateral blood flow at 10 min into the 40 min occlusion was 0.13 +/- 0.02 ml/min/g in the controls and 0.17 +/- 0.03 ml/min/g in the SOD group (p = NS); moreover, SOD did not alter collateral blood flow. In control dogs, infarct size was inversely related to collateral blood flow; analysis of covariance showed that SOD did not shift this relationship. Thus, SOD did not limit infarct size in this study. The results of the current study are consistent with our previous study in which allopurinol, a xanthine oxidase inhibitor, did not limit infarct size in this same experimental preparation. The results suggest that superoxide anions that are accessible to the infused SOD are not a major cause of myocyte death caused by 40 min of severe ischemia followed by reperfusion.

Animals↗
PubMed1986

Spinal cord infarction following intraaortic balloon support.

Infarction of the lumbar and sacral spinal cord was demonstrated at autopsy of a 72-year-old man in whom acute paraplegia developed following coronary artery bypass grafting and atrial septal defect repair with intraoperative insertion of an intraaortic balloon. Autopsy findings showed that infarcts of the spinal cord and other key organs were caused by critical occlusion of small arterioles by cholesterol emboli. These emboli apparently arose as a result of the fragmentation of atheromatous plaques within the aorta during use of the intraaortic balloon pump with subsequent embolization and occlusion of small blood vessels.

Aged↗
PubMed1986

Effect of repetitive brief episodes of ischemia on cell volume, electrolytes and ultrastructure.

The effects of repeated brief episodes of ischemia on myocardial cell volume, electrolytes and ultrastructure were studied in dogs. Seventeen animals were divided into five groups. Group 1 underwent a single 10 minute occlusion of the circumflex coronary artery, with no subsequent reperfusion. Group 2 was similarly subjected to a 10 minute coronary occlusion, but was allowed a 20 minute reperfusion period. Group 3 underwent two 10 minute occlusions separated by 20 minutes of reperfusion and Group 4 underwent four 10 minute occlusions, each separated from the next by 20 minutes of reperfusion. Group 5 was subjected to a single, uninterrupted 40 minute occlusion. The anterior and posterior papillary muscles in each heart were sampled to compare nonischemic versus ischemic myocardium. No changes in myocardial water or electrolytes occurred during ischemia. However, reperfusion was associated with slight increases in tissue water and potassium, loss of magnesium and minimal changes in sodium or calcium ions. Electron microscopic analysis revealed signs of mild ischemic injury (absence of normal intramitochondrial granules, partial loss of glycogen and slight clumping of the nuclear chromatin) in posterior papillary muscle from Groups 1, 3 and 4. Group 2 showed complete recovery with 20 minutes of reperfusion, whereas Group 5 showed evidence of irreversible injury. There was no difference in the appearance of myocardium that had been subjected to one, two or four 10 minute occlusions. It is concluded that intermittent periods of reperfusion between brief episodes of coronary ischemia have a protective effect and prevent a cumulative deterioration of myocardial ultrastructure.

Adenosine Triphosphate↗
PubMed1986

The spectrum of pathology associated with percutaneous transluminal coronary angioplasty during acute myocardial infarction.

The purpose of this study was to determine at necropsy the morphologic consequences of percutaneous transluminal coronary angioplasty performed during acute myocardial infarction. The heart was examined in four patients who died between 6 hours and 4 days after coronary angioplasty. The patients had angioplasty of the left main coronary artery (one patient), left anterior descending coronary artery (two patients) and left circumflex coronary artery (one patient). Necropsy revealed residual stenosis, intimal hemorrhage and plaque disruption in all four patients. Also noted were distal embolization of plaque elements (two patients) and thrombotic occlusion of the coronary artery (one patient). In conclusion, the morphologic changes after angioplasty are varied. These changes illustrate the mechanisms of angioplasty and some of the complications that can be expected in a small number of cases. The morphologic changes associated with coronary angioplasty are similar in patients undergoing elective or emergency angioplasty although medial dissection was not observed in these patients with an evolving myocardial infarction.

Aged↗
PubMed1986

Four brief periods of myocardial ischemia cause no cumulative ATP loss or necrosis.

The effect of repetitive periods of coronary occlusion on myocardial adenine nucleotides, lactate, and infarct size was studied. In one series of dogs, the circumflex artery was occluded for one, two, or four 10-min episodes, each separated by 20 min of reperfusion. Hearts were excised and sampled for metabolic assays after one or more periods of ischemia before or after reperfusion. One 10-min period of ischemia caused a 61% loss of ATP and 41% loss of adenine nucleotides from the most severely ischemic subendocardial zone. Reperfusion resulted in rapid restoration of the adenylate charge but in only slight repletion of the adenine nucleotide pool. However, two or even four 10-min periods of ischemia caused no further adenine nucleotide loss. In contrast, 40 min of continuous coronary occlusion caused an 87% depletion of ATP and 67% of the adenine nucleotide pool from the same subendocardial region. Collateral blood flow was similar during all occlusions, but lactate accumulation was less during later occlusions. In a second series of experiments, myocardial necrosis was quantitated 4 days after four 10-min periods of ischemia. Necrosis was observed in only one of six dogs and, in this dog, was only 1.5% of the anatomic area at risk. Thus intermittent reperfusion prevents cumulative metabolic deficits and myocardial ischemic cell death, perhaps by restoring the capacity for high-energy phosphate (HEP) production and/or washing out deleterious catabolites. A first episode of ischemia also slows HEP utilization in subsequent episodes.

Adenosine Diphosphate↗
PubMed1986

Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

We have previously shown that a brief episode of ischemia slows the rate of ATP depletion during subsequent ischemic episodes. Additionally, intermittent reperfusion may be beneficial to the myocardium by washing out catabolites that have accumulated during ischemia. Thus, we proposed that multiple brief ischemic episodes might actually protect the heart from a subsequent sustained ischemic insult. To test this hypothesis, two sets of experiments were performed. In the first set, one group of dogs (n = 7) was preconditioned with four 5 min circumflex occlusions, each separated by 5 min of reperfusion, followed by a sustained 40 min occlusion. The control group (n = 5) received a single 40 min occlusion. In the second study, an identical preconditioning protocol was followed, and animals (n = 9) then received a sustained 3 hr occlusion. Control animals (n = 7) received a single 3 hr occlusion. Animals were allowed 4 days of reperfusion thereafter. Histologic infarct size then was measured and was related to the major baseline predictors of infarct size, including the anatomic area at risk and collateral blood flow. In the 40 min study, preconditioning with ischemia paradoxically limited infarct size to 25% of that seen in the control group (p less than .001). Collateral blood flows were not significantly different in the two groups. In the 3 hr study, there was no difference between infarct size in the preconditioned and control groups. The protective effect of preconditioning in the 40 min study may have been due to reduced ATP depletion and/or to reduced catabolite accumulation during the sustained occlusion. These results suggest that the multiple anginal episodes that often precede myocardial infarction in man may delay cell death after coronary occlusion, and thereby allow for greater salvage of myocardium through reperfusion therapy.

Animals↗
PubMed1986

Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia.

To study whether myocardial infarction differs in patients with and without ventricular tachycardia, the hearts of 22 deceased patients with ventricular tachycardia and 21 deceased control patients were analyzed quantitatively. The hearts from the ventricular tachycardia group were heavier and more dilated than those from the control group. Histologic analysis of a representative cross section from each heart showed that the ventricular tachycardia group had larger, more solid infarcts than did the control group. The ventricular tachycardia group also had a greater area of spared subendocardium, more hydropic change of the spared subendocardium, and more "ribbon type" spared subendocardium, which was defined as spared subendocardium of uniform contour 1 mm thick or less. The ventricular tachycardia group was divided into a subacute subgroup (n = 14, dying less than or equal to 10 weeks after infarction) and a chronic subgroup (n = 8, dying greater than 10 weeks after infarction). The infarcts of the subacute ventricular tachycardia group were more solid and had a greater amount of ribbon type spared subendocardium than those of the chronic ventricular tachycardia group. This information can serve as a baseline for the evaluation of animal preparations of tachycardia and, when combined with knowledge of the location of the arrhythmogenic region furnished by intraoperative mapping, should lead to better understanding of the anatomic substrate for ventricular tachycardia.

Coronary Vessels↗
PubMed1985

Effects of calcium-channel blockers on myocardial preservation during experimental acute myocardial infarction.

Calcium antagonists have become accepted agents for the attenuation of myocardial ischemia when it becomes manifest as angina pectoris. However, it is not known whether these agents can protect ischemic myocardium during the early evolution of an acute myocardial infarct. Calcium antagonists could potentially improve myocardial perfusion, by relieving coronary spasm or improving collateral blood flow, and reduce the energy demands of the ischemic myocardium either directly or by reducing heart rate or contractility. In some studies, calcium antagonists have decreased the rate of adenosine triphosphate depletion in ischemia and reduced functional or structural indexes of ischemic injury after relatively brief periods (up to 2 hours) of injury. We have assessed the ability of verapamil to protect severely ischemic myocardium in dogs with a 40-minute test period of circumflex occlusion followed by reperfusion. After 4 days of recovery, infarcts were sized by histologic methods. Untreated dogs had subendocardial infarcts (the more moderately ischemic subepicardial region being salvaged by reperfusion). Pretreatment with verapamil reduced the size of these subendocardial infarcts from 34 +/- 8 to 8 +/- 3% of the ischemic circumflex vascular bed (anatomic area at risk). Thus, verapamil prevented cell death in a substantial proportion of the severely ischemic subendocardial region that otherwise would have died as a result of the 40-minute test period of ischemia. To establish whether verapamil could prevent cell death for a longer period of time in the less severely ischemic subepicardial region, a 3-hour period of coronary occlusion with reperfusion was studied.

Animals↗
PubMed1985

Right ventricular subendocardial infarction in a patient with pulmonary hypertension, right ventricular hypertrophy, and normal coronary arteries.

Right ventricular infarction is usually associated with coronary artery disease and concomitant left ventricular infarction. Isolated right ventricular subendocardial necrosis was discovered at autopsy in a 52-year-old woman with pulmonary hypertension, right ventricular hypertrophy, and normal coronary arteries, who died with septicemia 41 days after mitral valve replacement. This represents the first well-documented report of isolated right ventricular subendocardial infarction associated with normal coronary arteries.

Bioprosthesis↗