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Biomedical subjects

G J Grover

Publications and source records attributed to G J Grover.

At least 127 records · Page 7Linked to original sources
PubMed1987

Coronary adjustments to graded hypotension in rabbits.

The purpose of this study was to determine how the myocardium can compensate (change O2 supply/consumption parameters) regionally during acute hemorrhagic hypotension. Twenty-one open chest, anesthetized rabbits were subjected to one of three treatments: (1) control (nonhemorrhaged), (2) hemorrhage to 70 mm Hg, (3) hemorrhage to 50 mm Hg. Myocardial blood flows were determined by using radioactive microspheres before and during hemorrhage. At the end of the experiment the hearts were removed and stored in liquid N2 and analyzed for subepicardial and subendocardial arterial and venous O2 saturation by using microspectrophotometry, and from this, O2 consumption was determined. During hemorrhage, blood pressures were significantly depressed for all groups compared to the control group. Myocardial blood flow was depressed 20% in the 70 mm Hg group and coronary resistance fell 15% compared to control. In the 50 mm Hg group, flow was reduced 38% and resistance decreased 31% compared to the 70 mm Hg group. No regional (subepicardial-subendocardial) differences in flow or resistance occurred during hypotension. These decreases in resistance were observed despite a 32% drop in O2 consumption in the 70 mm Hg group and 44% in the 50 mm Hg group compared to the control. O2 extraction remained unchanged for all groups as did the O2 supply/consumption balance. Thus, despite decreases in O2 consumption during acute hemorrhage, rabbit hearts decreased coronary resistance so as to maintain the O2 regional supply/consumption balance constant. Since O2 extraction did not change, these hearts were not ischemic, even in the subendocardium.

Animals↗
PubMed1986

Effect of aortic constriction on the oxygen supply-consumption balance in partially ischaemic myocardium.

A study was carried out to determine the effect of distal aortic constriction on the regional oxygen supply-consumption balance in ischaemic and non-ischaemic myocardium. Left anterior descending coronary artery flow was reduced by 50% in anaesthetised mongrel dogs, and half these animals were subjected to distal ascending aortic constriction (ventricular systolic-aortic systolic pressure gradient 50 mm Hg). Blood flows were determined using radioactive microspheres, and arterial and venous oxygen saturations were determined using microspectrophotometry. When left anterior descending artery flow was decreased by 50% tissue flow, as measured by microspheres in the ischaemic region in both control and aortic constricted animals, decreased. Aortic constriction increased flow in the non-ischaemic zone compared with the same region in control animals. The arteriovenous oxygen content difference increased similarly in the ischaemic region in control and aortic constricted animals compared with their respective non-ischaemic zones. Aortic constriction decreased this difference in the non-ischaemic region compared with these same regions in control animals. Oxygen consumption in the non-ischaemic and ischaemic regions of aortic constricted animals was higher than in control animals. The oxygen supply to consumption ratio was lower in the ischaemic zone in both control and aortic constricted animals than in their respective non-ischaemic regions. Aortic constriction does not appear to alter the oxygen supply-consumption balance in the ischaemic myocardium compared with control animals. Thus the increased work performed by the heart in response to the aortic constriction is adequately matched by an increased flow even in the flow restricted region.

Animals↗
PubMed1986

Effect of hemorrhage on regional morphometric indexes of cerebral capillarity.

This study was performed to determine whether the brain can increase the number of perfused capillaries and arterioles supplying it regionally during hemorrhage. This was done using a technique to simultaneously determine total and perfused regional arteriolar and capillary morphology. Conscious Long-Evans rats served as unbled controls or were bled 65 mmHg or to 40-45 mmHg and stabilized for 30 min. Regional cerebral blood flow was determined using [14C]iodoantipyrine in half of these animals and fluorescein isothiocyanate-dextran was injected in the other half for determination of perfused cerebral microvascular morphometric indexes. The total microvasculature was labeled postmortem via an alkaline phosphatase stain. Regional cerebral blood flow was significantly increased in animals bled to 65 mmHg. During hemorrhage to 40-45 mmHg, cerebral blood flow was reduced 50% (from 59 +/- 28 to 26 +/- 11 ml X min-1 X 100 g-1, mean +/- SD) with no regional redistribution. For all treatments, total capillary density ranged from 400 to 500 capillaries/mm2, and in controls 47% were perfused. Animals bled to 65 mmHg did not mobilize their unperfused microvascular reserve even though they showed a slight tendency to do so. During hemorrhage to 40-45 mmHg, this percent increased significantly to 57% with the largest increase occurring in the pons. Approximately 51% of arterioles were perfused in controls and this was not different compared with the percent perfused during hemorrhage. Despite the overall lack of mobilization of unperfused arterioles, some regions within the brain significantly mobilized their reserves with severe hemorrhage, e.g., hippocampus (78%), hypothalamus (67%), and medulla (73%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Beta adrenoceptor control of the microvascular reserve in rabbit myocardium.

This study was performed to determine if the unperfused microvascular reserve in the rabbit heart can be controlled by beta adrenoceptors. Anesthetized, open chest rabbits (N = 54) were subjected to saline i.v., 0.7 mg/kg of atenolol i.v., 1 mg/kg of practolol, 0.1 microgram/kg of salbutamol, 1 microgram/kg of salbutamol or 0.7 mg/kg of atenolol + 1 microgram/kg of salbutamol treatments. In half these animals coronary flows were determined before and after treatment using radioactive microspheres. The others were given 100 mg/kg of fluorescein isothiocyanate-dextran and the hearts were removed and analyzed for perfused and total microvascular morphology. The fluorescence marked the perfused microvessels and the slides were stained to show all vessels. Control group blood flow was 213 +/- 25 ml/min/100 g. Flows decreased 25% with atenolol and practolol whereas no change was seen with salbutamol or atenolol + salbutamol. Total capillary volume fraction ranged from 0.15 to 0.20 mm3/mm3 with 60% of this perfused in controls. Atenolol significantly reduced this to 47% whereas practolol (90%), high-dose salbutamol (97%) and salbutamol + atenolol (99%) resulted in a significant mobilization. Low-dose salbutamol resulted in a mobilization of capillaries to a degree intermediate (79%) between controls and high-dose salbutamol. Total arteriolar volume fraction ranged from 0.002 to 0.004 mm3/mm3 and in controls 65% of this was perfused. This percentage was reduced with atenolol and significantly increased with all other treatments except practolol. Thus, blockade of beta-1 adrenoceptors results in decreases in the percentage of perfused microvessels whereas stimulation of beta-2 adrenoceptors results in an increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuterol↗
PubMed1985

The effect of graded doses of norepinephrine on the O2 supply/consumption balance in ischemic and nonischemic rabbit myocardium.

The purpose of this study was to determine the effect of graded doses of norepinephrine on the regional O2 supply/consumption ratio in ischemic rabbit hearts. Open chested, anesthetized rabbits were used and regional flows, O2 extraction, consumption and O2 supply/consumption ratios were determined before and 1 h after occlusion of the left anterior descending coronary artery in controls and animals given 0.1, 1.0 and 10 micrograms/kg per min norepinephrine (NE). After occlusion in controls, mean myocardial blood flow decreased 40% in the occluded region. Blood flow was also depressed in the occluded region for all NE doses compared to their own preocclusion values, but was higher in these regions compared to control animals. O2 extraction was higher in the occluded region compared to the nonoccluded region for all groups; however these values were lower in the NE groups compared to controls. NE increased O2 consumption in the occluded and nonoccluded regions compared to control group values. The O2 supply/consumption ratio was depressed in the occluded region in all groups compared to the nonoccluded region, though no differences were seen between NE and control groups. Thus, increases in the blood flow to the occluded region were proportional to the increases in O2 consumption with infusion of NE, indicating that a reserve exists and can be utilized with NE.

Animals↗
PubMed1985

Effect of pacing on oxygen supply-to-consumption ratio in ischemic myocardium.

This study was performed to determine if the partially occluded myocardium could maintain its O2 supply-to-consumption ratio during atrial pacing. In 14 open-chest anesthetized dogs, the left anterior descending coronary artery was occluded to 50% of base-line flow, and in half of the dogs the hearts were paced to 50% above base-line heart rate. Blood flows were determined by use of microspheres before and after occlusion, and O2 supply-consumption variables were determined by use of microspectrophotometry. After occlusion in control and paced groups, blood flow was depressed in the ischemic region compared with the nonischemic region. In paced animals, blood flows in all regions were significantly higher compared with their respective values in nonpaced animals. After pacing, mean O2 consumption was 34% higher (53% in the occluded region) compared with control animals. The O2 supply-to-consumption ratio was similar in the occluded region of paced animals compared with the same region in controls. This ratio was lower in ischemic regions of both groups compared with their respective nonischemic regions. This indicates that, despite a reduced O2 supply-to-consumption ratio in the ischemic area, an unutilized reserve of flow exists.

Animals↗
PubMed1985

Effect of ibuprofen and indomethacin on the O2 supply/consumption balance in ischemic rabbit myocardium.

The purpose of this study was to determine if differences in the cardioprotective abilities of ibuprofen and indomethacin were due to their differing abilities to alter the O2 supply/consumption ratio in the ischemic myocardium. Experiments were done on 21 anesthetized open-chest rabbits. Regional flow (using radioactive microspheres), O2 extraction, O2 consumption, and O2 supply/consumption ratio were determined 1 hr after occlusion of the left anterior descending coronary artery in controls and animals given iv 10 mg/kg ibuprofen or iv 3 mg/kg indomethacin. Myocardial blood flow was depressed in the occluded region compared to the nonoccluded region after occlusion for all treatments. O2 extraction in the occluded region was elevated compared to the nonoccluded region for all treatments after occlusion. No differences in O2 consumption were noted between any treatment within the occluded or nonoccluded regions. The O2 supply/consumption ratio was lower in the occluded region compared to the nonoccluded region for all treatments. No differences in this ratio were noted between any treatment. Thus, the effects of indomethacin or ibuprofen on ischemia are not related to acute changes in myocardial O2 supply/consumption balance.

Animals↗
PubMed1984

Effect of red blood cells and red blood cell ghosts on reticuloendothelial system function.

Previous studies have shown that hepatic phagocytosis of red blood cell (RBC) stroma can depress reticuloendothelial system (RES) phagocytic function and increase susceptibility to shock. Since the RBC stroma used in these experiments contained substantial amounts of adherent hemoglobin, the present study was carried out to evaluate the role of the hepatic uptake of RBC membrane material on RES phagocytic function and susceptibility to endotoxin shock in rats. Neuraminidase-treated RBC which contained normal amounts of hemoglobin and RBC ghosts which were hemoglobin-free were used. Both preparations were removed from the circulation primarily by the liver. RES phagocytic function was depressed following the hepatic uptake of 29 X 10(8) neuraminidase-treated RBC and 26 X 10(8) RBC ghosts. RES uptake of neuraminidase-treated RBC was associated with an increase in susceptibility to endotoxin shock, but RBC ghosts did not affect shock susceptibility. Thus, RBC ghosts and intact RBC are equally effective in depressing RES phagocytic function, but RBC ghosts did not affect susceptibility to endotoxin shock.

Animals↗
PubMed1984

Role of the liver in host defense to pneumococcus following splenectomy.

Splenectomy is associated with increased susceptibility to bacterial infection, and this is thought to be primarily due to a decrease in clearance of bacteria from the blood. The purpose of the present study was to determine if splenectomy could increase susceptibility to pneumococcus type 3, which is cleared primarily by the liver in rats, and if hepatic function is altered by splenectomy. Splenectomy increased the mortality of rats challenged iv with pneumococcus. Heat-killed, 51Cr-labeled pneumococci were rapidly cleared by the liver and splenectomy did not alter the initial clearance rate or the initial hepatic uptake of bacteria. Injection of viable pneumococci showed that blood levels were unchanged at 30 min but were much greater 5 hr after challenge in splenectomized animals. Hepatic uptake of viable pneumococcus was also not changed at 30 min after injection but at 5 hr the number of bacteria in the liver was greater in the splenectomized animals. This suggests an impairment in hepatic bactericidal function. Another contributing factor may have been that the hepatic bactericidal capacity was overwhelmed by the pneumococci which would normally have been killed by the spleen. Lung localization of viable bacteria was increased initially but there was no decrease in pulmonary bactericidal function. Thus, splenectomy increased susceptibility to a bacteria cleared primarily by the liver which was attributed to an impairment of hepatic bactericidal function and/or an inability of the liver to compensate for the loss of splenic function due to a saturation of the bactericidal system.

Animals↗
PubMed1984

Effect of T4-induced cardiac hypertrophy on O2 supply-consumption balance during normoxia and hypoxia.

The purpose of this study was to determine if thyroxine-induced hypertrophic hearts can maintain an adequate O2 supply-consumption balance both at rest and under hypoxic stress. New Zealand White rabbits were given 0.5 mg/kg L-thyroxine (T4) for 3 or 16 days, and a third group served as a control. Chests were opened under anesthesia, and myocardial blood flow was determined using microspheres. In half of these animals, microspectrophotometric determinations were made on left ventricular arterial and venous O2 saturation, and by combining this data with blood flows, O2 consumption was determined. The other animals were then subjected to hypoxia (8% O2 in N2), and flows and O2 consumption were again determined. T4 increased arterial pressure and heart rate in normoxic animals and also increased myocardial blood flow 65 and 210% for 3- and 16-day T4 groups, respectively, with no regional differences. O2 extraction was also increased in T4 animals. O2 consumption increased 134 and 280% in 3- and 16-day T4 groups. Only normoxic saline controls had a regional O2 consumption difference with subendocardial O2 consumption higher than subepicardial values. When compared with their respective normoxic groups, blood flow increased 49 and 101% for the hypoxic 3- and 16-day T4 groups. Hypoxia had no effect on saline control blood flow. Hypoxia decreased O2 extraction 29 and 41%, respectively, in the 3- and 16-day T4 groups and was unchanged in saline controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effect of red blood cell stroma on the reticuloendothelial system clearance and killing of Streptococcus pneumoniae.

Previous studies from this laboratory have shown that thermal injury can cause sufficient intravascular hemolysis to depress reticuloendothelial system (RES) phagocytic function and that the injection of red blood cell (RBC) stroma depresses RES function and increases susceptibility to experimental shock. The present study evaluated the effect of thermal injury and RBC stroma on susceptibility to infection with Streptococcus pneumoniae as well as the effect of RBC stroma on the RES clearance and killing of the bacteria. The mortality rate following pneumococcal infection was increased after thermal injury from 0% to 100% (P less than .01), and with the injection of RBC stroma (0.5 ml/100 g) mortality increased from 20% to 80% (P less than .01). Hepatic uptake of heat-killed S. pneumoniae was depressed from 64% to 44% of the injected dose following the injection of RBC stroma. RBC stroma depressed complement CH50 levels by 31%. The reduction in the number of viable S. pneumoniae present in the liver between 30 min and 4 hr following bacterial challenge was decreased in animals receiving RBC stroma. This was interpreted as an indication of impaired hepatic bactericidal function and was associated with an increase in the number of circulating viable S. pneumoniae. It is concluded that the increased susceptibility to pneumococcal infection induced by RBC stroma was probably due to an impairment in hepatic clearance and killing of the bacteria. The depressed bacterial clearance could have been contributed to by the stroma-induced decrease in complement levels. This study further supports the hypothesis that the intravascular hemolysis caused by thermal injury contributes to the increased susceptibility to infection following this form of injury.

Animals↗
PubMed1983

Effect of erythrocyte stroma on reticuloendothelial system phagocytic function.

Previous studies have demonstrated that intravenous administration of erythrocyte stroma is followed by a depression of RES phagocytic function. The present study evaluated the possibility that depression of hepatic blood flow, activation of the coagulation system, or depletion of opsonic factors mediates the RES depression induced by erythrocyte stroma. Stroma was prepared from washed rat erythrocytes and injected into rats at doses of 0.3, 0.5, 0.75, and 1.0 ml/100 gm. RES depression increased progressively after stroma doses greater than 0.3 ml/100 gm. Hepatic blood flow was decreased only after the 1.0 ml/100 gm dose. Fibrinogen levels were decreased with the 1.0 ml/100 gm dose but were unchanged with the 0.5 ml/100 gm dose of stroma, and the RES depression induced by the 0.5 ml/100 gm dose was not modified by the administration of heparin. Circulating fibronectin levels were not consistently depressed after stroma injection, and in vitro incubation of stroma with serum did not affect fibronectin levels. Erythrocyte stroma decreased hemolytic complement levels but depletion of complement with purified cobra venom factor did not depress RES phagocytic function. Preopsonization of the RES test particle did not modify the stroma-induced RES depression. These results indicate that decreased hepatic blood flow, activation of the coagulation system, or depletion of opsonins did not contribute to the RES depression induced by the 0.5 ml/100 gm dose of stroma. These results suggest that impairment of phagocytic cell function may mediate the effect of erythrocyte debris on RES phagocytic function.

Animals↗
PubMed1982

Effect of splenic sequestration of erythrocytes on splenic clearance function and susceptibility to septic peritonitis.

The effect of splenic sequestration of erythrocytes (RBC) on splenic clearance function and susceptibility to septic peritonitis was studied. Homologous RBC were treated with 20 mM phenylhydrazine hydrochloride in vitro and injected into rats at doses of 5, 15, 75, and 150 mg of hemoglobin per 100 g. Splenic 93, 23, and 13% of the injected dose, respectively, whereas less than 2.1% of the same doses of washed RBC were localized in the spleen. The total quantity of phenylhydrazine-treated RBC sequestered by the spleen was similar for the three larger doses (40 to 45 mg of hemoglobin per g of tissue), indicating that this is the capacity of the spleen to take up this type of RBC in 234 h. The phenylhydrazine-treated RBC in doses of 15, 75, and 150 mg of hemoglobin per 100 g depressed the clearance rate and splenic localization of a test dose of phenylhydrazine-treated RBC, whereas splenic clearance function was unchanged after a dose of 5 mg of hemoglobin per 100 g. Splenectomy or injection of doses of phenylhydrazine-treated RBC which depressed splenic clearance function increased the susceptibility to septic peritonitis induced by cecal ligation and puncture. After thermal injury, splenic clearance function was found to be depressed. Also, splenic localization of RBC 24 h after thermal injury was found to be approximately equal to that after injection of the doses of phenylhydrazine-treated RBC which depressed splenic clearance function. It is concluded that splenic sequestration of RBC can depress splenic clearance function and increase susceptibility to peritonitis, and that this may be one mechanism for the increased susceptibility to infection seen after thermal injury.

Animals↗
PubMedDate not supplied

The effect of the thromboxane A2 receptor antagonist SQ 29,548 on the severity of pacing-induced ischemia.

The effect of the thromboxane A2 (TXA2)/prostaglandin endoperoxide receptor antagonist, SQ 29,548 on pacing-induced ischemia was determined in anesthetized open-chest dogs. The dogs were subjected to a left anterior descending coronary artery (LAD) stenosis sufficient to result in ischemia as measured by epicardial ST-segment elevation only when the hearts were paced 70-80 beats/min above baseline. After a recovery (nonpacing) period, either 0.2 mg/kg + 0.2 mg/kg/hr SQ 29,548 or saline was infused i.v. The animals were subjected to 5 min periods of pacing before and 10, 40 or 70 min after the initiation of drug or saline treatment. Before drug treatment, pacing + LAD stenosis resulted in significant ST-elevation in both groups (11.5 +/- 1.1 mV and 12.4 +/- 0.6 mV for saline and SQ 29,548 groups, respectively). During drug treatment, SQ 29,548 significantly reduced ST-elevation during pacing + stenosis at 40 and 70 min. At 70 min, ST-elevation was 4.9 +/- 1.7 mV for the SQ 29,548 group vs 10.8 +/- 1.2 mV for the saline group (p less than 0.05). In separate experiments 0.2 mg/kg + 0.2 mg/kg/hr SQ 29,548 antagonized the activity of a TXA2 mimetic, U-46,619, for femoral vasoconstriction, causing 100-to-200 fold rightward shifts in dose response relationships. Thus, a dose of SQ 29,548 capable of strong TXA2-receptor blockade reduced the severity of ischemia, and this effect was independent of changes in arterial blood pressure and heart rate.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMedDate not supplied

Effect of complement depletion on O2 supply and consumption in ischemic dog myocardium.

The purpose of this study was to determine whether depletion of serum complement can decrease the severity of an ischemic episode by improving regional O2 supply and consumption parameters in the ischemic region of the heart. Fourteen anesthetized dogs with serum complement intact or depleted (100 U/kg cobra venom factor given 8 hrs before) were subjected to left anterior descending coronary artery (LAD) occlusion for 6 hrs. Myocardial blood flows were determined before and 6 hrs after LAD occlusion using radioactive microspheres. Regional arterial and venous O2 saturations were determined using microspectrophotometry. In control animals, flow decreased from 122 +/- 42 to 13 +/- 14 ml/min/100 g (mean +/- SD) in the occluded LAD region. With complement depletion, LAD occlusion resulted in a flow reduction in the ischemic region (38 +/- 29 ml/min/100 g), but to a lesser degree than seen in the same region in control animals, especially in the subendocardium. O2 consumption was decreased in the ischemic region of both treatment groups, though O2 consumption was higher in this region in complement depleted animals compared to the values in control animals. The O2 supply/consumption ratio was decreased similarly in the ischemic region of control and complement depleted groups. Thus, with complement depletion, flow to the ischemic zone was improved but this region was still flow restricted. The flow increase during complement depletion was sufficient to allow an increased O2 utilization in the ischemic region.

Animals↗
PubMedDate not supplied

Propranolol and thyroxine-induced hypertrophic rabbit hearts: effect on heart size and regional O2 supply/consumption variables.

The purpose of this study was to determine the effect of acute and chronic propranolol on heart size and regional O2 supply/consumption variables in thyroxine (T4)-treated rabbit hearts. New Zealand white rabbits were given 0.5 mg/kg T4 for 3 or 16 days with and without concomitant 2 mg/kg propranolol. Another group was given 16 days of propranolol alone and another 3-day T4 group was given 2 mg/kg propranolol 1 h before the experiment began. Another group served as control. Myocardial blood flows were determined using radioactive microspheres and small arteriolar and venous O2 saturations were determined using microspectrophotometry. Treatment with T4 for 3 or 16 days increased the heart weight/body weight ratio, myocardial blood flow, and regional O2 consumption. 16-day T4 treatment resulted in myocardial flow 195% and O2 consumption 300% above control group values. When propranolol was given chronically along with T4, heart weight/body weight ratios did not increase to the degree seen with 3 or 16 days of T4, alone. Propranolol given acutely in 3-day T4-treated animals, resulted in a reduced O2 consumption and O2 extraction, though not to the extent seen with chronic propranolol treatment of T4-treated animals. Acute propranolol treatment slightly reduced myocardial blood flow in 3-day T4-treated animals, while chronic treatment significantly reduced it. Chronic propranolol treatment in 16-day T4-treated animals resulted in a significant reduction in flow and O2 consumption. Thus, T4 treatment increased O2 consumption, flow, and heart size and these effects could be attenuated using acute and chronic propranolol.

Animals↗
PubMedDate not supplied

Regional oxygen supply and consumption balance in experimental left ventricular hypertrophy.

The aim of the present study was to determine if the relationship between myocardial O2 supply and O2 consumption was preserved after prolonged pressure overload due to aortic valve stenosis. This was examined in anesthetized open-chest dogs in which the aortic valve was plicated 6 months previously. We measured coronary blood flow with radioactive microspheres and regional small vessel O2 saturation with microspectrophotometry, to obtain O2 supply, and O2 consumption. Regional O2 consumption was calculated as the product of flow and O2 extraction. The left ventricular weight/body weight ratio was 81% greater in the dogs with aortic valve stenosis. There were no hemodynamic differences between the groups except that left ventricular systolic pressure was 38 +/- 22 mm Hg greater than aortic in the hypertrophied group. Coronary blood flow did not differ between the control and hypertrophied groups nor were there subepicardial vs subendocardial differences. When maximal coronary flow was determined with chromonar (10 mg/kg), the flow increase was significantly attenuated in the hypertrophied subendocardium (242.1 +/- 82.3 (hypertrophy) vs 512.4 +/- 204.1 ml.min-1.100 g-1 (control). There were no significant differences in O2 extraction or O2 consumption/g between control and hypertrophied animals. There was a significantly lower O2 supply/consumption ratio in the subendocardium compared to the subepicardium of both groups. However, the O2 supply/consumption ratio was not decreased by hypertrophy. Thus, despite significant hypertrophy, a loss of flow reserve and a high left ventricular pressure, O2 supply/consumption balance is preserved in valvular aortic stenosis at rest.

Animals↗