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K D Straub

Publications and source records attributed to K D Straub.

At least 19 recordsLinked to original sources
PubMed1998

Laser energy reaching the posterior pole during transscleral cyclophotocoagulation.

OBJECTIVE: To measure scattered laser energy reaching the posterior pole during transscleral cyclophotocoagulation. METHODS: Transscleral cyclophotocoagulation was performed on 4 cadaver eyes with Nd:YAG noncontact, Nd:YAG contact, and diode contact lasers. Energy was measured with a photodiode through a 7-mm trephined hole in the posterior pole. Average percentage power, average power, and average energy transmission were calculated. American Conference of Governmental Industrial Hygienists (ACGIH) guidelines were used to calculate allowable energy exposures for each laser. RESULTS: All 3 lasers transmitted 3% to 5% of the power to the posterior pole. The average energy transmission was 240 to 260 mJ for all lasers. The contact lasers had an average power transmission of 120 mW. The noncontact Nd:YAG laser, with shorter pulse duration, had an average power transmission of 13,000 mW, significantly greater than that of the other lasers. The ACGIH guidelines for allowable energy exposures were 93 mJ for the noncontact Nd:YAG laser, 1300 mJ for the contact Nd:YAG laser, and 440 mJ for the contact diode laser. CONCLUSIONS: Three percent to 5% of laser power delivered during cyclophotocoagulation reaches the posterior pole. Exposure energies may approach or exceed ACGIH guidelines. The clinical significance of these findings remains to be shown.

Aged↗
PubMed1990

Reperfusion injury in ischemic myocardium: protective effect of controlled reperfusion.

Restoration of coronary artery flow following a period of ischemia often results in further ultrastructural damage to cardiac fibers, a phenomenon known as reperfusion injury. We have compared the ultrastructural effects of uncontrolled reperfusion in vivo of ischemic pig myocardium with the ultrastructural effects of reperfusion controlled at flow rates comparable to preischemia levels. Myocardial ischemia was produced for 60 minutes in 9 pigs by means of a reversible coronary artery occlusion, after which coronary artery flow was restored for 120 minutes. This restoration of flow was complete in four pigs (resulting in uncontrolled reperfusion) and partial in five pigs, with constant monitoring and adjustment of flow to maintain rates near preischemia values (controlled reperfusion). Myocardial samples from the ischemic, reperfused region were examined by electron microscopy. Ischemic damage to nuclei, mitochondria, and myofibrils and ischemic depletion of glycogen were graded independently and blindly by two investigators using a simple, nonparametric three-point scale. Ischemic damage was greater in pigs receiving uncontrolled reperfusion than in animals receiving controlled reperfusion, and these differences were significant for ischemic effects on nuclei (p less than 0.01), glycogen (p less than 0.02), and myofibrils (p less than 0.05) but not for ischemic effects on mitochondria (p = 0.095). We conclude that uncontrolled, hyperemic flow during reperfusion of ischemic myocardium is responsible, in part, for the phenomenon of reperfusion injury.

Animals↗
PubMed1990

Microvasculature sparing with controlled reperfusion of ischemic myocardium.

Reperfusion of ischemic myocardium may result in further ultrastructural damage to cardiac fibers, a phenomenon known as reperfusion injury. We have recently shown that controlled reperfusion, with maintenance of reperfusion flow rates near preischemia levels, prevents much of this reperfusion damage. This observation suggests that mechanical damage to the myocardial microvasculature is important in the pathogenesis of reperfusion injury. In this study, we have used electron microscopy to examine the microcirculation of ischemic, reperfused pig myocardium under conditions of uncontrolled and controlled reperfusion. Animals receiving uncontrolled reperfusion (reperfusion flow 3-4 times preischemia levels) showed ultrastructural damage to myocardial capillaries after 1 hour of ischemia and 2 hours of reperfusion. This damage was manifested as depletion of endothelial cell pinocytotic vesicles, plugging of capillaries by erythrocytes, leukocytes, and fibrin-containing microthrombi, and perivascular microhemorrhages. None of these changes were found in animals receiving controlled coronary artery reperfusion. We conclude that mechanical damage to the myocardial microvasculature is important in the pathogenesis of reperfusion injury and that such damage is obviated under conditions of controlled coronary artery flow during reperfusion.

Animals↗
PubMed1990

Reperfusion injury in ischemic myocardium: effects of nifedipine and verapamil.

Coronary reperfusion following myocardial ischemia may result in further damage to injured myocytes, as judged by their ultrastructural appearance. Calcium entry into myocytes has been implicated in this effect, and calcium channel-blocking agents have been used in attempts to prevent or limit such damage. In this study, we produced myocardial ischemia in pigs by means of reversible coronary artery occlusion. The pigs were infused with either nifedipine or verapamil (both clinically employed calcium channel-blocking agents) prior to and during coronary reperfusion. During reperfusion, nifedipine produced a lowering of mean arterial pressure, while mean arterial pressure was constant in verapamil-treated pigs and rose in pigs not receiving drugs. Myocardial samples from the ischemic, reperfused region were examined by electron microscopy. Ischemic damage to nuclei, mitochondria, and myofibrils and glycogen depletion were independently graded on a three-point scale by two investigators. For each of the organelles studied, ischemic damage was significantly less for nifedipine-treated animals than for controls. Ischemic damage in verapamil-treated pigs was not different from that seen in control animals, except for a slight improvement in myofibrillar appearance. We conclude that nifedipine, administered prior to and during reperfusion of myocardium, protects against reperfusion injury. The mechanism of this protective effect may be attributable, in part, to afterload reduction and, in part, to inhibition of transmembrane calcium flux in cardiac fibers.

Animals↗
PubMed1989

Controlled versus hyperemic flow during reperfusion of jeopardized ischemic myocardium.

Controlled versus uncontrolled reperfusion of ischemic myocardium after experimental coronary artery occlusion was studied to determine the effect on regional ventricular wall motion and associated biochemical alterations. Fourteen pigs underwent coronary artery occlusion for 1 hour followed by 2 hours of reperfusion. In seven animals uncontrolled reperfusion was achieved by complete release of the arterial occlusion resulting in hyperemic flow. In seven other animals coronary flow during reperfusion was controlled at baseline levels eliminating hyperemic flow. Our results show that controlled reperfusion lessens end-diastolic wall thickness, reduces myocardial calcium deposition, increases the rate of mitochondrial oxidative phosphorylation, and preserves cellular high-energy phosphate stores in the ischemic-reperfused myocardium when compared to the uncontrolled reperfusion state. These data suggest that the magnitude of flow at an early stage of reperfusion is one of the important determinants in the outcome of ischemic myocardium.

Adenosine Triphosphate↗
PubMed1989

Reperfusion injury in ischemic myocardium: protective effects of ruthenium red and of nitroprusside.

Coronary reperfusion following myocardial ischemia may result in further damage to injured myocytes, as judged by their ultrastructural appearance. Ruthenium red is an inorganic dye with calcium flux-inhibiting properties which protects ischemic myocardium against reperfusion damage, as judged by biochemical indices of mitochondrial function. In this study, we produced myocardial ischemia in pigs by means of reversible coronary artery occlusion. The pigs were infused with either ruthenium red or nitroprusside (an after-load reducing agent with no known calcium flux-inhibiting properties) prior to and during coronary reperfusion. During reperfusion, both ruthenium red and nitroprusside produced similar lowering of mean arterial pressure, while mean arterial pressure rose in pigs not receiving these drugs. Myocardial samples from the ischemic reperfused region were examined by electron microscopy. Ischemic damage to nuclei, mitochondria, and myofibrils and glycogen depletion were graded independently on a three-point scale by two investigators. For each of the organelles studied, ischemic damage was significantly less for treated animals than for controls. This protective effect was similar for both ruthenium red-treated animals and nitroprusside-treated animals. These results suggest that the protective effects of ruthenium red treatment are attributable to its afterload reducing properties rather than to inhibition of transmembrane calcium flux in cardiac fibers.

Animals↗
PubMed1988

The relationship between hypertrophy and dilatation in the postmortem heart.

Confusion may exist at the time of postmortem examination as to whether the diseased heart is dilated, hypertrophied, or both. Ventricular dilatation and ventricular hypertrophy were therefore evaluated by cardiac partition techniques in 441 subjects at autopsy to determine their relationship. Specific weight and surface area of each ventricle were obtained and patients were divided into categories of disease. Wall thickness measurements, a parameter routinely used in the ordinary autopsy, were found to be unreliable in defining hypertrophy. Ventricular surface area (an index of dilatation) was highly correlated with ventricular weight in most disease categories. Exceptions were cardiomyopathy and aortic stenosis, in which hypertrophy predominated. We conclude from these data that dilatation and hypertrophy occur proportionately in the postmortem heart in most disease categories except in cardiomyopathy and aortic stenosis. These findings clarify the relationship of dilatation and hypertrophy at the time of autopsy in most cases. Therefore, uncertainty as to whether cardiac dilatation or hypertrophy is present or which predominates is usually related to the inability to assess these states critically at the time of autopsy when the ordinary pathological methods are used.

Cardiomegaly↗
PubMed1988

Evaluation of biochemical functions and ventricular performance in regional ischemic-reperfused myocardium by afterload reduction: differential effects of calcium blocking and non-calcium blocking vasodilators.

The effects of afterload reduction with and without calcium blockade on reperfusion injury were studied in the pig. Reversible occlusion of the left anterior descending coronary artery was performed for 60 minutes followed by 120 minutes of reperfusion. For 15 minutes prior to and throughout reperfusion, treatment was administered with a calcium blocker (nifedipine or verapamil), a metallic organic dye and Ca2+ antagonist (ruthenium red), a vasodilator (nitroprusside), or saline. Biochemical functions, i.e., mitochondrial oxidative phosphorylation, myocardial ATP and Ca2+ content, and sarcoplasmic reticulum Ca2+ uptake were determined. Regional left ventricular wall motion was measured echocardiographically. Nifedipine and ruthenium red improved biochemical indices of ischemic myocardium in part by reducing afterload and thereby reducing oxygen demand and in part by reducing calcium entry into cells and mitochondria. Verapamil in the doses used failed to reduce afterload and demonstrated no salutary effect on biochemical parameters in ischemic myocardium. Nitroprusside reduced afterload, improved mitochondrial ATP production and increased percent wall thickening. Our findings suggest that afterload reduction with and without calcium blockade during the early reperfusion phase improves ischemic myocardium. These changes are predominantly biochemical in nature.

Adenosine Triphosphate↗
PubMed1986

Effects of reperfusion on myocardial wall thickness, oxidative phosphorylation, and Ca2+ metabolism following total and partial myocardial ischemia.

Coronary artery reperfusion following acute myocardial ischemia may salvage ischemic jeopardized cells. We studied the effects of early brief reperfusion on totally ischemic and on partially ischemic myocardium of open-chest pigs. In 10 animals, coronary flow was reduced to 0% for 30 minutes and was followed by 10 minutes reperfusion (group A). In another 10 animals, coronary flow was reduced to 25% of the baseline value for 30 minutes followed by 10 minutes of reperfusion (group B). In another eight animals coronary flow was reduced to 25% of the baseline value for 60 minutes and followed by 10 minutes of reperfusion (group C). Results showed that a brief 10-minute period of reperfusion of ischemic myocardium after total occlusion caused abnormal diastolic wall thickening with only partial return of systolic wall thickening. However, reperfusion of ischemic myocardium after partial occlusion, whether 30 or 60 minutes, caused little diastolic wall thickening and a partial return of systolic thickening. A marked elevation of myocardial Ca2+, a decrease in mitochondrial adenosine triphosphate (ATP) production and cellular ATP concentration, and a reduction in the rate of Ca2+ uptake by sarcoplasmic reticulum vesicles occurred in the totally ischemic myocardium but not in the partially ischemic myocardium. These results demonstrate that reperfusion of ischemic myocardium after 1 hour of coronary flow reduction to 25% of baseline is less damaging than reperfusion after a 30-minute total coronary occlusion, and suggest that preexisting states affecting coronary flow need to be evaluated in assessing the outcome of reperfusion.

Animals↗
PubMed1986

Effects of early reperfusion on the mechanical and biochemical characteristics of ischemic myocardium.

Coronary reperfusion of ischemic myocardium may be beneficial but is highly dependent upon occlusion and reperfusion times. To study the effects of early reperfusion on ischemic myocardium, 24 open chest pigs underwent coronary occlusion; one group was occluded for 40 min, and the other was occluded for 30 min followed by 10 min of reperfusion. Left ventricular wall thickness during systole and diastole was determined by ultrasound. Mitochondrial energy production and calcium content were evaluated from ischemic and nonischemic areas. Results showed: There was an absence of systolic thickness, a slight decrease of diastolic thickness from baseline, and a decrease in energy production in the ischemic myocardium. Reperfusion resulted in a diverse pattern of systolic and diastolic wall thickness in the ischemic area and a variable Ca2+ accumulation and mitochondrial ATP production. The variability of myocardial Ca2+ accumulation in the ischemic reperfused group correlated inversely with mitochondrial ATP production (r = -0.94) and directly with diastolic wall thickness (r = 0.65). Similarly, calcium accumulation, ATP production, and diastolic wall thickness correlated with mean blood pressure during reperfusion. These results suggest that many factors including individual characteristics of the animal and experimental conditions such as the level of blood pressure and the degree of calcium accumulation may determine outcome of reperfusion even in as brief a period as 10 min.

Adenosine Triphosphate↗
PubMed1984

Comparison of the canine tissue distribution of digoxin after acute and chronic administration: implications for digitalis therapy.

Digoxin is often used as an antiarrhythmic and inotropic agent. It produces significant neuroexcitatory responses that influence both its therapeutic and toxic effects. Patients receiving digoxin can be separated into 2 groups: those who receive it acutely and those who receive it chronically. The therapeutic and toxic responses to digoxin vary between these groups. The neural tissue distribution of digoxin was compared in dogs after both acute and chronic injections. Acute administration of digitalis in this study was associated with preferential uptake of digoxin into peripheral sympathetic nerves. Chronic administration was associated with continued selective uptake into the central nervous system despite decreasing serum levels. Therefore, acute (experimental or suicidal) or chronic (maintenance) digoxin administration produces different neural responses. The peripheral sympathetic nervous system will be the primary area of interaction with acute digoxin administration and the central nervous system will have a greater involvement with chronic digoxin administration. Our results indicate that the uptake of digoxin into the peripheral nervous system and central nervous system depends upon the duration of digoxin administration. The time course of digoxin accumulation influences both its therapeutic and toxic actions.

Animals↗
PubMed1983

The adverse effect of systemic hypertension following myocardial reperfusion.

Transient myocardial ischemia in postoperative hypertension is relatively common with coronary artery bypass surgery. This study examines the effect of hypertension during reperfusion of transiently ischemic myocardium. The animal model was open chest pigs with myocardial ischemia induced by the occlusion of the left anterior descending coronary artery for 30 min followed by 2 hr of reperfusion. A normotensive control group was compared with animals rendered hypertensive with phenylephrine during the ischemic and reperfusion times. In the hypertensive group, systolic blood pressure was raised from 106 to 161 mm Hg and peripheral vascular resistance from normal to 3600 dyn-sec-cm-5. Regional left ventricular wall thickness, mitochondrial function, sarcoplasmic reticulum Ca2+ uptake, tissue calcium, water content, and hemorrhage were evaluated. Compared to controls the hypertensive group had (1) loss of systolic wall thickening with increased diastolic wall thickness in the reperfused zone, (2) intramyocardial hemorrhage in the area of reperfusion, (3) significant impairment of oxidative phosphorylation by mitochondria isolated from the reperfused zone, (4) a marked reduction in the rate of Ca2+ uptake by sarcoplasmic reticulum vesicles, and (5) an increase in ischemic tissue calcium. Thus, hypertension associated with revascularization of acutely ischemic myocardium may accentuate myocardial damage.

Animals↗
PubMed1982

Ventricular performance and biochemical alteration of regional ischemic myocardium after reperfusion in the pig.

Reperfusion of acutely ischemic myocardium may cause profound alterations in left ventricular wall performance and metabolism. This study evaluates regional left ventricular wall thickness, analyzes metabolic and biochemical alterations, and examines tissue hemorrhage during 15, 30, and 120 minutes of myocardial ischemia, each followed by 120 minutes of reperfusion. Reperfusion after 15 minutes of ischemia showed nearly normal ventricular wall thickening and motion, intact metabolic and biochemical function, and no tissue hemorrhage. However, reperfusion after 30 and 120 minutes of ischemia was associated with ventricular wall thickening and failure to resume systolic and diastolic wall motion. Furthermore, adverse metabolic and biochemical alterations and reperfusion zone hemorrhaging increased proportionally with the duration of ischemia. These findings suggest critical myocardial damage occurring between 15 and 30 minutes of ischemia in an animal model without preexisting coronary collateral circulation. The observed metabolic and biochemical changes are consistent with irreversible cell membrane defects, allowing calcium ion accumulation and thus adversely affecting diastolic relaxation and systolic thickening.

Adenosine Triphosphate↗
PubMed1982

Divalent cation-activated ATP hydrolysis by mitochondrial ATP'ase--mechanism for energy depletion in ischemic reperfused myocardium.

Recovery of high-energy compounds by ischemic myocardium is believed to be important for its return to normal functioning. While it has been previously shown that oxidative phosphorylation is markedly reduced in mitochondria isolated from ischemic myocardium in the presence of all substrates, alterations in ATPase activity have not been confirmed. This study demonstrates that, although the rate of ATP hydrolysis produced by mitochondria isolated from 2-hr ischemic myocardium does not significantly differ from that produced by non-ischemic mitochondria, the rate produced by 2-hr ischemic, 2 hr reperfused mitochondria is significantly higher. Also, Ca++ content was observed to be higher in reperfused than in non-reperfused ischemic mitochondria. The addition of EDTA, EGTA, or oligomycin to the reperfused ischemic mitochondria resulted in the inhibition of ATPase activity. These results indicate that mitochondrial ATPase in ischemic myocardium is activated by Ca++ ions and that ischemic reperfused myocardium may contain mitochondria with uncontrolled ATPase activity such that high energy phosphate supplies are excessively depleted when the cells are reperfused.

Adenosine Triphosphatases↗
PubMed1982

Picosecond spectroscopy of Cu(II) cytochrome c.

We have observed a strong pH dependence in the relaxation rate of Cu(II) cytochrome c following excitation at 532 nm. At pH 8.0 the excited state relaxes with a lifetime of 10 +/- 5 ps while at pH extremes of 2.5 and 13.0 we find that the lifetime becomes longer than 1 ns. This change of more than two orders of magnitude in the lifetime may be due to the Cu coordination number, which is six at neutral pH but five at pH extremes.

Cytochrome c Group↗
PubMed1982

Adrenergic and cholinergic mechanisms in digitalis inotropy.

In anesthetized dogs, the effects of peripheral cardiac nerves upon cardiotonic steroid-induced contractile force increases were determined by comparing the effects seen with cardiac nerves intact, cardiac denervation, stellate ganglia removed or vagi sectioned. Additionally, structure-activity relationships among four cardiotonic steroids were determined by comparing the contractile force effects of bolus i.v. injections of digitoxigenin (the genin), digitoxigenin-galactose (genin-neutral sugar combination), digitoxigenin-aminogalactose (ASI-222, genin-aminosugar combination) and digoxin. The effects of these drugs upon cardiac rate, mean blood pressure and cardiac contractile force were recorded. Cardiotonic steroids differ in their interaction with cardiac nerves. Digitoxigenin, in addition to its direct contractile force effect on the myocardium, modulates contractile force through adrenergic mechanisms. In contrast, both digoxin and ASI-222 influence their direct inotropic responses through cholinergic mechanisms. Neither adrenergic nor cholinergic mechanisms significantly affect the peak inotropic response of digitoxigenin-galactose. Our data indicate that alterations in both the aglycone and the sugar moieties can significantly alter the contribution of the autonomic nervous system to the contractile force response.

Animals↗