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Biomedical subjects

J B Scott

Publications and source records attributed to J B Scott.

At least 37 records · Page 2Linked to original sources

Carotid sinus reflex vasoconstriction in right coronary circulation of dog and pig.

This study was designed to evaluate the effects of the sympathetic nervous system on right ventricular and right coronary hemodynamics in the anesthetized vagotomized dog and pig during constant-pressure coronary perfusion. Carotid occlusion in the dog resulted in an increase in heart rate, aortic pressure, right ventricular dP/dt, and a sustained 13% decrease in right coronary artery blood flow and a 14% increase in coronary vascular resistance. This coronary vasoconstriction was not modified during beta-blockade with propranolol but was prevented by alpha- blockade with phentolamine. Similar hemodynamic data was obtained in the pig and, in addition, it was found that the O2 consumption of the right ventricle is low (4.8 +/- 0.4 ml O2.min-1.100 g-1) and is only slightly increased (5.l5 +/- 0.8 ml.min-1.100 g-1) during carotid occlusion. These data suggest that baroreflex-mediated sympathetic stimulation to the heart evokes only a minor increase in metabolic activity in the right ventricular myocardium so that the direct neural (alpha-vasoconstrictor) effect predominates over the metabolic vasodilator mechanism.

Animals↗

Flow through collapsible tubes at high Reynolds numbers.

The pressure-flow relationships of collapsible tubes were studied utilizing the Starling resistor model. Reynolds numbers much higher than previously reported were used to simulate high cardiac output states. Alterations which occur in vivo, including longitudinal tension, stretch, tubing diameter, length, and outflow resistance were also simulated and systematically investigated. The pressure-flow curves showed an initial rising phase, a plateau phase, as well as a late-rising phase which has not been reported previously. Self-induced oscillations occurred during the plateau phase and persisted throughout the late-rising phase. These perturbations were markedly increased by longitudinal tension and stretch, but were attenuated by increased diameter, length, and outflow pressure. These instabilities may prove to be an explanation for the "venous hum."

Animals↗

Systemic and digital vascular effects of intravenous histamine in the pony.

The effects of a 60-minute IV infusion of histamine (0.5 mg of histamine base/minute) on the systemic, pulmonary, and digital vasculature were investigated in mature ponies. Immediately after the start of histamine infusion, there were a transient decrease in systemic pressure lasting less than 1 minute and then a brief period of systemic hypertension. Systemic pressure then returned to preinfusion levels for the remainder of the infusion period. Pulmonary arterial pressure increased transiently coincident with systemic hypotension. Histamine increased cardiac output and decreased both total peripheral and pulmonary vascular resistances. In the digit, blood flow increased for the duration of the systemic hypertension, but was otherwise unchanged. Digital lymph flow and protein concentration were unchanged by histamine. Hematocrit increased significantly after 60 minutes of histamine infusion, but plasma and blood volumes were unchanged. Histamine caused cyanosis, hyperpnea, and sweating in all ponies. The effects of histamine given IV do not mimic the systemic and digital vascular effects of acute alimentary laminitis.

Animals↗

Effect of pulmonary venous pressure on steady-stage collateral resistance.

Steady-state collateral resistance (Rcoll), residual volume (RV), and lung pressure-volume (PV) relations were determined in an isolated perfused dog lung as pulmonary venous pressure (Ppv) was increased. Increased Ppv had no effect on the lung PV curve except for a significant increase in RV when Ppv equaled or exceeded 20 Torr. When compared to the value at Ppv = 5 Torr, significant decreases in Rcoll occurred when Ppv was raised to 15 Torr or above at transpulmonary pressure, PL = 0 cmH2O, to 20 Torr or above when PL = 2 cmH2O, and to 25 Torr or above when PL = 4 cmH2O. In most dogs the decrease in Rcoll with increased Ppv could be explained by increased lung volume.

Animals↗

Flow through collapsible tubes at low Reynolds numbers. Applicability of the waterfall model.

The applicability of the waterfall model was tested using the Starling resistor and different viscosities of fluids to vary the Reynolds number. The waterfall model proved adequate to describe flow in the Starling resistor model only at very low Reynolds numbers (Reynolds number less than 1). Blood flow characterized by such low Reynolds numbers occurs only in the microvasculature. Thus, it is inappropriate to apply the waterfall model indiscriminately to flow through large collapsible veins.

Blood Vessels↗

Evidence from bioassay studies indicating a role for adenosine in cardiac ischemic and hypoxic dilation in the dog.

Previous studies using bioassay demonstrated the presence of a vasoactive substance or substances in coronary sinus blood during myocardial reactive hyperemia which had, on bioassay, characteristics of adenosine and/or AMP. In the present studies, specific blockers were applied to an improved bioassay system to define more precisely the nature of the substance or substances and to determine whether it also appears during local cardiac hypoxia. In the anesthetized dog, coronary sinus blood was bioassayed in an isolated autologous kidney during reactive and hypoxic dilation. During reactive dilation, the bioassay kidney responded with a large resistance increase which was blocked by theophylline and adenosine deaminase and converted to a decrease by adenosine autoblockade. The same was true for hypoxic dilation, except in this instance, only adenosine deaminase reduced the response (40%). Theophylline and adenosine autoblockade eliminated responses of the bioassay organ to both exogenous adenosine and exogenous AMP, but adenosine deaminase was specific for adenosine. These results confirm that one or more vasoactive substances appear in sinus blood in vasoactive quantities during cardiac reactive dilation, and that the peak concentration correlates roughly with the peak flow. In addition, they show that this also is the case for hypoxic dilation. More importantly, they demonstrate that the substance almost certainly is adenosine in the case of reactive dilation, and that increased adenosine levels also are present during hypoxic dilation, but in addition, suggest that AMP sometimes appears in coronary sinus blood during severe cardiac hypoxia in the dog heart.

Adenosine↗

Antagonism of histamine edema formation by catecholamines.

Histamine (4 microgram base/min) infused into the brachial artery for 60 min greatly increases skin lymph flow and lymph protein concentration in forelimbs perfused either naturally or at constant inflow. In contrast, the simultaneous intrabrachial infusion of histamine and norepinephrine (4 microgram base/min of each) or histamine and isoproterenol (4 microgram base/min and 3 microgram/min, respectively) for 60 min failed to alter lymph protein concentration in forelimbs perfused either naturally or at constant inflow. The edema in forelimbs naturally perfused by histamine (4 microgram base/min) infused into the brachial artery for 60 min was also greatly reduced by the simultaneous histamine-catecholamine infusions. Phentolamine (in concentrations that antagonize the vascular actions of norepinephrine) failed to prevent the antagonism of histamine protein efflux by norepinephrine. Hence, it must be concluded that catecholamines antagonize the protein efflux by locally infused histamine, independent of alpha-adrenergic receptor activity.

Animals↗

Cardiovascular, acid-base, electrolyte, and plasma volume changes in ponies developing alimentary laminitis.

Twelve Shetland ponies were fed a high-starch ration. Seven ponies which had a transitory metabolic acidosis developed laminitis 56 hours (+/- 3.5, SEM) after overfeeding. These ponies also developed persistent hypokalemia, hyperthermia, and increased heart rate 24 hours before the onset of lameness. Serum sodium, serum chloride, hematocrit, plasma volume, and blood volume were unchanged. At the onset of clinical signs of laminitis, cardiac output and blood pressure increased, but total peripheral resistance was unchanged. None of the measured or calculated values predicted the onset of laminitis. Hypertension appeared to be a response to, rather than a cause of, lameness. Three of the remaining ponies apparently died of shock 29.3 +/- 2.7 hours after overfeeding. All 3 had severe metabolic acidosis; decreased cardiac output, systemic arterial pressure, and plasma volume; and increased hematocrit, total peripheral resistance, and pulmonary vascular resistance. The 11th pony was unaffected and the 12th pony was euthanatized.

Acid-Base Imbalance↗

Effects of systemically infused histamine on transvascular fluid and protein transfer.

Histamine (4-64 microgram base/min) infused into the brachial artery clearly promotes edema formation in forelimbs perfused at natural flow. In contrast, intravenously administered histamine, even in blood concentrations exceeding those achieved by local infusion, not only fails to promote edema formation, but rather causes net extravascular fluid reabsorption. In this study, high concentrations of histamine were infused into the left ventricular chamber to bypass the pulmonary circuit. Histamine (400-800 microgram base/min) infused into the left ventricle of the heart for 90 min produced marked hypotension and only very slight increases in forelimb skin lymph flow and lymph protein concentration and failed to produce visible signs of edema. Thus the differential actions of local and intravenous histamine on lymph flow, protein efflux, and fluid fluxes cannot be explained by uptake or destruction of histamine in the lung during intravenous infusions of this agent. It seems more likely that they result from different actions on microvascular pressure, surface area, and/or permeability to plasma proteins. Prior hypotension produced either by acetylcholine, systemically infused histamine, or arterial hemorrhage almost completely prevents the increase in skin lymph flow and lymph protein concentration by histamine infused locally into the brachial artery, even in forelimbs perfused at constant flow.

Animals↗

An extracorporeal shunt for the measurement of coronary flow in the closed-chest dog.

An extracorporeal shunt circuit interposed between the left carotid artery and the left coronary ostium employs an electromagnetic flowmeter to measure coronary blood flow in the closed-chest anesthetized dog. Flow may be measured with the animal's arterial pressure as the driving force; introduction of a roller pump, or a roller pump and a negative feedback pressure controller allows for constant flow or constant pressure modes. During occlusion of the circuit or cessation of pump flow, retrograde coronary blood flow can be collected for measurement. The construction of the circuit is relatively simple and inexpensive, using common laboratory materials and a commercially available electromagnetic flowmeter and probe.

Animals↗

Digital vascular responses and permeability in equine alimentary laminitis.

Digital vascular pressures, blood flow, and vascular resistances were measured in 11 control ponies and in 8 animals (7 ponies and 1 horse) affected with laminitis created by feeding a high starch ration. Animals with laminitis had increased digital blood flow, increased arterial, small vein, and large vein pressures, and decreased vascular resistances. Comparison of digital lymph flow rates and protein concentrations in animals with laminitis and control animals revealed no differences. Digital vascular responses of the 2 groups to acetylcholine, epinephrine, histamine, or serotonin also did not differ. Thus, the increased digital blood flow observed in animals with laminitis could not be attributed to altered responsivenss to the previously mentioned vasoactive agents. The studies also provided no evidence for increased capillary permeability in digits of animals affected with laminitis.

Acetylcholine↗

Reflex vascular responses in kidney, ileum, and forelimb to carotid body stimulation.

Reflex vascular responses to local carotid chemoreceptor stimulation with hypoxic-hypercapnic, hypoxic, or hypercapnic blood were investigated in pentobarbitalized dogs. Bilaterally isolated carotid chemoreceptors were perfused via an extracorporeal lung circuit. Oxygen and carbon dioxide tensions of blood perfusing the carotid bodies were altered by ventilating the isolated lung with various O2-CO2 mixtures. Ventilation of the whole animal maintained normal systemic O2 and CO2 tensions. Perfusion pressures of the isolated kidney, ileum, forelimb, gracilis and hindpaw were measured during constant-flow perfusion. Carotid chemoreceptor stimulation with hypoxic-hypercapnic blood before vagotomy increased renal vascular resistance but caused no change in intestinal or forelimb resistance. Following vagotomy, hypoxic-hypercapnic, hypoxic, or hypercapnic carotid body stimulation increased renal, intestinal, and forelimb vascular resistance. Forelimb skin and muscle vascular beds contributed about equally to the increase in forelimb resistance. Gracilis muscle and hindpaw resistance also increased during hypoxic-hypercapnic stimulation after vagotomy.

Animals↗

Interaction of O2 and CO2 in sustained exercise hyperemia of canine skeletal muscle.

The relative contribution of O2 and CO2 to the metabolic control of blood flow in long-term exercise was examined in the denervated gracilis muscle of the anesthetized dog. The data show that 1) on initiation of heavy exercise, the effluent blood PO2 and pH fall markedly and then rise slowly but remain depressed relative to control during 60 min of exercise hyperemia, while the initial increases in [K+] and osmolality rapidly approach and eventually reach preexercise levels. 2) The enhanced vasodilator activity of venous blood from exercising muscle is attenuated when effluent blood PO2 or pH is corrected to preexercise levels; it is completely abolished when both are corrected. 3) Induced reduction PO2 or pH in the arterial inflow, and thus venous outflow, of resting muscle produces a fall in resistance; simultaneous reductions of both to levels seen in heavy exercise produce a fall in resistance to near that observed during exercise. Since the enhanced vasodilator activity of venous blood from the contracting muscle was abolished by simultaneous correction of the PO2 and pH, it seems likely that these factors, acting directly or indirectly, are the principal chemicals responsible for the maintenance of the vasodilation seen in canine skeletal muscle during heavy exercise.

Animals↗