Biomedical subjects

K Kanamasa

Publications and source records attributed to K Kanamasa.

At least 55 records · Page 3Linked to original sources

PubMed1987

[Time constant of the left ventricular pressure fall, and onset and rate of expansion of the left ventricular segment in hypertrophic cardiomyopathy].

The left ventricular diastolic properties of patients with hypertrophic cardiomyopathy are impaired. Since there is degeneration or disarray of myocardial fibers in patients with hypertrophic cardiomyopathy (HCM), the rate of expansion in diastole may become asynchronous. Biplane coronary cineangiograms were performed in eight normal subjects and nine patients with HCM. The coordinates (x,y,z) of the ramifying points of the left coronary artery were measured, and the distance between any two of the points of the coronary artery was calculated (segment length). Fifteen segment lengths were calculated for each subject. Since the onsets of expansion of these 15 segment lengths were not simultaneous, they expanded at different times and the onsets of expansion occurred within a very short period of time, nearly at end-diastole. The variance (standard deviation) of the timing of expansions of these 15 segments and the rate of expansion within the late 40 msec of the isovolumic relaxation period (% delta L) were calculated. The time constant of the left ventricular pressure fall (T) in normal subjects was 41.3 +/- 7.7 (SD) msec, T in HCM was prolonged to 52.7 +/- 11.1 msec. The variance was 47 +/- 17 msec in normal subjects, but it increased to 99 +/- 26 msec in HCM. The rate of expansion again decreased in HCM (Normal 2.24 +/- 0.60 vs HCM 1.40 +/- 0.96%). The conspicuous diastolic asynchrony in the onset of expansion and the reduced rate of diastolic expansion in HCM may be the mechanism of impairing the diastolic properties of the left ventricle.

Adult↗

PubMed1986

The beneficial effects of 40% and 100% O2 inhalations on acutely-induced myocardial ischemia in dogs.

The effectiveness of O2 inhalation on the acutely-induced ischemic myocardium in dogs was investigated. In 22 open-chest mongrel dogs, the left anterior descending coronary artery was partially occluded to reduce coronary flow. The regional coronary vein accompanying the artery was cannulated to obtain coronary venous blood. Switching of inspiratory gas from room air to 40% O2 produced an elevation of coronary venous O2 saturation from 35.8 +/- 12.7 (S.D.) to 41.1 +/- 11.9% and shifting of myocardial lactate production to utilization (from -0.9 +/- 36.9 to 5.0 +/- 36.7%), indicating that 40% O2 inhalation ameliorated ischemia. Application of 100% O2 inhalation caused even more beneficial effects; coronary venous O2 saturation was elevated to 50.6 +/- 12.6% and myocardial lactate extraction was improved to 7.8 +/- 40.5%. The present study indicated that 40% O2 inhalation was effective and 100% O2 inhalation even more effective in ameliorating acutely-induced myocardial ischemia. Decreases in myocardial contractile force and left ventricular size and suppression of sympathoadrenal activity might be possible mechanisms for these beneficial effects.

Animals↗

PubMed1986

[Effects of nitroglycerin on left ventricular geometry and compliance in man].

The effects of nitroglycerin (NTG) on relaxation characteristics of the infarcted and non-infarcted myocardium were investigated by calculating a segment length on the epicardium of the left ventricle for 16 patients with old myocardial infarction. The spatial segment length was measured between two points which were identified as a junction of ramifying branches of the left coronary arteries using biplane coronary cineangiography. Regional myocardial stiffness was expressed as delta P/delta L, where delta P was an increment of left ventricular (LV) diastolic pressure from the lowest LV diastolic pressure to the pressure at the maximal segment length, and delta L was the difference of two segment lengths corresponding to those pressures. Myocardial stiffness decreased from 0.0402 +/- 0.0293 mmHg/mm to 0.0212 +/- 0.0157 with intracoronary NTG (p less than 0.01) and from 0.0220 +/- 0.0090 to 0.0136 +/- 0.0124 with sublingual NTG (p less than 0.001) in the non-infarcted portions. However, it was unchanged with both intracoronary and sublingual NTG in the infarcted portions. NTG may cause venous pooling and may decrease diastolic wall tension of the left ventricle as its indirect effect on the non-infarcted myocardium. Also, the non-infarcted myocardium may be influenced by dilatation of the epicardial coronary artery. Muscle stiffness of the infarcted myocardium was unchanged, probably due to the rigidity of myocardial fibrosis. It was concluded that in myocardial infarction diastolic distensibility of the non-infarcted portion can be improved by NTG both through indirect and direct effects.

Compliance↗

PubMed1986

[Reduction of myocardial segment shortening during angina-free period in patients with angina pectoris].

In 16 patients with angina pectoris who had no histories of myocardial infarction, myocardial segment shortening was studied during angina-free periods. Myocardial segment length in the anterior wall of the left ventricle was calculated by measuring the spatial length between two points identified as junctions of ramifying branches of the left coronary arteries using biplane coronary cineangiography. Segment shortening was classified according to the severity of coronary arterial stenosis. The patients were categorized according to the severity of coronary arterial stenosis: as 1) the 0% stenosis (normal); 2) the 50% stenosis group; and 3) the 75-90% stenosis group. Total segment shortening in the normal group was the same as that in the 50% stenosis group (10.4 +/- 2.5%). However, in the 75-90% stenosis group, segment shortening was reduced to 7.3 +/- 2.5%. Effective segment shortening during the ejection period was reduced (5.0 +/- 1.8%) in the 75-90% stenosis group, as compared with the normal group (8.4 +/- 2.4%) and the 50% stenosis group (7.2 +/- 3.6%). This study demonstrated that segment shortening was reduced at rest in patients with angina pectoris who had had no previous infarction. A possible mechanism of this reduced segment shortening during angina-free periods may be irreversible myocardial alteration from recurrent ischemic attacks.

Angina Pectoris↗

PubMed1984

Reduction of left ventricular size following oxygen inhalation in patients with coronary artery disease as measured by biplane coronary cineangiograms.

Left ventricular size is one of the major determinants of myocardial oxygen consumption, therefore if oxygen inhalation reduces myocardial oxygen demand, such might be beneficial in the treatment of acute myocardial infarction. Routine diagnostic biplane left coronary cineangiograms were obtained during air or oxygen breathing in 11 patients with old myocardial infarction or angina pectoris. Coordinates of the points on the left coronary artery were measured and throughout one cardiac cycle frame by frame. The spatial distance (segment length: L) between any two of these points was calculated. Segment length at R wave on the electrocardiogram (LECG R) and minimum value (Lmin) for each segment were calculated. Arterial pO2 was elevated by oxygen breathing from 91 +/- 4 (+/- SE) to 427 +/- 18 mmHg. Left ventricular segment length was significantly reduced by oxygen breathing: LECG R being reduced following oxygen breathing from 62.3 +/- 3.0 to 60.6 +/- 3.0 mm (a decrease of 3.3 +/- 0.8%) and Lmin also being reduced from 55.9 +/- 2.8 to 54.4 +/- 2.8 mm (a decrease of 3.1 +/- 1.0%). These figures indicate that left ventricular size was reduced. Reduction in left ventricular size through oxygen inhalation, by reducing myocardial oxygen demand, should therefore be beneficial in coronary artery disease.

Adult↗

PubMed1984

[Early relaxation of the left ventricular wall in coronary artery disease].

A mechanism for the genesis of early relaxation of the left ventricle was assessed. For 18 patients with coronary artery disease, biplane left coronary cineangiography was performed and the coordinates (x, y, z) of the points of the artery were measured by frame to frame basis throughout one cardiac cycle. The spatial distance (segment length) between any two points was calculated on each frame as (Formula: See text) to investigate shortening and relaxation characteristics of the ischemic and nonischemic segments. Coronary angiography was repeated during right atrial pacing to aggravate ischemia, and following nitroglycerin administration to ameliorate ischemia. From data of six normal subjects, 43 segments were calculated. All showed shortening during systole and lengthening in diastole. Right atrial pacing caused early relaxation in only two of the 43. Two hundred and fifteen segments were calculated for 18 patients with coronary artery disease. All but eight segments showed normal relaxation on control angiography. Following pacing, 115 segments showed early relaxation, and in 107 of the 115, normal relaxation were restored after nitroglycerin. Among the 107 segments, 44 were ischemic and 63 were normal. For 34 segments with early relaxation by pacing, pacing was repeated after administering nitroglycerin, and 15 did not reproduce early relaxation. The present study showed that early relaxation was observed in patients with coronary artery disease, which was effectively ameliorated by nitroglycerin, suggesting this phenomenon is closely related to the development of myocardial ischemia. The decreased active tension, reduced duration of tension, development and delay in electrical depolarization in the ischemic segment can be a reasonable inducement to early relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cineangiography↗

PubMed1984

[Intrathoracic movement of the normal and hypertrophied hearts measured by biplane coronary cineangiography].

The shift of the heart during systole within the thorax was measured using bifurcations of the left coronary artery as cineangiographic markers. Biplane coronary cineangiography was performed in 13 normal subjects and 6 patients with non-obstructive hypertrophic cardiomyopathy (HCM). The spatial coordinates (X, Y, Z) of the bifurcations on the cineangiograms were measured using a motion analizer-digitizer-computer system. The systolic excursion of the motion of a bifurcation located at the anterior-basal point of the heart was 1.4 +/- 0.1 (+/-SD) cm leftward, 3.0 +/- 0.3 cm caudally and 2.5 +/- 0.1 cm anteriorly in normal subjects. In the cases with HCM, on the other hand, the bifurcation moved 2.2 +/- 1.1, 2.7 +/- 1.2 and 2.2 +/- 0.6 cm during systole, respectively. The movement at the apex in the normal subjects was 1.7 +/- 0.2 cm rightward, 1.5 +/- 0.2 cm caudally and 1.5 +/- 0.2 cm posteriorly, although the direction was reversed as compared to that of the anterior wall of the cardiac base. The amplitude of the excursion was also reduced at the apex, suggesting the systolic twist of the ventricular wall. The excursion of the apex in HCM was 0.6 +/- 1.7, 1.5 +/- 1.8 and 2.5 +/- 1.4 cm, respectively, toward the base of the heart as in the normal subjects. The maximum speeds of these motions were 34.0 +/- 9.2 cm/sec leftward, caudally and anteriory at the anterior-basal point and 36.2 +/- 7.3 cm/sec rightward, caudally and posteriorly in the normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗

PubMed1983

Regional differences in shortening and relaxation characteristics of the left ventricular wall of normal subjects as studied by biplane coronary cineangiograms.

The coordinates of the ramifying points of the left coronary artery were measured using biplane coronary cineangiograms in 19 patients who were later diagnosed as normal. The spatial distances (segment length) between any two of these points were calculated and one cardiac cycle was plotted frame by frame in order to investigate shortening and relaxation characteristics of the segments. In most instances, the segments evidenced shortenings during systole and prolongations during diastole. The extent of shortening, as a percentage of maximum length ranged from 7.8 to 18.0%. The segments measured at the apex started shortening 77 msec sooner than those at the base, in other words, 90.3 +/- 6.2 msec before the R wave peak on the electrocardiograms. This indicates that the initial shortening at the apex contributes to the build up of left ventricular pressure. While at the base, since it begins to shorten after the completion of the build up in left ventricular pressure, it contributes more to the ejection of blood from the left ventricle. On the other hand, there is little systolic shortening at the atrioventricular groove and in some instances there is systolic expansion, suggesting that in comparison to the other portions of the left ventricle it is assigned an entirely different role.

Cineangiography↗

PubMed1983

The failure of oxygen breathing to decrease the myocardial contractile force in denervated dogs.

This study was done to discover whether or not the oxygen-induced depression of sympathoadrenal activity contributes to a reduction of myocardial contractile force during oxygen breathing. In 10 open-chest dogs, myocardial contractile force was measured using a myocardial strain gauge arch during air and oxygen breathing before denervation (intact heart) and after bilateral vagotomies, sympathectomies and adrenalectomies with the intravenous administration of propranolol, phenoxybenzamine and atropin (denervated heart). One hundred percent oxygen breathing caused similar increases in arterial pO2 in both the intact (from 94 +/- 10 to 442 +/- 25 mmHg) and the denervated dogs (from 113 +/- 11 to 456 +/- 15 mmHg). Coronary blood flow measured at the left anterior descending coronary artery was reduced by oxygen breathing from 28.4 +/- 3.4 to 21.7 +/- 2.3 ml/min in the intact dogs, and from 19.4 +/- 3.4 to 14.9 +/- 2.6 ml/min in the denervated dogs. Myocardial contractile force was significantly reduced by oxygen breathing in the intact dogs (a reduction of 5.8 +/- 1.4%). In the denervated dogs, on the other hand, no significant changes in myocardial contractile force was seen. This study suggests that the reduction in myocardial contractile force is mediated through sympathoadrenal activity, and thus, is abolished by sympathoadrenal blockade.

Adrenalectomy↗

PubMed1983

[Characteristics of left ventricular regional wall relaxation at the infarction site].

In order to investigate relaxation characteristics of the infarcted wall, segment lengths of the left ventricular wall were calculated in 6 patients with anterior myocardial infarction and in 9 angiographically normal subjects. The biplane left coronary cineangiography was performed and coordinates of ramifying points of the left coronary artery on the infarcted or non-infarcted wall were measured and the spatial lengths (segment lengths) on each wall were calculated. If the two points are on the left anterior descending artery (LAD) in infarcted patients, a calculated length is regarded as a segment length in the infarcted portion, while if the length is calculated between the two points located on the coronary artery other than LAD, it is a non-infarcted segment. Each segment length was calculated in frame by frame covering one cardiac cycle. The maximum length (Lmax), minimum length (Lmin) and the length at the beginning of P wave of the electrocardiogram (LECG P) were calculated. The extent of relaxation of the segment caused by atrial kick was calculated as (Lmax--LECG P)/Lmax X 100, (% delta Lla). This value was 2.8 +/- 1.5 and 3.5 +/- 1.4% on anterior and inferior walls, respectively, in 9 normal subjects and 3.6 +/- 1.2 and 4.0 +/- 0.9% in 6 patients with anterior infarction, revealing no significant difference among 4 values. This indicates that the amount of lengthening of the segment by atrial kick remains unchanged even if the wall is infarcted. The extent of diastolic lengthening of the segment by rapid and slow fillings, which excludes atrial filling, was calculated as (LECG P--Lmin)/Lmax X 100, (% delta L1-la).(ABSTRACT TRUNCATED AT 250 WORDS)

Cineangiography↗

PubMed1982

Reduction of left ventricular epicardial segment length by 100% oxygen breathing in open-chest dogs.

We conducted this study in order to learn whether or nt oxygen inhalation reduces left ventricular size, one of the major determinants of myocardial oxygen demand. In 11 open-chest dogs, a Mercury-in-Silastic gauge was applied to measure left ventricular circumferential length while the dogs were being ventilated with either room air or 100% oxygen. Four characteristic notches were identified on the resulting length curve: L1, length at the beginning of ejection; L2, length at the end of ejection; L3, length in early diastole; and L4, length at end diastole, L1 was shortened from 24.9 +/- 10.5 to 24.4 +/- 9.9 mm (a decrease of 1.4 +/- 2.1%) by oxygen breathing, L2 was also shortened from 26.8 +/- 11.5 to 26.2 +/- 10.7 mm (a decrease of 1.5 +/- 2.9%), L3 from 17.5 +/- 4.4 to 17.4 +/- 4.3 mm (a decrease of 0.7 +/- 2.7%) and L4 from 17.7 +/- 4.8 to 17.5 +/- 4.7 mm (a decrease o 1.3 +/- 2.4%). These changes all disappeared when the inspiratory gas was changed from oxygen back to air. Heart rate and left ventricular end-diastolic pressure showed no significant changes but were accompanied by a slight reduction in aortic pressure and myocardial contractile force. This study demonstrated a small but consistent reduction in left ventricular circumferential length by oxygen breathing. This reduction in left ventricular size will reduce left ventricular tension and thus result in reduction of left ventricular myocardial oxygen demand when oxygen inhalation is applied to patients with ischemic heart disease.

Animals↗

PubMed1982

[Effect of nitroglycerin on epicardial and endocardial shortening characteristics in dogs].

In 8 dogs, several paired lead beads as radiopaque markers were implanted in the subepicardial and subendocardial regions, and biplane cineradiograms were obtained after closure of the chest. The spatial distance (segment length) between the two markers in the outer and inner sides of the myocardium was calculated using a digitizer-computer-plotter system, and the effect of nitroglycerin on regional left ventricular geometry was assessed. Segment length at the R wave of the electrocardiogram (LECG R) was reduced from 39.7 +/- 11.8 (mean +/- SD) to 38.8 +/- 12.1 mm at the subepicardium and from 31.9 +/- 9.5 to 29.5 +/- 10.4 mm at the subendocardium 3 minutes after intravenous injection of 0.5 mg of nitroglycerin. Segment length at endsystole (LES) was also reduced from 38.9 +/- 11.7 to 38.2 +/- 11.8 mm at the subepicardium and from 29.6 +/- 9.2 to 27.9 +/- 9.9 mm at the subendocardium by nitroglycerin. Systolic shortening [(LECG R--LES)/LECG R] x 100) showed a slight reduction after nitroglycerin. Left ventricular wall thickness measured as a distance between subepicardial and correspondent subendocardial markers showed a slight but significant increase by nitroglycerin: Maximal thickness was increased from 10.9 +/- 3.2 to 11.4 +/- 3.3 mm, and thickness at the R wave of the electrocardiogram was also increased from 10.9 +/- 3.1 to 10.5 +/- 3.2 mm. Thickening of the wall was markedly increased at the anterior mid portion of the left ventricle but not at the base, suggesting nitroglycerin has larger effect on the former position than the latter.

Animals↗

PubMed1982

[Left ventricular outer wall motion in hypertrophic cardiomyopathy assessed by biplane coronary cineangiograms].

Left ventricular wall motion in patients with hypertrophic cardiomyopathy may show a characteristic movement since this condition is characterized by a disproportionate thickening of the wall and disorientation of myocardial muscle fibers. Biplane coronary cineangiograms were performed in 5 patients with hypertrophic cardiomyopathy and the spatial distance between the bifurcation of the left coronary artery was calculated using a digitizer-computer-plotter system as a measure of epicardial chord segment length. Systolic shortening of the segment was calculated as (LECG R--LES)/ECG R x 100 (%), where LECG R and LES represent segment lengths at the R wave of the electrocardiogram and at the end of systole, respectively. The value amounted 6.9 +/- 5.1 (+/- SD)% on the average which was significantly lower than the previously described values (9.0 +/- 4.1%) in 19 normal subjects. In all of 3 segments at the apex, systolic shortening showed nearly zero or negative indicating systolic expansion. Reduced shortening in patients with hypertrophic cardiomyopathy observed at the epicardial segment in the present study might be a reflection of geometrical difference between endocardial and epicardial segments because shortening of the epicardium will be reduced even the endocardium shortens considerably if the thickness of the wall is markedly increased. Anterior surface of the interventricular septum might be unable to shorten freely along the long axis since it is a junction of trifurcation among right and left ventricular free walls and the interventricular septum if these three walls are thickened. The present study indicated that shortening characteristics in the outer myocardium in patients with hypertrophic cardiomyopathy is markedly impaired possibly due to geometrical difference between endocardial and epicardial segments caused by marked thickening of the wall and also due to the degeneration or disorientation of myocardial fibers.

Cardiomyopathy, Hypertrophic↗

PubMed1982

[Difference of the shortening characteristics between left ventricular endocardium and epicardium as measured by radiopaque markers in experimental dogs].

This study was performed to clarify the difference of shortening characteristics between left ventricular epicardium and endocardium. Four to five pairs of radiopaque markers (lead beads, phi 0.3- 0.8 mm) were implanted just beneath the epicardium and endocardium, respectively in eight open-chest dogs. After the pericardium and thorax were closed, biplane cine-roentgenograms were obtained. The spatial distance (segment length) between any two of the markers was calculated using a digitizer-computer-plotter system. Left ventricular wall thickness (Th) was measured as a distance between epicardial and endocardial markers. The maximum left ventricular thickness (Thmax) was 9.4 +/- 3.4 mm (mean +/- SD), the minimum (THmin) 8.4 +/- 3.1 mm, and a percent increase of wall thickness [(Thmax-Thmin)/Thmin] was 12.7 +/- 6.5%. The value of epicardial segment length divided by endocardial segment length as normalized by each length at R wave of ECG was 1.088 +/- 0.071 at the end of systole and 0.979 +/- 0.016 at end diastole, indicating that endocardial segment shortened and distended more than epicardial segment during systole and diastole, respectively. Epicardial segment began to shorten 3 +/- 26 msec earlier and distend 4 +/- 50 msec earlier than endocardial one. This study revealed a small but consistent difference in the amount of shortening and its initiation and termination between the epicardium and endocardium.

Angiocardiography↗

PubMed1981

Myocardial contractile force at high coronary arterial oxygen tension in dogs.

In 34 mongrel dogs, the left anterior descending coronary artery was perfused with the dog's own femoral arterial blood at a constant flow rate and the myocardial contractile force was measured using a myocardial strain gauge arch. When the femoral arterial blood was oxygenated (pO2 61.7 kPa (463 mmHg)) using an artificial lung, so that the perfused myocardium became hyperoxic, the myocardial contractile force was increased by 11.1 +/- 2.3%. When the perfusion rate was reduced by approximately 20%, there was a smaller increase in myocardial contractile force, 8.0 +/- 2.3%. If, in addition, oxygen inhalation was performed the myocardial contractile force decreased by 4.1 +/- 2.1%. In 10 mongrel dogs, the carotid arteries were perfused at a constant flow rate with femoral arterial blood from a donor dog. Oxygen inhalation by the donor dog caused a reduction in the myocardial contractile force of the experimental dog of 5.9 +/- 1.6%. It is suggested that oxygen has a direct effect in increasing myocardial contractile force. This increase is counteracted by oxygen-induced coronary vasoconstriction in some part and by a neurohumoral effect or suppression of chemoreceptor activity.

Animals↗

PubMed1981

Coronary artery constriction by oxygen breathing in patients with coronary disease.

This study was conducted to find whether or not oxygen breathing induces coronary vasoconstriction in diseased as well as in normal coronary arteries. Coronary angiograms were repeated in 14 patients with coronary artery disease during successive air and oxygen breathings and the diameters of the coronary arteries as displayed by film projection were measured and compared. Arterial oxygen tension was elevated from 91.3 +/- 16.8 to 457.2 +/- 26.5 mmHg by oxygen breathing but was not accompanied by any significant changes in mean arterial pressure. The diameters of coronary arteries without significant narrowing were reduced from 2.89 +/- 1.05 to 2.65 +/- 1.02 mm by oxygen breathing (a decrease of 8.9 +/- 7.0%) and that of coronary arteries distal to a narrowing of more than 50% was reduced from 2.24 +/- 0.53 to 2.02 +/- 0.57 mm (a decrease of 10.1 +/- 10.7%). These findings suggest that oxygen breathing and constrict a large coronary artery even if it has atherosclerotic lesions and the myocardium needs more flow.

Coronary Circulation↗

PubMed1981

[Change of left ventricular segment length by nitroglycerin measured by biplane coronary cineangiography in man (author's transl)].

Left ventricular size at different portions was evaluated following the administration of nitroglycerin to find whether there is any regional difference in the amount of shortening. In 6 patients with old myocardial infarction, biplane coronary cineangiograms were obtained before and after sublingual administration of nitroglycerin of 0.3 mg. The coordinates of the bifurcations of the left coronary artery at multiple sites were measured on the postero-anterior and lateral films and the spatial lengths (L) between any paired two points were calculated frame by frame covering one cardiac cycle. The maximum length (Lmax) was 63.2 +/- 3.1 (SE) mm before nitroglycerin as a whole and was 61.4 +/- 2.9 mm after nitroglycerin, showing no significant change. The minimum length (Lmin) also showed no significant change after nitroglycerin; from 56.1 +/- 2.9 to 54.9 +/- 2.6 mm. However, at the free wall, Lmax after nitroglycerin was reduced by 4.5 +/- 2.5%, and Lmax at the anterior septum was also reduced by 3.0 +/- 1.3%. Lmax at the base was unchanged after nitroglycerin. Lmin at the free wall and at the anterior septum were also reduced after nitroglycerin, 4.4 +/- 2.6 and 2.9 +/- 1.2%, respectively, and it was unchanged at the base. Since a reduction in the left ventricular size is effective in reducing myocardial oxygen demand and is effective in treating myocardial ischemia, it was suggested that nitroglycerin is more effective in relieving ischemia at the free wall and septum and less effective at the base.

Cineangiography↗

PubMed1980

Increases in coronary vascular resistance related to high arterial oxygen tension in dogs.

It is known that oxygen inhalation induces coronary vessel constriction as well as brings about a reduction in myocarial oxygen consumption. The present study was performed to clarify whether or not this constriction of the coronary vessels resulting from oxygen is secondary to the reduction in myocardial oxygen consumption. The regional myocardium in 12 mongrel dogs was perfused with femoral arterial blood at a constant rate of flow. While maintaining myocardial oxygen consumption equal by adjusting heart rate, coronary vascular resistance was compared under the two following conditions: 1) perfusion of the coronary artery with the dog's own femoral arterial blood (pO2 : 95 +/- 14 mmHg) and 2) perfusion with blood with a high level of oxygen tension (pO2 : 497 +/- 56 mmHg). Coronary vascular resistance was increased (p < 0.001) from 3.00 +/- 1.25 to 3.36 +/- 1.28 mmHg/ml/min by incresing the pO2 in the perfusing blood, even though myocardial oxygen consumption was kept at the same level. This increase in coronary vascular resistance resulting from the increase in oxygen tension was independent of the coronary perfusion rate as well as independent of the presence or absence of myocardial ischemia. This suggests that coronary vasoconstriction due to oxygen is not secondary to decreases in myocardial oxygen demand.

Animals↗