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Biomedical subjects

L O Lutherer

Publications and source records attributed to L O Lutherer.

At least 19 recordsLinked to original sources
PubMed2002

A citywide evaluation of identification of risk factors for cardiovascular disease in emergency department patients complaining of chest pain.

The local division of the American Heart Association in Lubbock, Tex, conducted a cooperative study involving all three local hospitals to assess how effectively risk factors for cardiovascular disease are identified in patients presenting in the emergency departments with a complaint of chest pain. The charts of 250 consecutive patients with chest pain were reviewed for risk factors identified by the triage nurse and by the emergency department physician or the attending physician or both. Although the rate at which risk factors were identified was good, identification was neither complete nor comprehensive. Comparison with statistics for the general population showed that some risk factors were over-reported, while others were markedly underreported. Each of the three specialties of health care professionals stressed different risk factors, and having all three involved markedly increased the level of identification. The data provide guidelines for improving risk factor identification, and the study led to the formation of strategic alliances among the different hospitals and health care professionals that should help improve secondary prevention of cardiovascular disease within the community.

Adult↗
PubMed2001

Adenosine induces initial hypoxic-ischemic depression of synaptic transmission in the rat hippocampus in vivo.

The present study was designed to investigate the role of adenosine in the hypoxic depression of synaptic transmission in rat hippocampus. An in vivo model of hypoxic synaptic depression was developed in which the common carotid artery was occluded on one side in the urethane-anesthetized rat. Inspired oxygen levels were controlled through a tracheal cannula. Rats were placed in a stereotaxic apparatus for stimulation and recording of bilateral hippocampal field excitatory postsynaptic potentials. The percent inspired oxygen could be reduced to levels that produced a reversible and repeatable depression of evoked synaptic transmission restricted to the hippocampus ipsilateral to the occlusion. Further reduction in the level of inspired oxygen depressed synaptic transmission recorded from both hippocampi. The adenosine nonselective antagonist caffeine and the A(1) selective antagonist 8-cyclopentyltheophylline prevented the initial depression in synaptic transmission. We conclude that the initial depression of synaptic transmission observed in the rat hippocampus in vivo is due to endogenous adenosine acting at neuronal adenosine A(1) receptors.

Acid-Base Equilibrium↗
PubMed1999

Two genetically selected strains of rats exhibit hypersensitivity or resistance to cocaine-induced fatal arrhythmias.

We identified for the first time two genetically selected strains of rats that differ markedly in sensitivity to cocaine-induced life-threatening cardiac arrhythmias and arrest. The two strains of rats, designated as Fast and Slow, were bred for sensitivity (Fast) or resistance (Slow) to electrically kindled seizures. Studies were performed on halothane-anesthetized, mechanically ventilated rats. Animals were given cocaine (3 or 4 mg/kg/min i.v.) until they died. Arrhythmias (atrioventricular conduction block) developed at much lower cumulative cocaine doses in Slow-kindling rats than in Fast-kindling rats (15 +/- 1 versus 42 +/- 3 mg/kg, p <.01). The lethal cocaine dose (the dose that caused cardiac arrest) was also markedly lower in Slow than in Fast strains (32 +/- 2 versus 62 +/- 6 mg/kg, p <.01). These differences between the two strains were not significantly altered by pretreatment of animals with either ganglionic blockers, hexamethonium (20 mg/kg i.v.) or chlorisondamine (5 mg/kg i.v.), or a nonselective beta adrenergic receptor blocker, propranolol (1 mg/kg i.v.). A nonselective alpha adrenergic receptor blocker, phentolamine (10 mg/kg i.v.), however, abolished the differences between the Fast and Slow strains in the doses of cocaine required to produced atrioventricular conduction block and cardiac arrest. The results provide the first evidence of genetically determined susceptibility or resistance to cocaine-induced cardiotoxicity. There appears to be a genetically determined difference in the alpha adrenergic receptor system between the two strains that is responsible for the differential sensitivity to cocaine-induced arrhythmias and cardiac arrest.

Animals↗
PubMed1994

Cerebellar lesions alter autonomic responses to transient isovolaemic changes in arterial pressure in anaesthetized cats.

In previous studies, bilateral lesions of the rostral fastigial nucleus (rFN) of the cerebellum impaired recovery of mean arterial pressure (MAP) after many forms of hypotension. This study examined effects of cerebellar lesions on baroreflex responses during transient, isovolaemic, non-orthostatic changes in MAP in anaesthetized cats. Bilateral rFN lesions did not alter the rate or extent of fall in MAP induced by nitroprusside, but reduced by 39% the reflex increase in heart rate per unit decrease in pressure (delta HR/delta MAP). Femoral artery resistance remained below control levels. Lesions prolonged the time for 50% MAP recovery after nitroprusside by 93%. During phenylephrine-induced MAP increases, bilateral rFN lesions augmented reflex delta HR/delta MAP by 68%. In intact cats, the reflex decrease in HR after phenylephrine was blocked by electrical stimulation of the rFN, but appeared immediately after stimulation was stopped. Stimulation alone increased both MAP and HR. Propranolol failed to block either the increased HR or the suppression of reflex cardiodeceleration induced by rFN stimulation. Decreases in resting HR after rFN lesions may reflect removal of tonic cerebellar inhibition of cardiac parasympathetic tone. Thus, the cerebellum can influence autonomic output and modify baroreflex sensitivity by augmenting cardiovascular responses mediated by the sympathetic nervous system and inhibiting those mediated by the parasympathetic nervous system.

Animals↗
PubMed1991

Electrocardiography and postextrasystolic potentiation: utilization of the two methods to predict postrevascularization segmental myocardial function.

We previously reported that postextrasystolic potentiation (PESP) is a useful predictor of changes in systolic wall function (SWF) following coronary revascularization. In the current study we analyzed ECG changes related to corresponding myocardial segments to determine their correlation with PESP and SWF. We found: (1) The PESP response in a jeopardized segment was a valid predictor of improved SWF even when Q waves, ST-segment changes, or T-wave changes were present. (2) However, when Q waves were present in two or more of the corresponding leads, positive PESP was less likely to be observed. (3) Thus Q waves in two leads predicted the least postrevascularization improvement. (4) Segments with no corresponding Q-wave postrevascularization usually improved SWF. (5) Furthermore, a continuum of responsiveness to PESP was found, ranging from T-wave changes, ST-segment changes to Q-wave changes, indicating dissociation between electrical and mechanical events. In conclusion, the ECG together with PESP provide good predictive information relative to the efficacy of revascularization. PESP is a more valuable predictive indicator. ECG alone may be of value in that the occurrence of Q waves in two or more corresponding leads predicts a low probability of improved SWF. Further studies are indicated to investigate the dissociation between electrical and mechanical events.

Blood Pressure↗
PubMed1989

Stimulating fastigial nucleus alters central mechanisms regulating phrenic activity.

In paralyzed, mechanically ventilated, anesthetized cats, 30-sec trains of electrical stimulation in the rostral fastigial nucleus caused either respiratory excitation or inhibition (apnea) of respiration. The response elicited by stimulation was dependent on the frequency of stimulation: the duration of apnea decreased and respiratory excitation occurred more frequently at lower frequencies of stimulation. Excitation was characterized by increases of f and the rate of rise and peak (TNA) integrated activity of the phrenic nerve. TI and TE decreased. TNA and f remained elevated for at least three minutes after excitatory respiratory responses. Also, respiration was frequently elevated after an inhibitory response. Brief stimulation (100-200 ms) administered during expiration or inspiration altered either TE or TI and TNA, respectively. In addition, brief stimulation elicited short-latency inhibition or excitation of phrenic nerve activity. These effects were often unassociated with other phase changes. We conclude that activation of neurons or axons within the rostral fastigial nucleus can modulate activity of the phrenic nerve by altering the activity of at least three separate central mechanisms.

Animals↗
PubMed1989

Neurons of the rostral fastigial nucleus are responsive to cardiovascular and respiratory challenges.

The rostral fastigial nucleus (rFN) of the cerebellum has been implicated in the neural control of the cardiovascular and respiratory systems. Electrical stimulation and electrolytic lesions of this region produce changes in both cardiovascular and respiratory function. It has been suggested that some of these changes may result from effects on fibers of passage rather than on cell bodies of origin within the rFN. In the present study, extracellular recordings demonstrated a high percentage of units within rFN, as well as in adjacent areas, which responded to induction of acute increases or decreases in arterial blood pressure. Furthermore, units were identified in rFN which responded to respiratory stimuli as well as to changes in blood pressure. Out of the population tested, no units responding to respiratory stimuli were found in areas adjacent to rFN. In addition, a high percentage of neurons tested for response to passive movement also showed changes in firing rate to either cardiovascular or respiratory challenges, or both. Several units were identified (mostly in rFN), whose basal firing pattern was respiratory-related. This suggests the presence of cell bodies of origin within the rFN whose function is related to cardiorespiratory activity.

Action Potentials↗
PubMed1986

Inhibitory effects of cerebellar lesions on respiration in the spontaneously breathing, anesthetized cat.

Acute cerebellectomy depressed spontaneous respiration in cats anesthetized with chloralose-urethane. After cerebellectomy there was an increased interbreath interval (TTOT) accompanied by increased inspiratory and expiratory durations (TI and TE, respectively). However, the change of TE exceeded that of TI so that TI/TTOT decreased. Tidal volume (VT) and mean inspiratory flow (VT/TI) were not affected. No respiratory variable was significantly altered when cerebellectomy was performed subsequent to bilateral vagotomy. Bilateral lesions of the rostral fastigial nuclei (FN) in cats with intact vagi also caused a reduction in ventilation due to increased TTOT. In this case TI and VT/TI increased, but VT and TI/TTOT remained unchanged. Bilateral control lesions that usually included portions of the dentate nuclei did not influence respiration. The results suggest that in the anesthetized cat the cerebellum tonically excites respiratory centers controlling respiratory rate and the termination of inspiration. A part of this influence may be mediated by the rostral FN. In addition, vagal input appears to be important in the expression of the cerebellar influence on spontaneous respiration.

Anesthesia↗
PubMed1986

"Isolength" postextrasystolic potentiation as a predictor of functional restoration following surgical revascularization for myocardial ischemia.

A previously developed method of programmed postextrasystolic potentiation (PESP) was assessed in eight patients with medically refractory unstable angina, as a predictor of functional restoration resulting from surgical revascularization. Prior to coronary arteriography, left ventricular segmental wall motion was determined during ventricular pacing and the first postextrasystolic beat following an extrasystole. The postextrasystole was induced at an interval calculated to occur at a time where ventricular preload was identical to the regular paced beat (isolength interval). The left ventricular wall was divided into six segments, each subscribing one area of the ventriculogram, and correction for rotation during systole was made. Of 48 segments, 21 were considered "jeopardized," due to greater than 70% reduction in cross-sectional lumen of the serving coronary arteries. Fifteen of these 21 responded to PESP, increasing their segmental area ejection fraction from 44 +/- 5 (paced "normal" beat) to 56 +/- 6 (postextrasystolic beat) (p less than 0.05). Following surgical revascularization, these segments showed an improvement in their baseline area ejection fraction from 44 +/- 6 to 58 +/- 5 (p less than 0.05). Six jeopardized segments that failed to respond to PESP prior to revascularization showed functional deterioration after revascularization. The 27 non-jeopardized segments (which were not revascularized) also showed functional improvement, suggesting improved collateral flow. This study demonstrates that isolength postextrasystolic potentiation obtained with a standardized pacing protocol may be used to predict the potential for improvement in cardiac function following surgical revascularization. Our results also show that lack of PESP predicts loss of left ventricular myocardial function following revascularization.

Aged↗
PubMed1986

Postextrasystolic potentiation: analysis of methods of induction.

Studies were conducted in 15 patients with coronary artery disease to determine if the type of pacing used to induce an extrasystole had a bearing on subsequent postextrasystolic potentiation (PESP) and if the fact that these were evaluated in jeopardized or nonjeopardized portions of the ventricle altered the ability to assess PESP. Two types of pacing were used. In the first group, all beats in the test sequence (basic heart rate, extrasystole, and postextrasystole) were delivered from a programmed external pacemaker. This group was termed the "all-paced" (AP) group, and the postextrasystole was introduced before a compensatory pause could occur, so that loading conditions within the ventricle at the last regular beat and after the extrasystole were not different. In the second group, the extrasystole was coupled to the sensed intrinsic heart rate of the patient, and the postextrasystole was allowed to occur spontaneously. This group was termed the "sensed-paced" (SP) group. Despite differences in basic heart rates and postextrasystolic intervals between the two groups, comparable results were obtained with the two techniques. However, the postextrasystole in the SP group occurred much earlier than expected, probably due to intrinsic cardioacceleration during ventriculography. The net result was that loading conditions in this group before and after the extrasystole were also not different from each other. Results from the pacing techniques were not influenced by whether they were obtained from jeopardized or nonjeopardized segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1986

Postextrasystolic potentiation: regional wall motion before and after revascularization.

We evaluated the augmentation of contractility which follows an extrasystole (postextrasystolic potentiation: PESP) in patients before and after coronary revascularization surgery for angina pectoris. PESP was induced by methods which result in essentially identical loading conditions of the ventricle for the beat before the extrasystole and the beat after the extrasystole. We evaluated regional ventricular function before and after revascularization in "jeopardized" segments (supplied by a coronary vessel with significant coronary disease) and "nonjeopardized" segments (supplied by a vessel without significant disease). All coronary lesions were proximal to all three anterior or all posterior segments. Those jeopardized segments with patent grafts which had augmented with PESP improved their baseline function following revascularization. Conversely, those jeopardized segments which failed to augment with PESP decreased their basic function following revascularization. Those segments in which the grafts were occluded failed to augment with PESP after attempted revascularization. Perioperative myocardial infarction resulted in a drop in ejection fraction and a failure to augment with PESP. The nonjeopardized segments responded to PESP similarly to the ischemic augmenting segments. The results of this study suggest that PESP does detect ventricular segments which will improve basic function following revascularization. Those segments which fail to augment with PESP are most likely more ischemic than the augmenting segments, will not improve, and may even decrease function following revascularization.

Angina Pectoris↗
PubMed1986

Stimulating fastigial nucleus pressor region elicits patterned respiratory responses.

Electrical stimulation of the ventromedial region of the rostral fastigial nucleus (FN) in the cat produced marked quantifiable changes in respiration that were highly correlated with the concurrently elicited cardiovascular responses. The threshold- and stimulus-response curves were very similar for the two responses. Stimulation at relatively low frequencies produced increases in respiratory rate at all active sites. At approximately half the sites biphasic responses were observed with increases in stimulus frequency. These were characterized by a transient period of apnea beginning with onset of the stimulus, followed by an increased respiratory rate. At the remaining sites respiratory rate increased at all stimulation frequencies tested. Inspiratory duration decreased, and mean inspiratory flow increased. Tidal volume was not significantly altered. Similar changes were also observed when the pressor response was blocked by phenoxybenzamine. These observations, together with the frequent demonstration of expiratory-to-inspiratory and inspiratory-to-expiratory phase switching with short-burst stimulation, suggest that the FN can influence a respiratory central pattern generator. Based on these findings, a possible role for the FN in integrating cardiovascular and respiratory responses is suggested.

Adrenergic alpha-Antagonists↗
PubMed1985

Pain threshold changes induced by acute exposure to altered ambient temperatures.

Our previous findings that the degree of endotoxin-induced hypotension in the dog is inversely related to ambient temperature (19 degrees through 30 degrees C) and that only increased doses of naloxone are effective at 19 degrees C suggested that opioid activity is also influenced by ambient temperature, increasing in the cold and decreasing in the warm. Others have reported increases in plasma beta-endorphin in rats with acute exposure to both 5 degrees and 36 degrees C. In this study we measured changes in pain thresholds after both acute and chronic exposures to lesser alterations in ambient temperature as a potentially more sensitive index of changes in central opioid activity. Compared to 24 degrees C there was a marked increase in pain threshold with acute exposure to 10 degrees C and marked decreases at 30 degrees and 35 degrees C. A slight decrease occurred after 30 minutes but not 60 or 120 minutes at 19 degrees C. All acute changes disappeared three hours after the animals had been returned from the altered ambient temperature to 24 degrees C. No changes were observed after six days chronic exposure to 10 degrees or 30 degrees C. These findings suggest that moderate, acute changes in ambient temperature can produce inversely related, adaptable alterations in central opioid activity.

Acclimatization↗
PubMed1985

Changes in ambient temperature alter the blood pressure response to endotoxin and the effectiveness of naloxone.

At room temperature, naloxone, a competitive opiate antagonist, ameliorates the hypotensive effect of endotoxin, suggesting that endotoxin increases the secretion of endogenous opioids that have a cardiodepressor action. It was previously observed in our laboratory that reducing the ambient temperature from 24 degrees C to 19 degrees C blocked this protective effect of naloxone in dogs. This suggested that activation of peripheral cold receptors might also increase endogenous opioid activity and together with the opioid activity induced by endotoxin might be sufficient to override the competitive blockage by naloxone. In support of this, it was found in the present study that an increased dose of naloxone was effective at 19 degrees C. Studies done at 30 degrees C revealed that the hypotensive effect of endotoxin is inversely related to the ambient temperature, and naloxone is effective in low doses at the higher temperature. Core temperature was not altered significantly by the ambient temperatures used by naloxone, by endotoxin, or by any combination thereof. These findings suggest that, at least within moderate ranges, acute changes in ambient temperature induce inversely related changes in endogenous opioid activity, representing a specific thermal rather than a generalized stress response.

Animals↗
PubMed1984

Use of a programmable calculator for rapid, low-cost processing of echocardiographic records.

A comparative study was performed to determine the accuracy of a programmable calculator with supplemental digitizer in echocardiographic analysis. Twenty separate measurements were collected per heart beat from five different dogs, taking five heart beats from each dog. The measurements were made by an echocardiographic technician (ET), echocomputer (EC), and by a programmable calculator (HP). In a triple comparison (ET-HP, ET-EC, HP-EC) there were no significant differences in the values obtained, suggesting that the programmable calculator can provide a highly accurate and rapid means of processing echocardiographic measurements, thereby providing the advantages of the echocomputer without the cost of such a device.

Animals↗
PubMed1984

Applicability of echocardiography in volume determinations in experimental animals.

A method is described for the use of echocardiography in volume determinations in the experimental animal. Suitability of the technique in both acute and chronically implanted animals was tested. Stroke volumes derived from calculations based on echo data were compared with those obtained by an electromagnetic flow probe placed around the aorta. High correlation was found in both the acute (r = 0.96, P less than 0.001) and the chronic (r = 0.89, P less than 0.001) preparations. Cardiac output computed from echocardiographic data and compared with those based on either flow probe or indicator-dilution techniques also showed a high degree of correlation in both the acute (r = 0.91 and 0.95, respectively; P less than 0.001) and chronic (r = 0.98 and 0.94, respectively, P less than 0.001) preparations. It is suggested that echocardiography, because of the potential to measure many indicators of myocardial function in addition to volume, represents a significant improvement in the techniques available for basic cardiovascular experimentation.

Animals↗