Biomedical subjects

H R Weiss

Publications and source records attributed to H R Weiss.

At least 127 records · Page 7Linked to original sources

PubMed1991

Effect of peripheral and central alpha-adrenoceptor blockade on cerebral microvascular and blood flow responses to hypoxia.

The purpose of this study was to evaluate the effects of vascular and central alpha-adrenoceptor blockade on cerebral blood flow (CBF) and utilization of brain arteriolar and capillary reserve in conscious rats during normoxia and hypoxia (8% O2 in N2). Animals were divided into three groups and administered either saline, N-methyl chlorpromazine (does not cross the blood-brain barrier), or phenoxybenzamine (crosses the blood-brain barrier) in equipotent doses. Neither agent affected regional CBF and the utilization of brain microvascular reserve during normoxia. CBF increased from 70.9 +/- 2.9 (SEM) ml/min/100 g in the control normoxic group to 123.8 +/- 4.2 ml/min/100 g in control hypoxic animals. In control, hypoxic flow to pons and medulla of the brain was higher than to cortex, hypothalamus or thalamus. The percent of arterioles/mm2 perfused increased from 49.6 +/- 2.0% during control normoxia to 65.6 +/- 3.0% during control hypoxia. The percentage of capillaries/mm2 perfused changed similarly. Hypoxic CBF was increased similarly after administration of N-methyl chlorpromazine or phenoxybenzamine. Administration of N-methyl chlorpromazine or phenoxybenzamine eliminated regional differences in hypoxic CBF and the utilization of arterioles, and did not affect capillary response. There was no difference between the effect of N-methyl chlorpromazine and phenoxybenzamine on cerebral microvascular and blood flow responses to hypoxia. It was concluded that peripheral alpha-adrenoceptors affect the distribution of regional microvascular and blood flow responses to hypoxia, and central alpha-adrenoceptors probably do not participate in this effect.

Adrenergic alpha-Antagonists↗

PubMed1991

Relationship between myocardial tissue norepinephrine and coronary flow heterogeneity.

The purpose of this study was to investigate the hypothesis that heterogeneity of myocardial tissue norepinephrine content exists and is one of the controllers of flow heterogeneity in the canine myocardium. Tissue norepinephrine content was measured simultaneously with coronary blood flow in multiple sections of the left ventricle of eight anesthetized open-chest dogs. Radioactive microspheres were used for the measurement of blood flow during baseline and sympathetic stimulation. The left ventricle was cut into 15 subepicardial and 15 subendocardial sections. Norepinephrine levels of these same tissue sections were measured using high-pressure liquid chromatography. The average control coronary blood flow was 92.4 +/- 19.5 ml/min/100 g. Ansa subclavia stimulation (10-msec duration, 18-24 V, 10 impulses/sec) increased coronary blood flow to 127.9 +/- 21.9 ml/min/100 g. The average of the norepinephrine levels was 2480 +/- 573 ng/g wet wt and the biological variation was almost four times the method variation. The within-animal coefficient of variation was 32.9%. No significant regional differences were found in flow or norepinephrine content. Regression analysis between the percentage of mean norepinephrine (PNE) and the percentage of mean control flow (Pflow) produced the equation: Pflow = 0.29 (PNE) + 70.4 (r = 0.44, P less than .0001). The equation for PNE vs percentage of stimulated flow is Pflow = 0.24 (PNE) + 76.2 (r = 0.48, P less than .0001). Thus, significant heterogeneity of tissue norepinephrine levels exists in the heart. There also appears to be a direct linear relationship between tissue norepinephrine content and coronary blood flow distribution in the canine myocardium.

Animals↗

PubMed1991

Cerebral blood flow and oxygen consumption in cortical spreading depression.

We determined the effects of spreading depression on local cerebral O2 supply, oxygenation, and O2 consumption in the anesthetized rat. Spreading depression was induced by application of 0.5 M KCl to the frontal cortex. Regional cerebral blood flow was determined with [14C]iodoantipyrine and regional O2 extraction was determined microspectrophotometrically. The passage of the spreading depression wave was determined with a multiprobe assembly that recorded NADH redox state (surface fluorometry), extracellular K+ activity, and DC steady potential (surface minielectrodes). As the wave of spreading depression passed, there was an increase in extracellular K+ and a decrease in NADH. Cerebral blood flow was significantly increased (120 +/- 51 ml/min/100 g, mean +/- SD) during the wave as compared with other regions. In the affected cortex, blood flow was not different from that in the contralateral cortex (69 +/- 28 ml/min/100 g) either before or after the wave of spreading depression passed. Arterial and venous O2 saturation were unaffected by the wave and the histogram of O2 saturations of examined veins followed a similar normal distribution in all regions. Oxygen extraction was not altered by the wave of spreading depression. Oxygen consumption was significantly increased during the wave to 7.4 +/- 3.7 ml O2/min/100 g compared with the contralateral cortex (5.1 +/- 2.6 ml/min/100 g) and other regions. It can be concluded that spreading depression caused an increase in cerebral O2 consumption that was adequately matched by an increase in local blood flow. Oxygen delivery was not limited during spreading depression and its effects were quickly over as evidenced by the lack of alteration in oxygenation after the wave of spreading depression passed.

Animals↗

PubMed1991

Augmented efficiency of regional myocardial work by ouabain.

STUDY OBJECTIVE: The effect of ouabain on regional myocardial mechanics and corresponding regional myocardial oxygen consumption was investigated. DESIGN: Regional myocardial segment length (ultrasonic dimension crystals) and force development (miniature strain gauge) were measured. The integrated multiples of myocardial shortening by corresponding force during an averaged beat was used to express regional segment work (= area under the systolic portion of the length-force loop). External cardiac work was calculated from aortic blood pressure and cardiac output. Global and regional myocardial O2 consumption (MVO2) were evaluated at baseline and during intravenous infusion of ouabain (7 micrograms.kg-1.min-1). Regional coronary blood flow was measured with radioactive microspheres, and microspectrophotometry of frozen myocardial biopsies was used to evaluate O2 saturation in small arteries and veins. These variables were used to calculate regional myocardial MVO2. Arterial and coronary sinus O2 saturation was used to calculate global left ventricular O2 consumption. Myocardial efficiency was expressed as regional work/regional myocardial MVO2. SUBJECTS: Ten open chest anaesthetised dogs, weight about 20 kg, were used. MEASUREMENTS AND MAIN RESULTS: Ouabain increased regional myocardial segment work [from 5291(SEM 1067) to 8916(2338) mm.g-1.min-1] to a greater extent than regional myocardial MVO2 [from 6.33(0.75) to 8.54(0.75) ml O2.min-1.100 g-1]. Regional efficiency was increased from 734(78) to 1036(160) g.mm.ml O2(-1).100 g-1. External efficiency was not raised. Percent shortening was increased to a greater extent than peak force development (+76% v + 38%), possibly indicating increased myocardial compliance. The length-force loop was shifted upward and to the right. CONCLUSIONS: Ouabain increases regional efficiency of myocardial contraction.

Animals↗

PubMed1991

Local adenosine infusion and myocardial oxygen supply and consumption in reperfused canine myocardium.

STUDY OBJECTIVE: The aim was to determine whether a local infusion of adenosine could increase coronary blood flow to restore fully the O2 supply to consumption balance in reperfused myocardium. DESIGN: The left anterior descending coronary artery was occluded for 2 h followed by a 4 h reperfusion with and without simultaneous local infusion of adenosine (50 micrograms.kg-1.min-1). In another group, adenosine was infused for 4 h. Small artery and vein O2 saturations (microspectrophotometry) and regional flow (radioactive microspheres) were determined. SUBJECTS: 25 anaesthetised open chest mongrel dogs, divided in three groups, were used in this study. MEASUREMENT AND MAIN RESULTS: In the central group, 2 h occlusion decreased regional blood flow below normal. After 4 h of reperfusion, blood flow was less than normal in the affected area, at 57(SD39) affected v 85(31) ml.min-1.100 g-1 control. O2 extraction was higher in the reperfused area, with 61% of veins having O2 saturations less than 35%. For the experimental group, adenosine was infused into the left anterior descending artery at a dose of 50 micrograms.kg-1.min-1. Adenosine coupled with reperfusion increased regional blood flow above control in the affected area, to 267(238) ml.min-1.100 g-1, but this was less than was found with adenosine alone. O2 extraction in this area was lower than with reperfusion alone, with only 1% of veins having O2 saturations less than 35%. CONCLUSIONS: A large flow reserve is present in reperfused tissue and the low O2 saturations found in reperfused myocardium cannot be due to vessel blockage (greater than 20 microns in diameter). Thus local adenosine can be used to mobilise the reserve to improve the O2 supply to consumption balance.

Adenosine↗

PubMed1991

The effect of an exercise program on vital capacity and rib mobility in patients with idiopathic scoliosis.

All 813 patients with idiopathic scoliosis who completed their first Schroth physiotherapeutic rehabilitation program at the Katharina Schroth Hospital between 1984 and 1987 were reviewed. The patients were divided into four age groups. In Group I (10-13 years, N = 278), vital capacity in patients treated for the first time improved by 18.94% (445 ml). In Group II (14-17 years, N = 264), the average increase in vital capacity after initial treatment was 16.33% (497 ml). In Groups III (18-24 years, N = 123) and IV (greater than 24 years, N = 148), the corresponding increases were 15.11% (501) and 13.77% (394 ml), respectively. In the 256 patients receiving repeat treatment, the increases in vital capacity in the respective age groups amounted to just more than half those in the patients treated for the first time. The average increase in chest expansion was more than 20% in all groups at all measuring points. These findings show that a course of inpatient treatment by the Schroth method can lead to an increase in vital capacity and chest expansion so that, even in adult scoliosis patients, effective treatment of the associated restrictive ventilatory disorder is possible.

Adolescent↗

PubMed1991

Effect of vasopressin on myocardial capillary recruitment and coronary blood flow in the anesthetized rabbit.

The effects of infusion of arginine vasopressin (20 mU.kg-1.min-1) on coronary blood flow and the proportion of the coronary microvasculature perfused was studied in rabbit myocardium. Fluorescein isothiocyanate--dextran was injected into anesthetized open-chest rabbits to identify the perfused vessels and an alkaline phosphatase stain was employed to locate the total microvasculature. Coronary blood flow (radioactive microspheres) was studied in separate groups of rabbits. Vasopressin infusion caused bradycardia (243 +/- 19 to 165 +/- 22 beats/min, mean +/- SD) and an increase in mean blood pressure (92 +/- 18 to 104 +/- 12 mmHg) (1 mmHg = 133.32 Pa). Coronary blood flow decreased significantly with vasopressin from 209 +/- 68 to 97 +/- 36 mL.min-1.100 g-1. The proportion of the arteriolar bed per millimeter squared perfused decreased significantly after vasopressin from 54 +/- 13 to 44 +/- 21%, while the percentage of capillaries per millimeter squared increased significantly from 57 +/- 6 to 67 +/- 11%. There were no subepicardial versus subendocardial differences in any measured parameter. Thus, both coronary blood flow and the proportion of the arteriolar bed perfused decreased with vasopressin. However, compensation occurred in that the proportion of capillaries perfused increased. This indicated an independent level of control of the coronary arteriolar and capillary beds. These microvascular changes may help to maintain oxygen supply-demand balance with vasopressin in the heart.

Alkaline Phosphatase↗

PubMed1991

Oxy- and carboxyhemoglobin saturation determination in frozen small vessels.

A four-wavelength microspectrophotometric method has been developed to determine both O2 and CO saturation of hemoglobin in frozen small vessels. This method compensates for the nonspecific light loss related to the ice crystals and in addition can simultaneously measure both hemoglobin O2 and CO saturation in frozen blood. By using four wavelengths in the 540-580 nm range, it is possible to determine both O2 and CO saturations in frozen blood. This four-wavelength method demonstrated an accuracy of 6-8% within 95% confidence limits (SE of estimate = 3-4%) for both CO and O2 saturation determinations in frozen blood. The linear regression of the hemoglobin O2 saturation calibration was significant with an r2 value of 0.989. The linear regression of the CO saturation calibration was also significant with an r2 of 0.996. The repeatability of each measurement was on the order of 1-6%. This method also represents an accuracy within 5% for measurements in the frozen rabbit heart for both CO and O2 in vessels between 20 and 100 microns in diameter. It compares favorably with other previously reported methods. It shows a similar accuracy but requires fewer repeat measurements than the three-wavelength method. This method can provide accurate measurement of O2 and CO saturation in small frozen arterioles and venules of any organ.

Animals↗

PubMed1991

Cerebral regional capillary perfusion and blood flow after carbon monoxide exposure.

Alterations in regional cerebral blood flow (rCBF) and percent perfused capillaries (indicative of functional intercapillary distance) were determined in conscious male Long-Evans rats after reducing their blood O2-carrying capacity by exposing them to 1% CO for 12 min. rCBF was determined by the iodoantipyrine method. rCBF increased from a mean of 106 +/- 8 (SE) ml.min-1.100 g-1 before CO exposure to 173 +/- 14 ml.min-1.100 g-1 after CO exposure. There was a greater flow increase (126%) in the cerebral cortex than in the lower brain stem [pons (45%), medulla (39%)]. Presence of fluorescein isothiocyanate-labeled dextran identified the perfused capillaries before and after CO exposure. The volume fraction (Vv) and number/mm2 (Na) of all capillaries (perfused and nonperfused) in a given area of brain were determined after staining for alkaline phosphatase. The percent Vv and percent Na of perfused capillaries increased uniformly (from approximately 50% to approximately 80%) in all parts of the brain after CO exposure. In the presence of tissue hypoxia with undiminished plasma PO2, the brain vasculature allowed greater flow of blood while the microvasculature adjusted to reduce the diffusion distance for O2.

Alkaline Phosphatase↗

PubMed1991

Effects of MK-801 on cerebral regional oxygen consumption in focal cerebral ischemia in rats.

This investigation tested in rats whether MK-801, an N-methyl-D-aspartate receptor antagonist, would improve the balance of oxygen supply and consumption in the focal ischemic area of the brain induced by occlusion of the middle cerebral artery. Fifteen minutes after middle cerebral artery occlusion, 5 mg/kg MK-801 was administered intravenously to the MK-801 group (n = 12), and normal saline was given to the control group (n = 12). One hour after the occlusion in each group, regional cerebral blood flow was determined in six rats using [14C]iodoantipyrine, and regional arterial and venous oxygen saturations were determined using a microspectrophotometric technique in the other six rats. In both groups of animals, the cerebral blood flow of the ischemic cortex was significantly lower than that of the contralateral cortex (36 +/- 16 [SD] and 67 +/- 14 ml/min/100 g for the control group; 33 +/- 10 and 58 +/- 11 ml/min/100 g for the MK-801 group, respectively). Oxygen extraction was significantly higher in the ischemic cortex (8.8 +/- 2.1 ml O2/100 ml blood) than in the contralateral cortex (5.6 +/- 0.3) for the control group. However, for the MK-801 group, there was no significant difference between the ischemic cortex (6.1 +/- 1.0) and the contralateral cortex (5.7 +/- 1.1). Oxygen extraction in the ischemic cortex of the MK-801 group was significantly lower than that of the control group. Calculated ischemic regional oxygen consumption was similar to the nonischemic values in the control group, whereas the ischemic value was reduced to 61% of the value of the contralateral cortex in the MK-801 group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Capillary recruitment and heterogeneity of perfused capillary distribution in dog myocardium.

To estimate functional diffusion distances, the distribution of perfused capillaries was calculated in dog myocardium. A fluorescent dye was injected via a femoral vein in 6 anesthetized, open-chest dogs, and passed once through the coronary circulation (23 +/- 3 s). In 6 animals the dye circulated 4-20 min. In 6 animals the dye circulated for one pass following 2-3 min of asphyxia. The heart was then removed and frozen. Frozen sections from the left ventricule were cut, illuminated to excite the dye to fluoresce, and photographed. They were then stained by silver methenamine to mark all capillaries. The density of all capillaries was compared to that of capillaries containing fluorescent label. The distributions of capillaries were estimated by morphometry. In one pass of the normoxic coronary circulation, 66(+/- 4 SE)% of subepicardial and 60(+/- 4)% of subendocardial capillaries were detectably labeled. Their distribution approached a random pattern, and maximal distances to the nearest labeled capillary were lengthened by 50% compared to all capillaries. With multiple passes of the dye, or with asphyxia 76-79% of the capillaries were detectably labeled and their distribution approached the ordered pattern of the total capillary bed. We speculated that the unlabeled capillaries represented a spatially heterogeneous blood flow reserve.

Animals↗

PubMed1991

Reduction of cardiac hypertrophy in renal hypertensive rabbits with pindolol.

Arterial pressure, cardiac mass and coronary flow reserves were measured in untreated and chronically pindolol-treated rabbits, prepared as either one-kidney one clip (1K1C) hypertensive or uninephrectomized (sham) controls. Pindolol (200 micrograms/kg/day) was administered for either 23 or 30 days, beginning 1 week after, or the day of initial surgery, respectively. Coronary flow was measured, at day 30, using radioactive microspheres, during base-line and adenosine infusion (0.4 mg/kg/min) in anesthetized open-chest preparations. Heart weight of untreated 1K1C animals (9.13 +/- 0.73 g) was significantly greater than the controls (7.19 +/- 0.77 g). Myocardial mass of 1K1C (9.93 +/- 0.86 g) and sham controls (7.40 +/- 0.31 g) were unaffected by chronic pindolol for 23 days. Cardiac hypertrophy was prevented in 1K1C animals treated with pindolol for 30 days (7.53 +/- 1.28 g). Untreated 1K1C animals were hypertensive compared to sham controls (116 +/- 12 and 78 +/- 7 mm Hg) and neither pindolol regime affected blood pressure. Bradycardia was evident in all pindolol-treated animals. Base-line coronary flow was higher in the untreated 1K1C animals compared to untreated controls (228 +/- 43 vs. 182 +/- 31 ml/min/100 g). After chronic pindolol treatments, 1K1C base-line blood flows were reduced (158 +/- 48 and 175 +/- 59 ml/min/100 g, for 23- and 30-day protocols). Adenosine vasodilated flows were not different between the untreated 1K1C and sham animals and were not affected by pindolol treatment. Therefore, hypertension and cardiac hypertrophy were dissociable in this model when pindolol was administered from the onset of hypertension. This suggests immediate involvement of beta adrenergic activation in the development of hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Effect of salbutamol on regional cerebral oxygen consumption, flow and capillary and arteriolar perfusion.

This study quantitatively determined the effect of salbutamol (1 microgram kg-1), a beta 2-adrenoceptor agonist, on the perfusion of the brain microvasculature, cerebral O2 consumption, O2 extraction and cerebral blood flow (CBF) in conscious rat. Indices of arteriolar and capillary structure and the percentage of the total cerebral microvascular volume/mm3 (% Vv) and number/mm2 (% Na) perfused were determined. These parameters were obtained from the perfused microvessels, identified by the presence of fluorescein isothiocyanate (FITC) - dextran, and compared with the entire microvascular bed, identified by alkaline phosphatase stain. Cerebral O2 extraction was determined microspectrophotometrically and CBF was determined using 14[C]iodoantipyrine in another group of salbutamol-treated rats. The acute administration of salbutamol did not alter systemic arterial blood pressure. Significant tachycardia was noted in the salbutamol-treated rats. Salbutamol resulted in a significant increase in the percentage of arterioles perfused. Average percentage perfused capillary Na increased significantly from 46 +/- 2 to 88 +/- 1%; %Vv increased significantly and similarly in the arteriolar and capillary beds in all brain regions examined. Average cerebral O2 consumption increased significantly from 3.0 +/- 0.2 to 7.4 +/- 0.7 ml O2 min-1 100 g-1 with salbutamol, while cerebral O2 extraction was unchanged. Average CBF increased from 50 +/- 2 to 142 +/- 9 ml min-1 100 g-1 with salbutamol. Salbutamol may increase the perfusion of the regional microvasculature by increasing cerebral O2 consumption (metabolic vasodilation) and CBF and microvascular perfusion secondarily, although a direct effect of salbutamol on cerebral microvessels cannot be ruled out.

Albuterol↗

PubMed1990

Alterations in the regional beta adrenergic system in experimental left ventricular hypertrophy.

STUDY OBJECTIVE - The aim of the study was to determine the changes in the beta adrenergic system induced by cardiac hypertrophy due to valvular aortic stenosis. DESIGN - Density of beta adrenoceptors, cardiac tissue noradrenalime concentrations, coronary blood flow (using radioactive microspheres), and haemodynamic variables were compared in a model of experimental aortic valve stenosis of 6 month's duration and in sham operated controls. SUBJECTS - 14 mongrel dogs with aortic stenosis and eight sham operated litter mates were used in the studies. MEASUREMENTS and RESULTS - Heart weight to body weight ratio was 33% greater in dogs with aortic valve stenosis than in controls. There were no haemodynamic differences except for a left ventricular to aortic systolic pressure gradient of 38 (SD 22) mm Hg in the aortic stenosis group. Response of left ventricular dP/dtmax to dopamine was similar in the two groups, as was coronary flow. Density of beta adrenoceptors (Bmax) as measured by (125I)-iodopindolol binding was reduced in ventricles from the aortic stenosis group compared to control: 41.2(13.3) v 59.1(8.1) fmol.mg-1 protein, p less than 0.005. Affinity of receptor for ligand (Kd) was not affected by cardiac hypertrophy. Tissue noradrenaline concentration was reduced in the hypertrophy group: 1108(402) (control) v 438(13) ng.g-1 initial wet weight (aortic stenosis), p less than 0.05. There were no significant subepicardial v subendocardial differences in any variable. CONCLUSIONS - Cardiac hypertrophy induced by aortic valve stenosis over a 6 month period is accompanied by a decrease in the density of ventricular beta adrenoceptors per gram and a decrease in ventricular noradrenaline concentration, though responsiveness of the whole heart is maintained.

Animals↗

PubMed1990

Effect of hyper- and hypovolaemia on regional myocardial oxygen consumption.

STUDY OBJECTIVE - The purpose of the investigation was to study the effect of preload on coronary blood flow and myocardial oxygen consumption in subendocardial and subepicardial regions of left ventricular free wall. DESIGN - Ventricular volume in anaesthetised open chest dogs was altered over a range of 20% to produce hypovolaemia (10-15% exsanguination) or hypervolaemia (colloid infusion), allowing measurements of regional blood flow and oxygen consumption with varying preloads. beta Adrenergic blockade was used to limit changes in inotropy, and heart rate was kept constant by pacing at 150 beats.min-1. SUBJECTS - 9 mongrel dogs of either sex weighing 24.9 (SEM 4.1) kg were studied. MEASUREMENTS and RESULTS - Left ventricular volume was calculated from ultrasonic measurements of long and short axis end diastolic diameters and wall thickness. Regional myocardial blood flow was estimated using radioactive microspheres, and oxygen consumption in each region was determined from microspectrophotometric measurements of oxygen saturations in small arteries and veins. Hypervolaemia increased subepicardial blood flow from 66.8(6.9) (normovolaemic) to 114.1(13.5) ml.min-1.100 g-1, and regional oxygen consumption from 4.08(0.57) to 6.44(1.08) ml.min-1.100 g-1. Values in the subendocardium were similar, except for oxygen consumption, which increased less than in the subepicardium. Left ventricular end diastolic volume, pressure, and output were each increased in hypervolaemia, but not dP/dt and systolic aortic pressure. Hypovolaemia reduced blood pressures without reducing end diastolic volume. CONCLUSIONS - Augmented flow work produced by increased preload (even in the absence of changes in pressure work) increases myocardial oxygen supply equally in the subepicardium and the subendocardium, while oxygen extraction and consumption are preferentially augmented in the subepicardium.

Animals↗

PubMed1990

Isoproterenol and myocardial O2 supply/consumption in hypertension-induced myocardial hypertrophy.

Myocardial oxygen supply, O2 consumption (MVO2) and function were determined during base-line and isoproterenol infusion (0.5 microgram.kg-1.min-1) 30 days after New Zealand White rabbits were prepared as one-kidney, one-clip (1K,1C) Goldblatt hypertensive or uninephrectomized (sham) controls. Coronary blood flow and cardiac output, using radioactive microspheres, and small vessel O2 saturations, using microspectrophotometry, were measured in hypertrophied and nonhypertrophied hearts. After 30 days, 33% myocardial hypertrophy was evident in the 1K,1C animals. Base-line blood pressure was significantly higher in the 1K,1C animals compared with sham controls and remained higher during isoproterenol infusion. Base-line heart rate was not different between animal groups, and heart rate increased in both groups during isoproterenol. Cardiac output was similar between sham and 1K,1C animals during base-line conditions (316 +/- 40 vs. 365 +/- 51 ml/min, respectively). After isoproterenol, cardiac output increased in the sham animals (494 +/- 119 ml/min) but not in the 1K,1C group (317 +/- 85 ml/min). Isoproterenol elevated MVO2 threefold in both the sham and 1K,1C animals. Coronary blood flow was significantly increased to similar levels in both animal groups. O2 extraction significantly increased during isoproterenol in both groups. Therefore, impaired cardiac function was evident during isoproterenol stress in the hypertrophied myocardium independent of myocardial O2 supply or consumption restrictions.

Animals↗

PubMed1990

Pacing during reperfusion elevates regional myocardial oxygen consumption.

Reperfusion after 2 h of coronary artery occlusion has been shown to result in depressed coronary blood flow to the reperfused region and elevated regional myocardial extraction. This suggests that reperfused myocardium, even after 4 h of reperfusion, possesses limited flow and O2 consumption reserves. We studied the capacity of reperfused myocardium to elevate regional blood flow and regional O2 consumption in response to sustained increased O2 demand, produced by atrial pacing. Two groups of anesthetized open-chest dogs were subjected to 2 h of left anterior descending coronary artery occlusion followed by 4 h of reperfusion. One group was subjected to atrial pacing (40% increase in heart rate) during the entire 4-h reperfusion period. Regional O2 saturation was measured by microspectrophotometry in samples of reperfused and nonoccluded subepicardium and subendocardium, which were taken at the end of the reperfusion period. In the paced group, regional blood flow (radiolabeled microspheres) to reperfused myocardium was significantly higher than to corresponding regions of unpaced hearts (110 +/- 22 vs. 40 +/- 9 ml.min-1 x 100 g-1 in the subendocardium). In the control group, O2 extraction of reperfused subendocardium was significantly higher than that measured in the corresponding nonoccluded region (11.0 +/- 0.9 vs. 8.0 +/- 0.6 ml O2/100 ml). Pacing did not elevate O2 extraction of reperfused myocardium (8.7 +/- 0.6 vs. 8.3 +/- 0.7 ml O2/100 ml). Myocardial O2 consumption was significantly elevated in all regions of the paced heart. It is concluded that reperfused myocardium possesses significant unutilized O2 supply and consumption reserves.

Animals↗

PubMed1990

Hypertension-induced cardiac hypertrophy. Oxygen supply and consumption with pacing.

The purpose of this study was to determine if hypertrophied myocardium was associated with diminished cardiac function, restricted oxygen supply, or oxygen consumption during tachycardia. Myocardial oxygen supply and oxygen consumption were determined during baseline and atrial pacing conditions 30 days after New Zealand White rabbits were prepared as one-kidney, one clip Goldblatt hypertensive or uninephrectomized sham control rabbits. Coronary blood flow and cardiac output, using radioactive microspheres, and small vessel oxygen saturations, using microspectrophotometry, were measured in hypertrophied and nonhypertrophied hearts. After 30 days, baseline blood pressure was significantly higher in the Goldblatt rabbits compared with sham controls, and hypertension was maintained during pacing. The myocardium was hypertrophied in the Goldblatt hypertensive rabbits compared with sham controls. Baseline heart rates were not different between animal groups (242 +/- 32 and 244 +/- 24 beats/min, respectively). Both groups were paced 35% above baseline heart rates; during pacing, cardiac output was similar to baseline values in the sham controls (304 +/- 99 versus 321 +/- 116 ml/min, respectively) but reduced in the hypertensive rabbits (248 +/- 43 versus 325 +/- 62 ml/min). Myocardial oxygen consumption increased twofold in both nonhypertrophied and hypertrophied ventricles during tachycardia. Oxygen extraction was significantly elevated, but coronary blood flow was not altered during pacing in either animal group. Therefore, at the pacing level chosen the diminished function in cardiac hypertrophy was not associated with reduced oxygen consumption. Conversely, reduced efficiency during pacing in the hypertrophied myocardium was suggested.

Animals↗