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Biomedical subjects

I Y Liang

Publications and source records attributed to I Y Liang.

At least 19 recordsLinked to original sources
PubMed1994

Thromboxane A2 receptor-specific antagonism in hypothermic cardiopulmonary bypass.

Using a thromboxane A2 receptor-specific antagonist, SQ 30,741, this study was undertaken to define the role of thromboxane A2 in postischemic myocardial reperfusion injury and in the heparin-protamine reaction. Eighteen heparinized (300 units/kg) sheep were placed on cardiopulmonary bypass (CPB) after complete instrumentation, cooled to 28 degrees C, and had their aortas crossclamped for 1 hour. They were then rewarmed to 36 degrees C and weaned from CPB without inotropic support. Control sheep (n = 6) received a saline infusion throughout the procedure. Bolus animals (n = 6) received 5 mg/kg of SQ 30,741 at 5 minutes after discontinuation of CPB and before protamine sulfate administration. Infusion animals (n = 6) received an SQ 30,741 bolus of 5 mg/kg followed by a continuous infusion of 5 mg.kg-1 hr-1 of SQ 30,741 initiated before CPB. All animals received 5 mg/kg of protamine sulfate over a 15-second period 15 minutes after being weaned from CPB. Control animals exhibited significantly decreased global myocardial function after the 1-hour ischemic interval. Further significant functional decline and increase in pulmonary pressure occurred after protamine sulfate administration. Bolus animals experienced a similar postischemic injury, but had no further decrease in function following protamine infusion. Infusion animals had significantly improved global myocardial function after bypass compared with both other groups and were also protected from the deleterious effects of protamine sulfate administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Response to brief coronary stenosis in conscious dogs after ventricular sympathectomy.

Left ventricular responses to 2-min circumflex occlusion were studied in conscious dogs. In nonsympathectomized controls at 2, 4, and 8 wk after surgery for cardiac instrumentation, segmental shortening in the posterior ventricle significantly decreased by 111, 87, and 81% of the preocclusion values, respectively (P less than 0.05). The decrease in shortening was associated with increases in end-diastolic pressure of 9, 9, and 8 mmHg (P less than 0.05), decreases in the maximal rate of pressure generation of 305, 272, and 340 mmHg/s (P less than 0.05), and increases in heart rate of 28, 21, and 20 beats/min, respectively (P less than 0.05). After 2 and 4 wk of ventricular sympathectomy, posterior segmental shortening declined by 38 and 31%, respectively (P less than 0.05), but these decreases were less than in controls (P less than 0.05). Shortening did not change during occlusion after 8 wk of sympathectomy. Diastolic pressure increased by 6 mmHg (P less than 0.05), and the rate of pressure generation decreased by 232 mmHg/s (P less than 0.05) in the 2-wk sympathectomized ventricle. These variables did not change significantly after 4 and 8 wk of sympathectomy. After 2, 4, and 8 wk of sympathectomy, the increases in heart rate during circumflex occlusion were not different from controls (P greater than 0.05). Thus chronic sympathectomy preserved ventricular function during occlusion. This effect was attributable to a reduced preocclusion mechanical performance with a reduction in blood flow requirement and to an increased collateral perfusion, as indicated by a higher peripheral coronary pressure during occlusion in sympathectomized ventricles.

Animals↗
PubMed1987

Effects of alpha-adrenergic blockade on coronary autoregulation in dogs.

In alpha-chloralose-anesthetized, open-chest dogs, left coronary blood flow and oxygen extraction were measured at perfusion pressures from 25 to 175 mmHg. Pressure-flow relationships were obtained before and after alpha-blockade with prazosin or alpha 2-blockade with yohimbine in the presence of beta-blockade with propranolol. The efficiency of flow autoregulation with increments in pressure was calculated as the closed-loop gain and as the slope of flow to pressure. In all animals the highest gain and the lowest slope were seen when pressure increased from 75 to 125 mmHg. In the prazosin group before alpha-blockade the gain with this pressure increase was 0.76 +/- 0.05, whereas in the yohimbine group before alpha-blockade this gain was 0.75 +/- 0.03. Prazosin reduced the gain within the pressure range of 75-125 mmHg by 41%, and this reduction was statistically significant (P less than 0.05). Prazosin also significantly increased the flow to pressure slope within this range. In addition, at all pressures greater than or equal to 50 mmHg, the level of coronary flow was significantly increased by prazosin. The increase in flow and the reduction in autoregulatory efficiency with prazosin were not attributable to an increase in myocardial oxygen consumption. Yohimbine had no effects on the level of coronary flow or on the autoregulatory efficiency. These data indicate that an alpha 1-adrenoceptor mediated coronary constriction modulates coronary autoregulation.

Adrenergic alpha-Antagonists↗
PubMed1987

Effect of beta 1-receptor blockade on coronary resistance in partially trained dogs.

Selective beta 1-receptor blockade with atenolol (1 mg X kg-1, i.v.) was used to determine the effect of partial exercise training on diastolic coronary resistance (DCR) during sub-maximal exercise. Seven conscious dogs were studied in the untrained (UT) and partially trained (PT) conditions. The conditioning regime consisted of treadmill running 5 d X wk-1 for 4 to 5 wk. Left circumflex coronary flow, aortic pressure, and heart rate were measured, and DCR and myocardial oxygen consumption were calculated. During sub-maximal exercise, DCR in the UT dogs decreased from a resting value of 4.08 +/- 0.18 mm Hg X ml-1 X min-1 to 1.91 +/- 0.17 mm Hg X ml-1 X min-1 at a workload of 6.4 kph (speed)/16% (grade). During exercise, DCR was significantly greater in UT than in PT dogs. Atenolol significantly increased DCR at all levels of sub-maximal workload in both UT and PT dogs. However, the percent increase in DCR with atenolol was significantly greater in the PT dogs compared to UT dogs. These findings suggest that daily exercise for 4 to 5 wk may decrease beta 2-receptor activity of the coronary vasculature during sub-maximal exercise.

Adaptation, Physiological↗
PubMed1986

Cardiac and coronary effects of prazosin and phenoxybenzamine during coronary hypotension.

Left coronary perfusion pressure was reduced to 50 mm Hg in alpha-chloralose-anesthetized open chest dogs, causing significant reductions in coronary blood flow and left ventricular oxygen consumption (P less than .05). Infusion of the specific alpha-1 adrenergic antagonist prazosin (0.1 mg/min i.c.) during coronary hypotension significantly increased coronary flow and oxygen consumption within 6 to 8 min. These effects of prazosin were not attenuated by beta adrenergic blockade with propranolol. In the absence of propranolol, infusion of the nonspecific alpha adrenergic antagonist phenoxybenzamine (0.37 mg/min i.c.) increased coronary flow and oxygen consumption within 10 to 15 min, and these increases were significantly greater than with prazosin. In the presence of propranolol, phenoxybenzamine caused increases in coronary flow and oxygen consumption that were not different from those caused by prazosin. The results indicate that 1) prazosin increases coronary flow and oxygen delivery by abolition of a coronary constrictor tone mediated by postsynaptic alpha adrenoceptors; 2) the increases in coronary flow and oxygen consumption caused by phenoxybenzamine in the absence of beta adrenergic blockade were due to antagonism of pre- and postsynaptic alpha adrenoceptors; and 3) the increases in coronary flow and oxygen consumption caused by phenoxybenzamine after beta adrenergic blockade were due entirely to antagonism of coronary postsynaptic alpha-1 adrenoceptors.

Animals↗
PubMed1985

Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion.

Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6-8 min of prazosin infusion (0.6-0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.

Adrenergic alpha-Antagonists↗
PubMed1984

Maximum coronary blood flow and minimum coronary resistance in exercise-trained dogs.

Exercise training has been found to increase coronary vascularity of the heart in experimental animals. Maximum coronary flow and minimum coronary resistance were determined in 16 dogs with the injection of microspheres (15 micron) into the left atrium at rest and during the intravenous infusion of adenosine (0.7 mg X min-1 X kg-1). Heart rate was paced at 150 beats/min. Dogs were divided into three groups with microsphere injections made before and after 4-5 wk of daily exercise (group 1); before and after 8-10 wk of daily exercise (group II); and before and after 8-10 wk of cage rest (group III). Results of average left ventricular maximum myocardial flow before and after daily exercise were 4.08 +/- 0.34 and 4.89 +/- 0.33 ml X min-1 X g-1 for group I, 5.13 +/- 0.32 and 5.55 +/- 0.56 ml X min-1 X g-1 for group II, and 5.24 +/- 0.43 and 4.34 +/- 0.55 ml X min-1 X g-1 for group III. Arterial pressure, maximum coronary flow, and minimum coronary resistance were not significantly different before and after any condition in all three groups of dogs. Peak reactive hyperemia coronary flow was not altered by daily exercise. These results indicate that maximum coronary flow and minimum coronary resistance were not altered by either 4-5 or 8-10 wk of exercise training.

Adenosine↗
PubMed1983

Changes in diastolic coronary resistance during submaximal exercise in conditioned dogs.

Diastolic coronary resistance (DCR) was studied in 10 conscious dogs in the untrained (UT) and partially trained (PT) condition. The PT regime consisted of treadmill running 5 days/wk for 4-5 wk. Left circumflex coronary flow, aortic pressure, and heart rate were measured, and diastolic coronary resistance (DCR) was calculated. Adrenergic blockade was achieved with propranolol (1 mg/kg, iv) (beta B) and phentolamine (1 mg/kg, iv) (alpha B). During submaximal exercise in the UT condition, DCR fell from a resting value of 3.84 +/- 0.24 Torr . ml-1 . min with increasing work load to 1.57 +/- 0.12 Torr . ml-1 . min at 6.4 km/h (speed)/16% (grade). The decrease in DCR during submaximal exercise was greater in the PT than in the UT condition. DCR following alpha-adrenergic blockade was not significantly changed in the UT and PT conditions (e.g., at 6.4 km/h (speed)/16% (grade), 1.10 +/- 0.141 vs. 1.03 +/- 0.107 Torr . ml-1 . min, whereas following beta-adrenergic blockade, DCR was larger in the UT compared with the PT condition (e.g., at 6.4 km/h (speed)/16% (grade), 2.03 +/- 0.091 vs. 1.73 +/- 0.073 Torr . ml-1 X min). Myocardial oxygen consumption was not significantly different in the PT and UT conditions, indicating no difference in metabolism with partial training. The present study suggests that during submaximal exercise in the PT condition there is a change in the neurogenic control of the coronary vasculature by a reduction in sympathetic neural activity on the coronary resistance vessels.

Animals↗
PubMed1982

Effect of exercise conditioning on coronary resistance.

Diastolic coronary resistance (DCR) was determined in seven conscious dogs in the untrained state and after 4-5 wk of daily exercise conditioning (partial training). The conditioning regime consisted of treadmill running 5 days/wk. The dogs were instrumented to measure aortic pressure and left circumflex coronary flow during atrial pacing with implanted electrodes. Heart rate was varied from the resting value to 240 beats/min before and after adrenergic blockade with propranolol (beta B, 1 mg/kg) or phentolamine (alpha B, 1 mg/kg); myocardial oxygen consumption (MVO2) was measured in three dogs under the same condition in both the untrained (UT) and partially trained (PT) condition. DCR decreased with increasing heart rate [from 4.75 +/- 0.56 (SE) to 2.48 +/- 0.22 Torr . ml-1 . min at 240 beats/min]; alpha B reduced DCR, whereas beta B increased DCR. In the PT condition, DCR decreased to 4.02 +/- 0.40 Torr . ml-1 . min at rest and was decreased to 1.82 +/- 0.16 Torr . ml-1 . min at 240 beats/min (P less than 0.05 compared with UT). alpha-Adrenergic and beta-adrenergic blockade in the PT condition resulted in parallel reduction in DCR compared with the UT condition. MVO2 was unaffected by either PT or adrenergic blockade but increased as heart rate increased with atrial pacing. These data suggest a change in caliber of the coronary resistance vessel because of the parallel shift in the relationship between DCR and heart rate.

Animals↗
PubMed1979

Parasympathetic cholinergic vasodilator mechanism in the terminal liver microcirculation in rats.

Changes in the diameter of liver sinusoids were studied by an intravital television microscope method in pentobarbital-anaesthetized rats. Dilatation of liver sinusoids was observed during parasympathetic neural stimulation and during acetylcholine administration. Frequency-dependent stimulation-effect relationships were obtained by electrical excitation of intact vagus nerves at supramaximal intensity from 2 to 8 Hz. Acetylcholine concentration-effect relationships were also obtained by intraportal venous infusions of acetylcholine 30 microliter for 5 s from 10(-9) to 10(-2) mol.1(-1). Systemic cholinergic receptor blockade with atropine (1 mg.kg-1) markedly reduced dilatation of liver sinusoids produced by both vagus nerve stimulation and acetylcholine administration. Changes in diameter of liver sinusoids with frequency of neural stimulation and with concentration of administered acetylcholine were also expressed as percentage of observed maximum effect and the respective stimulation-effect curves were constructed such that at a certain percentage of diameter change, the equivalent level of vagus nerve activity was represented by a given concentration of administered acetylcholine. Liver plasma concentration of acetylcholine presumably released during electrical vagal stimulation and reaching liver sinusoids was also estimated and found to be within physiological range. It is therefore proposed that rat liver sinusoids have the capacity for parasympathetic cholinergic vasodilatation.

Acetylcholine↗
PubMed1979

Microvascular filling pattern in rat liver sinusoids during vagal stimulation.

1. The terminal microcirculation in the transilluminated ventral margin of the rat liver was observed and recorded by a video-microscope system. The volumetric flow rate in a liver sinusoid was calculated from the observed diameter of the sinusoid and the intra-sinusoid erythrocyte flow velocity. 2. The topographic distribution of liver sinusoids within an arbitrary boundary of a microscopic field of terminal liver microcirculation was observed and the total inflow and outflow in the field were determined. 3. Both vagus nerves at the lower end of the oesophagus were stimulated at supramaximal voltage. Vagal stimulation dilated the calibre of liver sinusoids and paradoxically diminished the erythrocyte flow velocity in each individual liver sinusoid, but the total volumetric flows in a microscopic field remained unchanged. 4. Vagal stimulation also increased the number of liver sinusoids in a microscopic field by opening previously closed liver sinusoids. This recruitment contributed two-thirds of the total increase of the sinusoidal capacity while the other one third was the result of distension of existing liver sinusoids.

Animals↗
PubMed1979

Stimulation and blockade of cholinergic receptors in terminal liver microcirculation in rats.

This study was designed to establish the existence of cholinergic vascular receptors in the terminal portion of the rat liver microcirculation. The liver microcirculation was observed in vivo by a transillumination technique through a television microscope. The changes in the caliber of the liver sinusoids were measured directly on the television screen. Infusion of the parasympathetic neurotransmitter acetylcholine into the portal venous circulation caused a concentration-dependent dilation of liver sinusoids. Similar dilatation effects were observed for other cholinergic receptor agonists. Atropine, the specific cholinergic receptor blocker, inhibited this dilator effect, displacing the acetylcholine concentration-effect curve to the right. In contrast, physostigmine, the cholinesterase inhibitor, caused displacement of the curve to the left. In conclusion, cholinergic receptors are present in the terminal portion of the liver microcirculation, subserving the functional role of vasodilatation.

Acetylcholine↗
PubMed1978

Microvascular responses to norepinephrine in skeletal muscle of cold-acclimated rats.

The microcirculation of the spinotrapezius muscle in normal and cold-acclimated (4 degrees C) rats was observed by an in vivo microscopic technique. The responses of the arterioles and venules in the skeletal muscle microcirculation to topical application of norepinephrine (NE) were recorded by a photomicrographic method. Results show that the skeletal muscle microcirculation possesses both alpha- and beta-adrenergic vascular receptors. Stimulation of the alpha-receptor results in vasoconstriction, and of the beta-receptor, vasodilatation. These microvascular responses are antagonized by specific alpha- and beta-adrenergic blockers. Cold-acclimation (4 degrees C) for 3 wk decreases the responses of the skeletal muscle microvessels to NE stimulation. This diminished sensitivity is due to an attenuation of the alpha-adrenergic receptor mechanism.

Acclimatization↗
PubMed1977

Adrenergic mechanisms in the hepatic microcirculation in the rat.

The in vivo hepatic microvascular bed of the rat was observed microscopically in the transilluminated liver and the diameter of the hepatic sinusoids was measured by serial photomicrography. Intraportal infusion of tyramine induced concentration-dependent constriction of the hepatic sinusoids, but also dilatation of the sinusoids when the dose was small. These effects were attributed to the release of endogenous noradrenaline which activated either alpha- or beta-adrenergic receptors and caused constriction, or dilatation, of the sinusoids respectively. Adrenaline and noradrenaline induced similar changes in the hepatic sinusoids as tyramine, while phenoxybenzamine induced dilatation, and propranolol constriction, of the sinusoids. All the above responses were abolished by pretreatment with reserpine. A possible noradrenaline-mediated basal vasomotor tone in the hepatic sinusoids for autonomic control of the blood flow in the sinusoids was postulated.

Animals↗