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Biomedical subjects

O A Smiseth

Publications and source records attributed to O A Smiseth.

At least 73 records · Page 4Linked to original sources
PubMed1990

Effect of intracoronary contrast medium on left ventricular diastolic pressure-volume relationships.

The purpose of this study was to investigate the effect of intracoronary injection of the contrast medium sodium-meglumine diatrizoate (CM) on left ventricular (LV) diastolic pressure-volume relationships. Seven closed-chest dogs were instrumented with pressure catheters in the left ventricle and aorta, a balloon transducer to measure pericardial pressure, and an aortic flow meter to determine stroke volume. We estimated LV volume from two diameters by sonomicrometry. Six milliliters of CM was injected into the left main coronary artery. Transmural LV end-diastolic pressure increased from 3.3 +/- 1.1 to 7.2 +/- 0.9 mm Hg and LV end-diastolic volume index from 40.8 +/- 6.8 to 44.7 +/- 7.4 ml. There was only a minor increase in pericardial pressure. Stroke volume decreased by 31 +/- 7%. There was no change in the intracavitary or transmural diastolic pressure-volume relationship, indicating unchanged LV "compliance." Increased LV filling pressure by CM reflected reduced systolic function.

Animals↗
PubMed1990

Left ventricular filling at elevated diastolic pressures: relationship between transmitral Doppler flow velocities and atrial contribution.

The relationship between transmitral Doppler blood flow velocities and atrial contribution to left ventricular (LV) filling was investigated in seven open-chest dogs. At LV filling pressures greater than 15 to 20 mm Hg, LV volume approaches a maximum. Thus we hypothesized that when LV pressure before the onset of atrial systole exceeds this level, the atrial contribution would decrease and the ratio between peak early (E) and atrial-induced (A) mitral velocities would increase. Atrial contribution was measured as LV diameter increase during atrial contraction expressed as a percentage of the total LV diameter change during diastole (sonomicrometry). When left ventricular end-diastolic pressure (LVEDP) was progressively increased from 10 +/- 1 (mean +/- standard deviation) to 28 +/- 3 mm Hg by intravenous saline solution, the atrial contribution decreased from 34 +/- 14% to 8 +/- 10% (p less than 0.001). Concomitantly the A velocity decreased from 39 +/- 7 to 24 +/- 8 cm.sec-1 (p less than 0.01), and the E/A ratio increased from 1.8 +/- 0.3 to 3.6 +/- 1.5 (p less than 0.001). The E/A ratio and the atrial contribution were constant until LVEDP exceeded 17 to 20 mm Hg, at which level marked changes in both parameters were noted. Thus when LV filling pressure was increased, the E/A ratio increased, indicating a filling shift towards early diastole. The reduced atrial contribution during increased preload was explained by the curvilinear shape of the LV pressure-volume curve. At markedly elevated filling pressures, near-maximum LV diameter was achieved before atrial contraction; hence the atrial contribution decreased and the E/A ratio increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

A comparison of changes in esophageal pressure and regional juxtacardiac pressures.

The relationship between esophageal pressure and juxtacardiac pressures was studied during positive end-expiratory pressure (PEEP) ventilation applied to both lungs or selectively to one lung. The experiments were performed in eight anesthetized dogs with balloon catheters in the esophagus and in the left and right pericardial and overlying pleural cavities and with an open-ended liquid-filled catheter in the pleural cavity. Bilateral PEEP (10, 20, and 30 cmH2O) caused progressive and similar increments in left and right pleural pressure. Selective PEEP, however, increased ipsilateral pleural balloon pressure more than contralateral pressure. The increase in ipsilateral pleural balloon pressure markedly exceeded the increase in esophageal pressure. There was a small increase in pleural open-ended catheter pressure that approximated the increase in esophageal pressure. During selective PEEP, pericardial balloon pressure remained uniform because of a decrease in ipsilateral pericardial transmural pressure. In conclusion, selective PEEP caused nonuniform increments in regional pleural balloon pressure. Left and right pericardial balloon pressure, however, increased uniformly with selective PEEP because of reduced ipsilateral pericardial transmural pressure. The esophageal balloon did not reflect the marked regional increments in pleural balloon pressure with selective PEEP and consistently underestimated the changes in pleural balloon pressure with general PEEP.

Animals↗
PubMed1990

Assessment of left ventricular relaxation by Doppler echocardiography. Comparison of isovolumic relaxation time and transmitral flow velocities with time constant of isovolumic relaxation.

Isovolumic relaxation time (IVRT) and events of early transmitral flow measured by Doppler echocardiography were validated against the time constant of left ventricular relaxation (tau) in open-chest dogs. During increased inotropy (by isoproterenol infusion) at constant preload, enhancement of relaxation was indicated by a decrease in tau from 48 +/- 12 (mean +/- SD) to 33 +/- 5 msec (p = 0.04) with a concomitant decrease in IVRT from 74 +/- 18 to 38 +/- 8 msec (p = 0.03). During decreased inotropy (by propranolol infusion) at constant preload, slowing of relaxation was indicated by an increase in tau from 40 +/- 8 to 51 +/- 13 msec (p = 0.02) with a concomitant increase in IVRT from 71 +/- 15 to 83 +/- 21 msec (p less than 0.05). A significant correlation between changes in tau and changes in IVRT was found (r = 0.66, p less than 0.001). In contrast, when left ventricular end-diastolic pressure was increased from 7 +/- 2 to 24 +/- 4 mm Hg at constant inotropy, tau increased from 47 +/- 14 to 64 +/- 25 msec (p = 0.03), whereas no change in IVRT was observed (76 +/- 19 and 71 +/- 19 msec, respectively). Aortic pressure was not significantly changed during any intervention, and heart rate was kept constant by pacing. Peak early transmitral velocity was unchanged by propranolol but increased during isoproterenol and saline infusion (p less than 0.001 and p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The dependence of the time constant of left ventricular isovolumic relaxation (tau) on pericardial pressure.

The purpose of this study was to investigate the dependence of tau, the time constant of left ventricular (LV) isovolumic relaxation, on pericardial pressure and to compare values of tau as determined by the methods of previous investigators and by a standard exponential curve fit. All of the more recent methods involve an additional parameter--the pressure to which the exponential relaxation finally declines (PB, the pressure intercept in the method of Craig and Murgo and the asymptote in the exponential fits). An additional purpose of the study was to determine the relation of these parameters to pericardial pressure. In eight closed-chest anesthetized dogs, tau was calculated from intracavitary (Plv) and transmural LV pressure (Plv = Plv-Pper) by each method as pericardial (Pper) and LV end-diastolic pressure were changed by pericardial infusion and intravenous volume loading. The time constant determined by the method of Weiss et al was dependent on pericardial pressure; the time constants determined by the other methods were not. PB and the asymptotes were found to be similar and to increase almost equally with pericardial pressure. When pericardial pressure was zero, these values were approximately -20 mm Hg. Thus, both these parameters seem to indicate the same baseline pressure, a pressure that increases pari passu with pericardial pressure. Reported changes in the value of tau calculated from intracavitary LV pressure by the method of Weiss et al may reflect factors other than changes in LV diastolic function.

Animals↗
PubMed1990

Assessment of the splanchnic vascular capacity and capacitance using quantitative equilibrium blood-pool scintigraphy.

A series of human and animal experiments were carried out to assess the usefulness of equilibrium blood pool scintigraphy (EBPS) to study acute changes of the splanchnic vascular capacity and the splanchnic vascular pressure-volume (P-V) relationship. Corrected regional abdominal count rate changes, before and after various pharmacologic interventions, were used to assess regional splanchnic vascular volume changes. Animals were instrumented to manipulate and record splanchnic venous pressures. In patients, splanchnic vascular capacity increased by 5.2 +/- 6.9% (p less than 0.001) after 0.6 mg sublingual nitroglycerin while no significant change was noted after sugar pills (0.9 +/- 5.2%, p greater than 0.3). In dogs, splanchnic vascular capacity decreased by a mean of 16% during infusion of angiotensin (p less than 0.001) and increased by a mean of 32% during infusion of nitroprusside (p less than 0.001). The splanchnic vascular P-V curve was shifted rightwards during nitroglycerin administration. Thus, using the radionuclide technique we detected the expected qualitative and quantitative shifts in splanchnic capacity and capacitance. We conclude that EBPS is a useful method to assess acute changes of 1) the splanchnic vascular P-V relationship, in invasive animal studies, and 2) the splanchnic vascular capacity in noninvasive human and animal studies.

Adult↗
PubMed1989

[Treatment of unstable angina pectoris].

We present the results of an acute revascularisation program for unstable angina. Of the 63 consecutive patients included in the program 61 had significant coronary artery disease. Coronary bypass grafting was performed in 39 and percutaneous transluminal angioplasty in 9. There were two perioperative myocardial infarctions and one death in hospital. 13 patients were found unsuitable for revascularisation. At follow-up (14-26 months) 60 patients were still alive (95%). In the revascularised group 30 patients (65%) were free of angina pectoris. Accordingly, in patients who do not respond to medical therapy, acute revascularisation may be performed with low operative mortality, low incidence of perioperative myocardial infarctions, and good long term results.

Angina Pectoris↗
PubMed1989

Inosine causing insulin release and increased myocardial uptake of carbohydrates relative to free fatty acids in dogs.

The aim of the present study was to determine the effect of i.v. inosine on myocardial substrate uptake and function in the in situ dog heart. Inosine was infused i.v. at a rate of 5 mg kg min-1 in eight closed-chest pentobarbital anaesthetized dogs. Inosine caused a 46% decrease (P less than 0.01) in plasma free fatty acids (FFA), a 15% decrease (P less than 0.05) in plasma glycerol, an 18% decrease (P less than 0.05) in plasma glucose and a 46% increase (P less than 0.01) in blood lactate. This was associated with a 55% decrease (P less than 0.01) in myocardial FFA uptake and a 72% increase in lactate uptake, while glucose uptake remained unchanged. These metabolic changes were associated with a five-fold increase (P less than 0.05) in arterial insulin. Inosine caused an 18% increase (P less than 0.01) in myocardial blood flow without changing MVO2. There was a 33% increase (P less than 0.01) in LV dP/dtmax, a decrease in LVEDP from 4.9 +/- 0.9 (mean +/- SEM) to 0.9 +/- 0.3 mmHg (P less than 0.05) and a 24% decrease (P less than 0.01) in systemic vascular resistance. Inosine caused a transient 38% increase (P less than 0.05) in pulmonary vascular resistance. In conclusion, in addition to a positive inotropic effect and vascular effects inosine was found to cause release of insulin and to shift myocardial metabolism towards increased uptake of carbohydrates relative to FFA.

Animals↗
PubMed1988

Plasma concentrations of atrial natriuretic factor in acute left ventricular failure in the dog.

Acute ischemic left ventricular failure was induced in anesthetized dogs by repeated coronary embolization with 50 microns microspheres. Plasma concentrations of atrial natriuretic factor (ANF) were measured by radioimmunoassay of arterial and venous samples before and after failure induction. Heart failure was accompanied by a doubling of arterial ANF concentration, whereas there were only insignificant changes on the venous side. The increase in arterial ANF correlated significantly to the increase in left ventricular end-diastolic pressure, but not to the increase in right atrial pressure. Measurements of pericardial pressure indicated that a pericardial constraint acted to reduce atrial distension and thereby cardiac ANF release during failure.

Animals↗
PubMed1988

Increased pulmonary vascular capacitance with beta-adrenergic receptor stimulation: an experimental study of the effect of isoproterenol on the pulmonary vascular volume-pressure relationship.

The present study is an investigation of the effect of beta-adrenergic receptor stimulation by isoproterenol on pulmonary vascular capacitance. The experiments were done in six intact-chest, anaesthetized dogs in which pulmonary and cardiac blood volumes were assessed by blood pool scintigraphy. Isoproterenol (0.150 microgram.kg-1.min-1) significantly (p less than 0.005) lowered pulmonary capillary wedge pressure (PPCW) and pulmonary artery pressure (PPA) but did not significantly change pulmonary blood volume (PBV). Left ventricular end-diastolic pressure and total cardiac volume both significantly (p less than 0.005) decreased. Pulmonary vascular volume-pressure (V-P) relationships before and during isoproterenol were described by means of blood transfusions and hemorrhage. In individual dogs the PBV-PPCW and the PBV-(PPCW + PPA)/2 relationships were significantly shifted upward by isoproterenol (p less than 0.05 or less); slope changes were variable. Pooled data from all dogs also showed a significant (p less than 0.001) upward shift in the pulmonary vascular V-P relationship regardless of which measure of distending pressure was used. These results suggest that beta-receptor stimulation by isoproterenol increases pulmonary vascular capacitance by increasing the unstressed volume.

Adrenergic beta-Agonists↗
PubMed1988

Unstable angina pectoris. Experience with an acute revascularization program.

One year's experience of an acute revascularization program for unstable angina pectoris is presented. In the total material of 63 patients, significant coronary artery stenosis was found in 61 and normal coronary arteries in two. Coronary artery bypass grafting was performed in 39 patients (62%) and percutaneous transluminal angioplasty in nine (14%). There were two perioperative myocardial infarctions and one hospital death. Thirteen patients were not eligible for revascularization. At follow-up (14-26 months) 60 patients were still alive (95%). In the revascularization group, one patient had died, but of the remaining 46 patients, 30 (65%) were free of angina pectoris, and in addition six had only minor symptoms.

Adult↗
PubMed1987

Left ventricular external constraint: relationship between pericardial, pleural and esophageal pressures during positive end-expiratory pressure and volume loading in dogs.

Left ventricular (LV) diastolic filling is limited by the constraining effects exerted by the pericardium (PE) and the lung/chest wall. The aim of the present study was to assess the validity of various estimates of external cardiac constraint, compared to pericardial surface pressure (Ppe) measured lateral to the LV myocardium. In nine anesthetized dogs we measured Ppe, pleural surface pressure (Ppt) (lateral to the pericardium) and esophageal pressure (Pes) under conditions of volume loading and positive end-expiratory pressure (PEEP). We measured Ppe and Ppl with flat, liquid-containing silastic rubber balloons and Pes with an air-containing cylindrical balloon. After instrumentation, the chest was resealed and continuous suction (-5 mm Hg, 1 mm Hg = 0.133 kPa) was maintained. Volume loading with incremental intravenous infusions of saline was used to increase LV end-diastolic pressure to 20-25 mm Hg. PEEP of 0, 10 and 20 mm Hg were applied at baseline and after each increment of volume loading. At low volume, increases in PEEP caused simultaneous increases in LV end-diastolic pressure (P less than 0.01) and in Ppe (P less than 0.0001) but a reduction in transmural LV pressure (P less than 0.0005). Ppl and Pes both increased with PEEP (P less than 0.001 and P less than 0.01, respectively). However, Ppe always exceeded Ppl, while Pes remained at only approximately 1/3 Ppl throughout. Volume loading caused a significant increase in Ppe (P less than 0.0001) and a smaller, but significant increase in Ppl (P less than 0.05). Pes remained unchanged during volume loading. Thus external cardiac constraint increased markedly during volume loading and PEEP as evidenced by a marked elevation of Ppe. Both Ppl and Pes markedly underestimated this increase. Therefore, calculation of transmural LV pressure by subtracting pleural or esophageal pressure from intracavitary pressure can lead to overestimation of LV preload. The decrease in cardiac output during PEEP occurs secondary to decreased preload, i.e. decreased transmural pressure and end-diastolic dimension. Analysis of performance using cardiac function curves does not suggest a change in contractility with PEEP.

Animals↗
PubMed1987

Quantification of effect of pericardium on LV diastolic PV relation in dogs.

The aim of the present study was to quantify the effect of the pericardium on the left ventricular (LV) diastolic pressure-volume relation. The experiments were done in 10 anesthetized closed-chest dogs. Pericardial and cardiac volumes were determined by computed tomography. Pericardial effusion (n = 5) and volume loading (6% dextran iv; n = 5) were used to increase pericardial volume. Volumes were normalized as multiples of the LV volume measured when LV transmural pressure was 6 mmHg (VLV6). Using the data from the pericardial effusion experiments, we calculated the best-fit exponential equations for the pericardial pressure-volume relations. From these equations we calculated that the changes in pericardial volume necessary to shift the LV diastolic pressure-volume curve upward by 2, 5, 10, and 20 mmHg were 0.6 +/- 0.1, 1.1 +/- 0.2, 1.6 +/- 0.2, and 2.2 +/- 0.3 times VLV6, respectively. Using the data from the volume loading experiments, we also calculated the degree of upward shift of the LV pressure-volume relation caused by volume loading, which increased LV mean diastolic pressure by 12 mmHg. (The upward shift is that increment in pericardial pressure caused by the total increase in volume of the extra-LV contents of the pericardium, i.e., the atria, the right ventricle, and any pericardial effusion.) This volume loading increased the total volume of the right ventricle and the atria by 1.0 +/- 0.1 VLV6, which, in itself, increased pericardial pressure by 3.6 +/- 0.8 mmHg. We conclude that in situations in which heart or pericardial volume increases acutely, the pericardium shifts the diastolic pressure-volume relation of the LV upward by a significant amount.

Animals↗
PubMed1987

Nonuniformity of pericardial surface pressure in dogs.

Previously, we have shown that pericardial constraint cannot be measured by true (hydrostatic) pressure except when an excess of pericardial fluid is present and that a device such as a balloon (which reflects radial contact stress as well as hydrostatic pressure) must be used. Since radial contact stress is the major component of the constraint exerted by the pericardium when little pericardial liquid is present, it follows that the pressure measured by the balloon might be different over different parts of the heart. In an attempt to test this hypothesis, in 11 anesthetized dogs we placed pericardial balloons over the right and left ventricular free walls, instrumented the animals to measure ventricular dimensions (sonomicrometry) and pressure, mounted pneumatic constrictors on the aortic and pulmonary artery, reapproximated the pericardium, and closed the chest under suction. We studied the transient effects of constrictions of the ascending aorta and pulmonary artery and of angiotensin infusion before and after intravenous saline infusion. Aortic constriction and, to a lesser degree, angiotensin increased pericardial pressure over the left ventricle more than over the right ventricle. Pulmonary artery occlusion increased pericardial pressure over the right ventricle but significantly decreased pericardial pressure over the left ventricle. We conclude that there are significant local differences in pericardial pressure (recorded by balloon) over the lateral ventricular surfaces during acute changes in afterload. These observations may be explained in part by decreased venous return to the contralateral ventricle, the tendency of the heart to resist lateral displacement, and the limited mobility of the pericardium.

Animals↗
PubMed1987

Modulation of vascular capacitance by angiotensin and nitroprusside: a mechanism of changes in pericardial pressure.

The aim of the present study was to test the hypothesis that vasoactive drugs may modify left ventricular diastolic function by shifting blood between the systemic vascular bed and the heart, thereby changing pericardial and left ventricular pressure. The experiments were done in 10 open-chest, anesthetized, previously splenectomized dogs in which changes in pericardial surface pressure in response to intravenous sodium nitroprusside and angiotensin were related to changes in blood volume in the abdominal region. Blood volume was determined by blood pool scintigraphy (99mTc) and regions of interest were drawn in the liver and in the mesenteric area. Angiotensin was infused at rates that were adjusted to increase mean aortic pressure by 20 and 30 mm Hg, and nitroprusside was infused at rates to decrease mean aortic pressure by 30 and 50 mm Hg. Angiotensin increased pericardial pressure by 3 and 5 mm Hg at the respective doses and there were increments in left ventricular end-diastolic pressure (LVEDP) and left ventricular diameter (sonomicrometry). Angiotensin decreased blood volume in the mesenteric region by 14% and 17%, but did not significantly change blood volume in the liver region. Angiotensin increased portal venous pressure and decreased mesenteric blood volume, suggesting decreased mesenteric venous compliance. Nitroprusside had opposite effects: pericardial pressure was decreased by 5.5 and 6.5 mm Hg by the respective doses. The doses of nitroprusside increased blood volume in the mesenteric region by 14% and 20%, but did not significantly change blood volume in the liver region.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

A mechanism for the nitroglycerin-induced downward shift of the left ventricular diastolic pressure-diameter relation.

Nitroglycerin has been shown to cause a downward shift in the left ventricular (LV) pressure-volume relation in patients. To test the hypothesis that this shift is mediated by an alteration in pericardial pressure, 13 patients undergoing diagnostic cardiac catheterization were studied. LV and right ventricular (RV) pressure (micromanometers) and LV diameter (2-dimensional echocardiography) were measured simultaneously before and after sublingual administration of 0.3 to 0.6 mg of nitroglycerin. In the 11 patients with hemodynamic effects from nitroglycerin, mean LV end-diastolic pressure decreased from 12.7 +/- 5 mm Hg (mean +/- standard deviation) to 7.3 +/- 3 mm Hg (p less than 0.002) and mean RV end-diastolic pressure declined from 7.7 +/- 3 mm Hg to 5.0 +/- 1 mm Hg (p less than 0.001). However, nitroglycerin caused only a slight (6%) reduction in LV minor axis diameter, from 52 +/- 8 mm to 49 +/- 9 mm (p less than 0.05). Diastolic pressure-diameter plots constructed from early and late diastolic measurements demonstrated a downward shift in the relation. However, when RV end-diastolic pressure was used as an estimate of pericardial pressure (a procedure validated by studies in our laboratory), the transmural pressure-diameter points before and after administration of nitroglycerin defined a single curve. These observations are in keeping with the conclusions that nitroglycerin did not alter the elastic properties of the myocardium and that the decrease in LV end-diastolic pressure induced by nitroglycerin was primarily attributable to a reduction in external constraint.

Adult↗
PubMed1986

Assessment of pericardial constraint: the relation between right ventricular filling pressure and pericardial pressure measured after pericardiocentesis.

Experimental studies have shown that right ventricular filling pressure (that is, intracavitary diastolic pressure) approximates pericardial surface pressure but, in many patients after removal of pericardial effusion, right ventricular filling pressure has been found to markedly exceed pericardial pressure recorded by an open catheter. The aim of this study was to determine whether this apparent contradiction was related to the technique of pericardial pressure measurement. Nine patients with chronic pericardial effusion were studied and, although these pressures diverged to varying degrees in individual patients, the previous observation was confirmed in that, although initially similar, right ventricular filling pressure and pericardial pressure (measured by means of an open catheter) tended to diverge during removal of the effusate; when the evacuation was as complete as possible pericardial pressure was 2.1 +/- 1.0 (mean +/- SE), while right ventricular filling pressure was 8.7 +/- 1.7 mm Hg (p less than 0.01). In six open chest, anesthetized, volume-loaded dogs with pericardial effusion (50 ml), right ventricular filling pressure and pericardial pressures measured with both open catheter and flat balloon were all equal. With decreasing volume of pericardial fluid, right ventricular filling pressure and pericardial pressure (by catheter) diverged as had been observed in patients. However, pericardial pressure (balloon) continued to be equal to right ventricular filling pressure. (With 0 ml in the pericardium, right ventricular filling pressure = 12.9 +/- 0.9 mm Hg, pericardial pressure [catheter] = 1.4 +/- 1.9 mm Hg and pericardial pressure [balloon] = 12.4 +/- 1.5 mm Hg.) Thus, these observations support the use of right ventricular filling pressure as an estimate of pericardial constraint in patients.

Adult↗