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Biomedical subjects

H J Priebe

Publications and source records attributed to H J Priebe.

At least 19 recordsLinked to original sources
PubMed1992

Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency.

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.

Alprostadil↗
PubMed1992

Splanchnic hemodynamics and oxygen supply during acute normovolemic hemodilution alone and with isoflurane-induced hypotension in the anesthetized pig.

Safety of combined hemodilution and isoflurane-induced hypotension was assessed by studying their effects on splanchnic hemodynamics and oxygenation in nine anesthetized (ketamine/flunitrazepam) pigs. Acute normovolemic hemodilution (decrease in hematocrit from 29% to 15%) with 6% hydroxyethyl starch decreased (P < 0.05) O2 delivery despite increases in cardiac output and all splanchnic flows, as measured by electromagnetic flow probes. Superimposed isoflurane (1.45% end-tidal concentrations) caused marked decreases in arterial blood pressure, cardiac output, and splanchnic flows. Oxygen uptake of the liver became O2 supply dependent. A liver surface PO2 histogram (Clark-type electrode) showed 38% of PO2 values between 0 and 5 mm Hg. Hepatic lactate uptake decreased by 75%. These data suggest that depression of cardiovascular function during reduced O2-carrying capacity adversely affects hepatic perfusion, oxygenation, and function. Combined hemodilution and isoflurane-induced hypotension may not be appropriate in patients.

Anesthesia↗
PubMed1991

Effects of acute normovolemic hemodilution on splanchnic oxygenation and on hepatic histology and metabolism in anesthetized pigs.

Perioperative hemodilution (HD) has become an accepted means of reducing transfusion requirements. Therefore, the effects of limited (decrease in hematocrit [Hct] from 30 to 20%, "HD1") and severe (decrease in Hct from 20 to 14%, "HD2") acute normovolemic HD with 6% hydroxyethyl starch on splanchnic blood flows (electromagnetic flow probes), O2 uptakes and deliveries, surface O2 tensions (PO2) (Clark-type electrode), hepatic metabolism (organic acids), and hepatic histology (liver biopsies) were studied in nine pigs anesthetized and paralyzed with ketamine/flunitrazepam and pancuronium. HD1 caused significant (P less than 0.05) increases in cardiac output and all splanchnic flows. Only hepatic arterial blood flow increased twice as much as did cardiac output. Except for hepatic arterial O2 delivery, all splanchnic O2 deliveries decreased. Splanchnic O2 extractions increased, and O2 uptakes remained unchanged. There were no changes in mean surface PO2 values or in surface PO2 histograms of liver and small intestine; in portal or hepatic venous pH; and in hepatic uptake of pyruvate and lactate. In contrast, during HD2 (despite further increases in flows and O2 extractions) portal and hepatic venous pH decreased; mean surface PO2 of liver and small intestine decreased; and the liver surface PO2 histogram showed broadening and a shift to the left. However, hepatic uptake of lactate and pyruvate, and splanchnic O2 uptake remained unchanged, and histologic examination did not reveal significant cell injury. These data indicate that in this experimental model limited acute normovolemic HD was well tolerated by the splanchnic organs. After severe HD, gross liver function remained intact, but there was evidence that compensatory mechanisms (increases in flow and O2 extractions) were no longer fully able to counteract the decrease in splanchnic O2 delivery.

Anesthesia↗
PubMed1990

Myocardial ischemia in a canine model of pulmonary hypertension and right coronary artery stenosis.

This study was performed to study the effects of acute pulmonary embolization (injection of autologous muscle) on global and regional (ultrasonic dimension technique) right ventricular (RV) performance, coronary hemodynamics (electromagnetic flow probes), and gas exchange during underlying critical stenosis (cuff occluder) of the right coronary artery (RCA) in eight open-chest dogs. Resting coronary blood flow (CBF) and regional myocardial performance remained unaffected by the induction of RCA stenosis. Following embolization pulmonary artery (PA) pressure, pulmonary vascular resistance, end-diastolic dimensions and pressure increased, and PA flow, stroke volume (SV), and aortic pressure (AoP) decreased (P less than 0.05). There was a marked decline (60%) in CBF accompanied by severe myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, postsystolic shortening) in the area supplied by the stenosed RCA. Gas exchange, lung compliance, and pH worsened. Release of the RCA constriction led to a fourfold increase in CBF, return of PA flow, SV, and AoP to baseline values, and disappearance of regional myocardial dysfunction despite continued pulmonary hypertension. These data indicate that RV function may deteriorate in response to even small increases in afterload if coronary vascular reserve is absent and aortic pressure is allowed to decrease.

Animals↗
PubMed1990

Differences in effects of isoflurane and enflurane on splanchnic oxygenation and hepatic metabolism in the pig.

The effects of end-tidal concentrations of 1.45% isoflurane and 2.12% enflurane on splanchnic blood flow (electromagnetic flow probes), oxygen (O2) extraction and surface PO2 (Clark-type electrode), and hepatic metabolism (organic acids) were compared in an animal model relevant to humans. Eighteen laparotomized, ventilated pigs, anesthetized and paralyzed with ketamine/flunitrazepam and pancuronium, were studied. Enflurane caused significantly (P less than 0.05) greater decreases in mean arterial pressure, cardiac output, and superior mesenteric arterial, portal, and total hepatic blood flows. In addition, hepatic arterial blood flow decreased during enflurane administration but increased markedly (40%) during isoflurane administration. However, mean surface PO2 of liver and small intestine decreased to similar degrees (20%) during isoflurane and enflurane. Summary histograms of surface PO2 values were leftward shifted but did not show O2 values in the hypoxic range (0-5 mm Hg). Except for a decrease in hepatic lactate uptake during enflurane, there were no changes in either hepatic uptake or release of organic acids during anesthesia with either agent. These data show that splanchnic O2 supply is better maintained during isoflurane than during enflurane. Although this was not reflected in differences in tissue oxygenation and metabolism, decreased portal and hepatic venous O2 contents during enflurane indicate that an increase in preportal and hepatic oxygen extraction was necessary to preserve tissue oxygenation.

Animals↗
PubMed1989

Adverse effects of halothane in a canine model of acute right ventricular hypertension.

The effects of acute right ventricular (RV) hypertension (RVH) induced by pulmonary artery (PA) constriction, and of two concentrations (mean inspired 0.8 and 1.5%) of halothane (HAL) during RVH on global and regional RV performance (ultrasonic dimension technique), and on coronary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Following PA constriction, RV systolic pressure more than doubled, RV end-diastolic and systolic dimensions increased, and stroke volume (SV) and segment shortening fell (P all less than 0.05). There was no evidence of regional myocardial dysfunction (i.e., akinesis, systolic lengthening, postsystolic shortening), and reactive hyperemia in response to right coronary artery occlusion was present. Subsequent addition of HAL (0.8%) resulted in further increases in end-diastolic and systolic dimensions, and in marked decreases in right coronary blood flow, segment shortening, SV, and aortic pressure. During HAL 1.5% (range: 1.2-1.6%), regional myocardial dysfunction developed in three animals, reactive hyperemia was abolished in five out of six animals tested, and metabolic acidosis developed. Release of PA constriction during 1.5% HAL in seven animals resulted in improved global and regional RV performance, disappearance of regional myocardial dysfunction, and restoration of reactive hyperemia. In this canine model of acute RVH, increasing concentrations of HAL led to increasing deterioration in global and regional RV performance most likely due to inadequate coronary perfusion.

Acute Disease↗
PubMed1988

Cardiovascular effects of diltiazem in the dog.

The effects of two bolus injections (0.2 mg kg-1) and two infusion rates (0.2 mg min-1 and 0.4 mg min-1) of diltiazem on global and regional left (LV) and right ventricular (RV) performance (ultrasonic dimension technique), on coronary (electromagnetic flow meters) and systemic haemodynamics, and on electrophysiology (PR, QRS, QTc intervals) were studied in eight open-chest dogs anaesthetized with droperidol and fentanyl. The two bolus injections of diltiazem resulted in plasma concentrations of 688 +/- 115 and 650 +/- 85 ng ml-1 (means +/- SE), respectively, and caused substantial decreases in systemic and coronary vascular resistances, and in aortic pressure, and increases in LV segment shortening, stroke volume and aortic flow. Electrophysiological variables were little affected. At the low infusion rate (plasma concentration 140 +/- 23 ng ml-1) coronary and systemic vasodilatation occurred, but global and regional RV and LV performance were little affected. PR interval increased by 15%. At the higher infusion rate (plasma concentration 282 +/- 33 ng ml-1) coronary and systemic vasodilatation were maintained. Aortic pressure decreased slightly. Whereas LV end-diastolic and end-systolic dimensions remained unchanged, they increased in the RV. In addition, the PR interval increased by 35%, and three animals developed atrioventricular block type I. The data indicate that diltiazem is a potent coronary and systemic vasodilator with little effect on global RV and LV performance. However, at a higher infusion rate RV dimensions clearly tend to increase, and conduction abnormalities develop.

Animals↗
PubMed1988

Isoflurane causes more severe regional myocardial dysfunction than halothane in dogs with a critical coronary artery stenosis.

The effects of 1) isoflurane (ISO)- and halothane (HAL)-induced hypotension to a mean aortic pressure (AoP) of 55 mmHg, and 2) of substituting ISO and HAL for each other at a mean AoP of 55 mmHg on global and regional left ventricular performance (ultrasonic dimension technique) and on coronary hemodynamics (electromagnetic flow probes) were studied in eight open-chest dogs (anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium) with a critical coronary artery stenosis (micrometer-controlled snare) of the left anterior descending coronary artery (LAD). The stenosis reduced resting coronary blood flow by 5% (P less than 0.05) without affecting global or regional myocardial performance. HAL- and ISO-induced hypotension caused comparable decreases in global cardiac function, but regional myocardial dysfunction in the area of stenosis and the reduction in coronary flow through the stenosed LAD were more pronounced during ISO. Substitution of HAL for ISO at constant mean AoP, heart rate, end-diastolic dimensions and pressures, and stroke volume resulted in significant (P less than or equal to 0.05) amelioration of regional myocardial dysfunction (improvement in contraction amplitude, disappearance of paradoxical systolic lengthening and akinesis), a 20% increase in flow through the stenosed LAD, and a 20% decrease in flow through the unobstructed left circumflex coronary artery. These data suggest that, in the presence of a critical coronary artery stenosis: 1) ISO- and HAL-associated hypotension result in comparable decreases in global cardiac function, 2) ISO-associated hypotension is more likely to cause severe regional myocardial dysfunction suggestive of ischemia than equal degrees of HAL-associated hypotension, and 3) the different effects of HAL and ISO on ischemic myocardial segments at equally reduced coronary perfusion pressure are primarily related to their different effects on coronary vasomotor tone.

Animals↗
PubMed1988

Efficacy of vasodilator therapy in canine model of acute pulmonary hypertension.

This study was performed to determine 1) the effects of acute pulmonary embolization (induced by injection of autologous muscle) on right ventricular (RV) performance, coronary hemodynamics, and gas exchange; and 2) the efficacy of subsequent administration of nitroglycerin, prostaglandin E1, and hydralazine with regard to improvement in RV function and gas exchange in eight open-chest dogs. After embolization, pulmonary artery (PA) pressure and vascular resistance (PVR) increased three- to fivefold without changes in RV end-diastolic dimensions (ultrasonic dimension technique) or pressure. However, systolic dimensions increased, and stroke volume (SV) fell. Gas exchange, lung compliance, and pH worsened. Subsequent administration of nitroglycerin (5 micrograms.kg-1.min-1) and prostaglandin E1 (0.2 micrograms.kg-1.min-1) caused further decreases in SV and pH. In contrast, hydralazine (mean 0.15 mg/kg) improved myocardial segment shortening, SV, PVR, pulmonary artery flow, and gas exchange. Coronary blood flow increased by 110%. Thus in this canine model of combined pulmonary hypertension and respiratory insufficiency, nitroglycerin and prostaglandin E1 exerted no beneficial cardiopulmonary effects. In contrast, hydralazine improved regional and global RV performance and gas exchange.

Alprostadil↗
PubMed1988

Effects of tracheal intubation on laryngeal acoustic waveforms.

To assess the feasibility of noninvasive detection of laryngeal injury after tracheal intubation through acoustic waveform measurements, we studied the effects of intubation on "time-expanded" acoustic waveforms of the larynx in 16 patients given general anesthesia, 9 with and 7 without tracheal intubation. Recordings of several utterances were obtained by means of a microphone and an accelerometer attached to the skin at the midpoint of the suprasternal notch. Recordings were taken the day before induction of general anesthesia, 20 minutes after extubation, and 2 and 4 days after extubation. Waveforms of the recordings were subsequently assessed visually for features different from those of normal phonation as determined in preliminary studies. Waveforms in several of the recordings taken soon after extubation showed marked intraperiod and interperiod irregularities. These abnormalities improved and disappeared over the following 4 days. No changes were observed in the acoustic waveforms of seven patients given general anesthesia without tracheal intubation. The analysis of time-expanded acoustic waveforms of the larynx indicates that this technique has considerable potential as a sensitive, noninvasive technique that helps to evaluate the effects of tracheal intubation on laryngeal function, a technique that warrants further study and evaluation.

Adult↗
PubMed1987

Cardiovascular and electrophysiologic interactions between diltiazem and isoflurane in the dog.

The effects of the calcium entry blocker diltiazem (iv loading dose 0.4 mg/kg, iv maintenance dose 0.4 mg/min) and subsequent isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right ventricular (RV) and left ventricular (LV) performance (ultrasonic dimension technique), on coronary (electromagnetic flow probes) and systemic hemodynamics, and on electrophysiologic parameters (PR, QRS, QTc intervals) were studied in eight open-chest dogs, anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Diltiazem at a plasma concentration of 282 +/- 33 ng/ml (mean +/- SE) caused significant (P less than 0.05) increases in coronary blood flows, and decreases in coronary and systemic vascular resistances with only little effect on global and regional RV and LV function. However, the PR interval increased by 40%, and three animals developed II degrees atrioventricular block type I. At stable diltiazem plasma levels, administration of isoflurane caused dose-dependent decreases in myocardial segment shortening and stroke volume with unchanged LV or increased RV preload, and little changed RV or reduced LV afterload indicating myocardial depression. Coronary and systemic vascular resistances remained unaffected. At the higher concentration of isoflurane (mean inspired 1.3 +/- 0.2%), seven animals developed intermittent sinus node arrests with pauses up to 12 s followed by intermittent junctional escape or sinus rhythms. Similar interactions might develop in patients on diltiazem receiving isoflurane.

Animals↗
PubMed1987

Differential effects of isoflurane on regional right and left ventricular performances, and on coronary, systemic, and pulmonary hemodynamics in the dog.

The effects of isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right (RV) and left (LV) ventricular performance (ultrasonic dimension technique), and on coronary, systemic, and pulmonary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Isoflurane caused dose-dependent decreases in LV and RV dP/dt, and in myocardial segment shortening in the presence of unchanged heart rate, unchanged or increased (RV) preload, and unchanged (RV) or decreased (LV) afterload. RV and LV functions were affected differently: at a mean aortic pressure of 70 mmHg (mean inspired isoflurane 1.2%), RV end diastolic dimensions and pressure remained unchanged, whereas those of the LV decreased. At a mean aortic pressure of 55 mmHg (mean inspired isoflurane 1.8%), RV end diastolic dimensions and pressure increased above control, whereas those of the LV remained unchanged. Within the RV, inflow and outflow tract were affected quantitatively similarly, but dyssynchrony developed in four animals. Isoflurane caused dose-dependent decreases in coronary and systemic vascular resistances, but no change in pulmonary vascular resistance. At the lower concentration of isoflurane, coronary blood flow did not fall despite decreased LV and RV dP/dt, unchanged heart rate, unchanged or decreased preload, and unchanged or reduced afterload. The data indicate that isoflurane is a myocardial depressant and a potent coronary vasodilator. At both concentrations, LV function was better preserved than RV function, most likely due to the different effects of isoflurane on RV (unchanged) and LV (reduced) afterload.

Animals↗
PubMed1987

Isoflurane causes regional myocardial dysfunction in dogs with critical coronary artery stenoses.

The effects of isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right and left ventricular performance (ultrasonic dimension technique) and on coronary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs (anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium) with critical coronary artery stenoses (micrometer-controlled snares) of the right and left anterior descending coronary arteries. The stenoses reduced resting coronary blood flow by approximately 10% without affecting global or regional myocardial performance. During subsequent isoflurane administration, coronary blood flow fell markedly. In the areas supplied by the stenosed coronary arteries, segment length shortening decreased by 70% (P less than 0.01), and regional akinesis, paradoxical motion, or postsystolic shortening developed in 9 of 12 animals. In contrast, in the areas supplied by normal coronary arteries, myocardial segment length shortening decreased significantly less and did not show signs of dysfunction. In these non-ischemic areas at both concentrations of isoflurane, end diastolic and systolic dimensions were greater in the right than in the left ventricle, probably related to differences in right (unchanged) and left (reduced) ventricular afterloads. The data indicate that in the presence of coronary artery stenoses, isoflurane-induced hypotension may cause regional myocardial dysfunction suggestive of ischemia.

Animals↗