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Biomedical subjects

J T Reeves

Publications and source records attributed to J T Reeves.

At least 181 records · Page 10Linked to original sources
PubMed1979

Pulmonary vascular reactivity in the spontaneously hypertensive rat.

We examined the pulmonary vascular reactivity of normotensive rats (NR) and spontaneously hypertensive rats (SHR) to acute and chronic pressor stimuli. In rats kept at low altitude (1,520 m), SHR had a slight degree of right ventricular hypertrophy, but there was no difference between SHR and NR in either right ventricular systolic pressure or pulmonary artery wall thickness. When compared to blood-perfused lungs from low altitude NR, lungs from low altitude SHR were normoresponsive to acute airway hypoxia, hyporesponsive to intra-arterial angiotensin II, and hyperresponsive to intra-arterial prostaglandin F2alpha. After exposing rats to simulated high altitude (4--6 weeks at 4,270 m) to induce hypoxic pulmonary hypertension, SHR had a higher right ventricular systolic pressure, a greater degree of right ventricular hypertrophy, and more pulmonary artery medial thickening than did NR. The results indicate that although the pulmonary vasculature of SHR does not become hypertensive spontaneously, it might have an increased tendency to develop hypertension when exposed to an appropriate stimulus, i.e., chronic airway hypoxia.

Altitude↗
PubMed1979

Ultrasonic transesophageal measurement of hemodynamic parameters in humans.

A noninvasive method has been developed to monitor centerline blood velocity waveforms and vessel diameter in the descending aorta and pulmonary artery of conscious humans. An esophageal endoscope fitted with miniature ultrasound transducers is swallowed and positioned in the esophagus near vessels of interest. The transducers are connected to ultrasound Doppler velocimeters and echotrack instrumentation to obtain the pertinent hemodynamic parameters. This paper describes the design and fabrication of the esophageal ultrasound transducers and the techniques involved in human applications. In addition, blood velocity and wall motion measurements obtained in conscious men at rest and during exercise are described.

Aorta, Thoracic↗
PubMed1978

Decreased pulmonary vascular responses in dogs with increased pulmonary blood flow.

We wished to determine whether high pulmonary blood flow alters the pulmonary vascular responses to the vasoconstrictors, hypoxia and prostaglandin F2alpha (PGF2alpha). Acute or chronic left pulmonary artery (PA) occlusion was performed in dogs in order to create high pulmonary blood flow conditions. Right lung pulmonary vascular resistance (PVR) during normoxia was reduced by both acute and chronic left PA occlusion, suggesting passive vasodilatation. Increases in right lung PVR induced by hypoxia (10--15% O2) and PGF2alpha (0.8-4 microgram kg-1 min-1) were attenuated both in acute and chronic left PA occluded dogs. Since the reductions in responsiveness were similar with acute and chronic increases in blood flow, the attenuating effect of high blood flow was not dependent upon morphologic changes in the vasculature. Pulmonary vascular responsiveness was probably reduced in these animals due to their dilated pulmonary vascular beds, consequent to the increased blood flow, thereby decreasing the effectiveness of smooth muscle contraction.

Animals↗
PubMed1978

Lungs from chronically hypoxic rats have decreased pressor response to acute hypoxia.

We measured pressor responses in blood-perfused lungs from rats kept at low altitude (LA, 1,520 m) and from rats exposed to simulated high altitude (HA, 4-6 wk at 4,270 m) to see if lungs from chronically hypoxic rats were hyper- or hyporeactive to acute airway hypoxia. HA lungs had bigger pressor responses to intra-arterial angiotensin II, prostaglandin F2alpha, and norepinephrine, but smaller responses to airway hypoxia than did LA lungs. The dose-response curve to hypoxia in HA lungs was shifted to the right of that in LA lungs. Thus, HA lungs were hyperreactive to intra-arterial agonists, but were hyporeactive to acute airway hypoxia. In contrast, additional experiments with rats that had been exposed to HA for 5 wk and then returned to LA for 3 days showed that the lungs from such post-HA rats were hyperreactive to acute airway hypoxia. The decreased pressor responsiveness to acute hypoxia in lungs from chronically hypoxic rats could have been due to an increased activity of some endogenous vasodilator or to some abnormality in the mechanism that couples hypoxia to contraction of the vascular smooth muscle.

Acclimatization↗
PubMed1978

Potentiation of hypoxic pulmonary vasoconstriction by ethyl alcohol in dogs.

Pulmonary and systemic hemodynamics and arterial blood gases were measured in anesthetized and mechanically ventilated dogs before and after oral or intravenous administration of ethanol. Increases in mean pulmonary artery pressure and pulmonary vascular resistance occurred. Platelet antiserum-induced thrombocytopenia inhibition of prostaglandin synthesis with meclofenamate, or alpha-adrenergic blockade did not alter the pulmonary pressor response to ethanol. However, the increase in resistance following ethanol was abolished by hyperoxia and potentiated by hypoxia. Thus, it appears that the effect of ethanol is to augment hypoxic pulmonary vasoconstriction, whereas ethanol per se has no independent pulmonary pressor activity.

Administration, Oral↗
PubMed1978

Cold-induced pulmonary hypertension in cattle.

The frequency with which cattle develop right-heart failure during the winter at high altitude suggested that cold might contribute to hypoxic pulmonary hypertension. Indeed in a preliminary study conducted out-of-doors during early Spring, two calves with known hyperreactive pulmonary vessels showed elevated pulmonary arterial pressures attributed to their prior exposure to nighttime cold (-5 degrees C). In a second study five hyperreactive calves had increases in mean pulmonary arterial pressure from 29 to 45 Torr (+ 55%) during 48 h of exposure to cold (0 to -5 degrees C) in a climatic chamber. Three calves with less reactive lung vessels increased their pressures from 25 to 36 Torr (+ 44%). In a more complete study, six calves selected as potential hyperresponders showed increases in pulmonary arterial pressure (+ 60%), blood flow (+ 18%), and vascular resistance (+ 38%) during 48 h of cold exposure. Arterial PO2 decreased (-10 Torr) and PCO2 rose (+6 Torr) suggesting hypoventilation. Oxygen breathing returned pulmonary pressures and resistance to near control values, suggesting that cold had induced a hypoxic pulmonary vasoconstriction and an increased blood flow. Thus, a cold produced pulmonary hypertension in cattle at the modest altitude of 1,524 m and the pressor responses were greater in calves with more reactive lung vessels.

Altitude↗
PubMed1978

Lung mast cells and hypoxic pulmonary vasoconstriction in cats.

An attempt was made to reduce or eliminate lung mast cells in order to determine the involvement of mast cells in hypoxic pulmonary vasoconstriction. Anesthetized cats were exposed to acute hypoxia (10% O2) 20-24 h after no pretreatment, after total lung irradiation (3,000 r), after intravenous nitrogen mustard, or after combined lung irradiation and nitrogen mustard. None of the treatments reduced total or perivascular lung mast cell density, or reduced the pulmonary vasoconstrictor response to hypoxia. However, an inverse relationship between lung mast cell density and the pulmonary pressor response to hypoxia was observed. These results suggest that the presence of more lung mast cells may oppose hypoxic pulmonary vasoconstriction.

Animals↗
PubMed1978

Diagnosis of airflow obstruction at high altitude.

Using predicted sea level values for spirometry done at high altitude, underestimation of airway obstruction may result. We therefore established spirometric normal values for an altitude of 3,100 m for white men.

Adolescent↗
PubMed1978

Pulmonary vascular effects of endotoxin in leukopenic dogs.

We have demonstrated previously that in the dog, small doses of endotoxin abolish the pulmonary vasoconstrictor reponse to hypoxia, apparently by stimulating the production of a vasodilator prostaglandin. We previously ruled out platelets as mediators of this endotoxin effect. To evaluate leukocytes as possible mediators, we rendered dogs leukopenic by means of a leukocyte antiserum. However, this did not modify the inhibitory effect of endotoxin on hypoxic pulmonary vasoconstriction. Hence, neither leukocytes nor platelets appear to mediate the endotoxin effect. In the near absence of both platelets and leukocytes, the endotoxin effect can be prevented by inhibiting prostaglandin synthesis with meclofenamate. This suggests that endotoxin prevents hypoxic pulmonary vasoconstriction by acting on the systemic circulation or on the lung (possibly directly on the pulmonary blood vessels) to stimulate the production of a vasodilator prostaglandin.

Animals↗
PubMed1978

Platelet-mediated pulmonary hypertension and hypoxia during pulmonary microembolism: reduction by platelet inhibition.

The literature indicates that vasoactive substances released from platelets contribute to the pulmonary pressor response and hypoxemia during pulmonary microembolism. Hence, removal of the platelets or inhibition of their function should reduce these effects. The purpose of this study was, therefore, to investigate the pulmonary effects of experimental embolism with glass beads in dogs rendered thrombocytopenic with platelet antiserum and to compare these effects to the effects in dogs pretreated with sulfinpyrazone (Anturane) or heparin, both substances that affect the function of platelets, probably by inhibiting the release of platelets. In all three groups the pulmonary hypertension was reduced by more than half, and hypoxemia was lessened or abolished. The results of this study indicate the platelets contribute to the effects of pulmonary microembolism and that administration of sulfinpyrazone or heparin reduces the embolism-induced pulmonary hypertension to the same extent as the depletion of platelets. Platelet-inhibiting drugs might therefore be useful prophylactically in human pulmonary microembolism.

Animals↗
PubMed1977

Reduction of bovine pulmonary hypertension by normoxia, verapamil and hexoprenaline.

In calves with hypoxic pulmonary hypertension, resistance was reduced by 40 +/- 3% with normoxia, 19 +/- 4% with verapamil, and 60 +/- 1% with hexoprenaline. It is possible that the increased resistance during normoxia is due to partly to vasoconstriction rather than solely to vascular thickening, and that the vasoconstriction is due to an abnormality in calcium metabolism by the hypertensive vasculature.

Airway Resistance↗
PubMed1977

Vascular actions of histamine H1- and H2-receptor agonists in dogs and cats.

Systemic and pulmonary vascular responses to infusions of histamine, 2-methylhistamine (2-MeH), and 4-methylhistamine (4-MeH) were determined. In dogs, H1-receptor stimulation with 2-MeH induced pulmonary vasoconstriction, and a decrease in cardiac output. H2-receptor stimulation with 4-MeH induced pulmonary and systemic vasodilation, tachycardia, and an increase in cardiac output. In cats, 2-MeH caused slight pulmonary vasoconstriction and 4-MeH caused vasodilation. Both H1- and H2-receptors mediated the systemic vasodilation, tachycardia, and increase in cardiac output observed in cats.

Animals↗
PubMed1977

Histamine H1- and H2-receptors in the cat and their roles during alveolar hypoxia.

We sought to define the roles of H1-and H2-receptors in the cat and to evaluate the roles of these receptors during alveolar hypoxia. In pentobarbital anesthetized cats, we found that histamine infusion (1.1 microgram/kg/min for 3 min) increased cardiac output and decreased pulmonary and systemic vascular resistances. However, when cardiac output was held constant, histamine infusion induced pulmonary vasoconstriction. Histamine infusions after H1-and H2-receptor blockade (chlorpheniramine and metiamde, respctively) indicated that H2-receptors mediated systemic vasodilatation. In the lung, H1-receptors mediated vasoconstriction, and H2-receptors mediated vasodilatation. Hypoxia (10% O2) caused large increases in pulmonary vascular resistance which were not blocked by H1-, H2-, or combined H1- and H2-receptor blockade. In the intact cat, histamine does not appear to mediate hypoxic pulmonary hypertension.

Animals↗