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Fifteen postoperative surgical patients, in whom noncardiac pulmonary edema developed were studied. A presumptive diagnosis of left ventricle failure would have been based on historical evidence of heart disease (80%), electrocardiographic changes of ischemia or arrythmia (87%), or cardiogenic shock (20%). (see article) Fig. 6. PAEDP-PCW gradient. Note that arterial oxygen tension had an inverse relationship to this pressure differential. Roentgenographic findings included pulmonary edema (73%), pulmonary vascular congestion (60%), cardiomegaly or congestive heart failure (40%). Mean increase in A-aDO2 was 290 torr. Further cardiovascular investigation seemed to exclude left ventricular failure. Mean cardiac index was 4.1 plus or minus 1.3 L/min/m2; pulmonary capillary wedge pressure 4 plus or minus 2.7 torr, and stroke work was 87 plus or minus 8.7 gm-meters. Possible etiologic agents included elevated pulmonary artery pressure (67%), allergic reactions (27%), peritonitis or multiple system trauma (54%), or multiple transfusions (33%). Forty-seven per cent of the entire group survived. Therapy was directed toward the underlying noncardiogenic suspected etiology. Direct cardiovascular measurements were necessary to correct the erroneous though seemingly well founded suspected diagnosis of left ventricular failure in these patients.
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PMID:"Pseudocardiogenic" pulmonary edema. 111 52

As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was produced in the left ventricular dysfunction. The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin. Epinephrine (0.05 mug/kg per min) elicited a significant reduction in end-diastolic pressure and increase in stroke volume. The latter was not attended by an increased incidence of ventricular fibrillation, whereas fibrillation occurred in half of the group given strophantihidin. Thus, the catecholamine was selected to study pump failure. Severe ischemic heart failure was assessed in two groups with scar from previous infarction for up to 4 hours. By 60 minutes of ischemia the increase in end-diastolic pressure and volume and decrease in stroke volume and ejection fraction were comparable in both groups. Thereafter, alternate animals received small doses of epinephrine (0.05 to 0.15 mug/kg per min) with graded increments at 60 minute intervals to counter tachyphylaxis and findings were compared with those in control dogs. Over the subsequent 3 hours, there was progressive deterioration of left anterior descending coronary artery, affecting ventricular function in the untreated group with an increase in end-diastolic pressure from 10 plus or minus 1 to 33 plus or minus 2.4 mm Hg. End-diastolic volume increased by 63 percent; stroke volume and ejection fraction decreased by 48 and 66 percent, respectively. The infusion of epinephrine was attended by a significantly lower end-diastolic pressure of 20 plus or minus 2.5 mm Hg, whereas end-diastolic volume, stroke volume and ejection fraction were restored to control levels after 4 hours of ischemia. Mortality in the untreated group was 62 percent by 4 hours; all seven animals in the treated group survived.
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PMID:Ischemic heart failure: sustained inotropic response to small doses of I-epinephrine without toxicity. 111 1

The known risk factors for atherosclerosis do not possess the same significance in young people as in the elderly. Hypercholesterolemia, diabetes and cigarette smoking appear to have a greater bearing below the age of 50 than later, particularly in myocardial infarction but also in apoplexy. On the other hand, hypertension is an important factor in the young and, especially in the case of apoplexy, even more so in advanced age. There is marked difference with regard to preexisting heart disease, which scarcely plays a role in myocardial infarction of the younger patient but is a factor in some 50% of hemiplegia cases. Only one fifth of elderly patients with this disease have no preexisting carcdiopathy. The similarity of the risk factors in elderly patients either with or without apoplexy is due to the fact that arteriosclerosis is already established in both groups and the risk factors which give rise to ischemia, thrombosis or embolism assume prominence. The therapeutic implications are briefly discussed.
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PMID:[Risk factors and age]. 113 58

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133Xe concurrently with measurements of local cerebral blood flow (LCBF) after injection of 133Xe directly into the distal stump of the occluded middle cerebral artery (MCA) by the use of the gamma camera after producing experimental ischemia in baboons by occluding the MCA. Regional MCA stump pressure (rMCAP) was also measured. Regions of ischemia assessed by intracarotid injection of 133Xe correlated well with the territory of infarct defined by injection of 133Xe into the distal MCA stump. Flow values in ischemic regions obtained by direct injection of 133Xe into the MCA were 15% to 20% lower than those obtained by intracarotid injection of 133Xe. Possible explanations for these differences are discussed. During induced hypertension autoregulation in ischemic areas was abolished and paradoxical responses of LCBF and rMCAP to changes in arterial carbon dioxide tension (PaCO2) were confirmed.
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PMID:Regional cerebral blood flow measured by the gamma camera after direct injection of 133Xe into the distal stump of the occluded middle cerebral artery. 115 74

While left ventricular (LV) performance in patients with coronary artery disease (CAD) has been extensively investigated, little attention has been given to right ventricular (RV) function in this disease. For this purpose, a new geometric model for RV volume has been developed and RV end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI) and ejection fraction (EF) have been determined from biplane RV cineangiograms in 26 patients. Eight patients served as normal (control) subjects (group I). Eighteen patients with obstructive CAD comprised two other groups: six who had no significant disease of the right coronary artery (RCA) (group II) and 12 who had a high grade RCA lesion (group III). The mean values for EDVI, SVI and EF in group I were 76 +/- 11 ml/m2, 50 +/- 6 ml/m2, and 66 +/- 6%. The only significant difference between groups I and II was that SVI was lower in group II than in group I (P less than 0.01). No measurements in groups II and III were statistically different from each other. However, markedly subnormal values were found in group III (EDVI: 61 +/- 16 ml/m2, SVI: 33 +/- ml/m2 and ef: 52 +/- 7%); all values being significantly lower (SVI and EF: P less than 0.001; EDVI: P less than 0.05) than in group I. RV end-diastolic pressure was normal in all patients. These findings may related to 1) reduced RV compliance, 2) distorted LV geometry, 31 possible RV ischemia or 4) reduced Frank-Starling effect.
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PMID:Right ventricular performance in patients with coronary artery disease. 115 72

Male and female, arteriosclerotic (breeder) and nonarteriosclerotic (virgin), Sprague-Dawley rats were made severely diabetic with alloxan. Two weeks later experimental animals had both carotid arteries ligated to induce a state of acute cerebral ischemia. After six weeks of cerebral ischemia either with or without severe diabetes the animals were killed. Animals which survived either the acute induction of diabetes or cerebral ischemia did not manifest any new episodes of cerebral ischemia. Subjects with combined diabetes and cerebral ischemia manifested the greatest loss in body weight, adrenal hypertrophy and thymus gland involution, increased levels of serum CPK and SGOT, but decreased SGPT and LDH, hyperglycemia and hypertriglyceridemia, and the most extensive cerebral edema. It is suggested that diabetic rats may have a greater predilection toward cerebrovascular accidents because the diabetic state contributes not only to an exacerbation of atherosclerosis, but also complicates any condition of cerebrovascular ischemia by creating extracerebral edema.
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PMID:Chronic diabetes followed by chronic cerebral ischemia induced by bilateral carotid artery ligation in arteriosclerotic versus nonarteriosclerotic rats. 117 43

Amaurosis fugax (transient monocular blindness) is a symptom of retinal ischemia just as contralateral hemiparesis and sensory loss are symptoms of cerebral ischemia. These symptoms are produced by atherosclerotic stenosis of the carotid vessels at the ipsilateral carotid bifurcation and emboli from these areas causing focal, repetitive, retinal ischemia. A study of 31 endarterectomy patients was undertaken to see if eight patients with amaurosis fugax (25%) could be differentiated from 22 patients with transient cerebral ischemia. The patients with amaurosis fugax were found to be younger. They all had 75% or greater stenosis of the internal carotid artery at the bifurcation on the symptomatic side. They all had unilateral visual symptoms and these symptoms were relieved by surgery. The patients with amaurosis fugax were devoid of cardiac disease, while 45% of the cerebral ischemic patients had documented myocardial disease. Amaurosis fugax (transient monocular blindness) in the setting of clinically significant atheroslerosis of the carotid vessels is an indication for carotid endarterectomy.
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PMID:Amaurosis fugax: a clinical comparison. 117 55

Adenosine diphosphate (8 mg per minute for five minutes) was infused into the carotid artery of 63 rabbits. The effects were twofold: systemic hypotension and platelet aggregation in the cerebral circulation. As a consequence of the last effect, platelet emboli were produced which occluded cerebral arteries in a number and size sufficient to cause cerebral ischemia. Areas of focal ischemia were observed through a cranial window, and documented with antipyrine autoradiography. Platelet thrombi were almost entirely transient, being fragmented and removed within a very short time of cessation of ADP infusion. Consequently, no permanent tissue damage ensued. This experimental model approaches the spontaneous transient ischemia attacks (TIAs) in man, demonstrating that these can be caused by pure platelet emboli. A high cholesterol diet administered for two months prior to ADP infusion did not enhance the effect of the procedure or make the platelet aggregation and the following ischemia longer in duration or more severe.
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PMID:Animal model of TIA: an experimental study with intracarotid ADP infusion in rabbits. 119 26

The permissible duration of brain ischemia without sustaining damage is short. Less clear are the mechanisms accounting for the vulnerability of brain to ischemic insults. Neurochemical factors implicated include impairment of energy synthesis by mitochondria and of energy-dependent processes such as synaptic transmission, ATPase activity, membrane conductance and altered protein and lipid synthesis. To clarify the vulnerability of energy metabolism, we investigated energy availability and synthesis in our model of global cerebral ischemia. Our studies evaluated in vitro mitochondrial ATP synthesis and the in vivo quantitation of the cortical adenylate pool. Results of our investigations support a growing body of evidence showing the energy state to be relatively stable to ischemia. We conclude that an energy-dependent process of brain is primarily vulnerable to ischemia.
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PMID:Energy metabolism during brain ischemia. Stability during reversible and irreversible damage. 119 33


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