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Biomedical subjects

A Tucker

Publications and source records attributed to A Tucker.

At least 127 records · Page 7Linked to original sources
PubMed1984

Cardiovascular adjustments to various degrees of acute isocapnic hypoxia in dogs.

Cardiovascular responses to various degrees of acute isocapnic hypoxia were determined in spontaneously breathing anesthetized dogs. Cardiac output (CO), heart rate, stroke volume, systemic blood pressure, and systemic vascular resistance were measured at frequent intervals during 20-minute exposures to hypoxia (7% to 17% O2). Cardiac output increased during hypoxia, with the most severe degree of hypoxia producing the greatest increase in CO. Stroke volume increased significantly (P less than 0.05), whereas tachycardia was inconsistent. Systemic vascular resistance declined with hypoxia, with the greatest vasodilation observed with the most severe hypoxia. During the first 3 minutes of hypoxia, CO increased at all 3 degrees of hypoxia, whereas systemic vascular resistance remained relatively unchanged during this initial portion of the hypoxic exposures. Prevention of the hypoxia-induced increase in CO by partial caudal vena caval obstruction (reducing venous return) resulted in a maintenance of systemic vascular resistance at or above the base-line value before hypoxia. Seemingly, hypoxia can increase CO before systemic vasodilation is evident and systemic vasodilation depends, partly, on the increase in CO.

Acute Disease↗
PubMed1983

Density and ultrastructure of mast cells in lung vessels of aging rats exposed to and recovering from chronic hypoxia.

A decrease in pulmonary vascular responsiveness in aging animals during exposure to chronic hypoxia has been previously reported; however, morphological documentation is lacking. Lungs from young (3-5 months) and aging (12-14 months) Sprague-Dawley rats, exposed to and recovering from chronic hypoxia, were morphometrically analyzed at the light-microscopic level for changes in perivascular mast cells, and at the electron-microscopic level for cellular alterations. While young rat lungs showed proliferation of mast cells around elastic and muscular pulmonary arteries and arterioles, perivascular mast cell density in lungs of aging rats was significantly greater than in young rat lungs. At the ultrastructural level, perivascular mast cells in aging hypoxic rats showed numerous profiles of cellular extensions that contained remnants of discharged secretory vesicles. The results suggest that increased proliferation of perivascular mast cells as well as increased secretory activity of vasoactive substances in aging animals might represent a humoral determinant of the hyporesponsiveness of pulmonary vessels that occurs with increasing age during chronic hypoxia.

Aging↗
PubMed1983

Cardiopulmonary response to acute altitude exposure: water loading and denitrogenation.

In order to determine if a positive water balance would impair cardiovascular and ventilatory adjustments during acute altitude exposure, six healthy male subjects were exposed to 4570 m for 2 h with and without water loading. No significant differences in any of the measured variables were observed between normal and overhydrated subjects. In order to determine if rapid ascent to altitude involves the formation of nitrogen bubbles which could impair gas exchange, 11 subjects were exposed to 4570 m with and without denitrogenation (by breathing 100% O2 prior to ascent) and 6 subjects were exposed to normobaric hypoxia (14% O2). Prior O2 breathing reduced the hyperventilatory and alkalotic responses to altitude, tachycardia did not develop, and systemic blood pressure fell, despite the fact that arterial desaturation was similar to that during the untreated altitude exposure. Reduced urine flow and increased urine osmolality were observed in two subjects at 4570 m, but these changes were not observed in the same subjects after O2 breathing. Breathing 14% O2 also produced the same degree of arterial desaturation but the hyperventilatory response was significantly greater than in the prior altitude exposures. Heart rate, blood pressure, and urine flow and osmolality were not altered and symptoms of altitude illness were minimal. Thus, neither of our hypotheses proved to be correct; however, we did observe a prolonged effect of O2 breathing on the hypoxic ventilatory response, and a potential effect of hypobaria on ventilation.

Acclimatization↗
PubMed1983

Chemical sympathectomy and serotonin inhibition reduce monocrotaline-induced right ventricular hypertrophy in rats.

Young male rats were administered monocrotaline (40 mg/kg, s.c.) either after chemical sympathectomy with 6-hydroxydopamine (6-OHDA, 100 mg/kg), after serotonin synthesis inhibition with p-chlorophenylalanine (PCPA, 500 mg/kg), or after saline injection. Monocrotaline rats exhibited a loss of body weight, marked right ventricular hypertrophy (RVH), increased pulmonary vascular muscularization, but no change in left ventricular weight or hematocrit at 20 days post-monocrotaline. Pretreatment with 6-OHDA or PCPA reduced the degree of RVH; however, neither 6-OHDA nor PCPA pretreatment prevented or reduced the pulmonary vascular muscularization associated with monocrotaline. Control, 6-OHDA-, and PCPA-treated rats exhibited only changes in ventricular weights associated with changes in their body growth. Thus, the sympathetic nervous system and serotonergic mechanisms seem to be involved in the development of monocrotaline-induced right ventricular hypertrophy, but are not responsible for the pulmonary vascular lesion.

Animals↗
PubMed1982

Altered vascular responsiveness in isolated perfused lungs from aging rats.

Systemic vascular hyporesponsiveness has been well documented in aged rats, but a similar decreased vasoreactivity of the pulmonary vasculature has not been reported. Isolated lungs from young (3-5 months) and middle-aged (12-14 months) rats were perfused with whole blood and challenged alternately with alveolar hypoxia, angiotensin II, and 5-hydroxytryptamine. Hypoxic pulmonary vasoconstriction was less in the aging rats during both 5-min and 10-min hypoxic exposures. Likewise, log-dose response curves for angiotensin II and 5-hydroxytryptamine were right-shifted in the aging rats, indicating decreased responsiveness to the vasoactive agents. Since the vascular responses to all three vasoconstrictors were lower in the older animals, a generalized pulmonary vascular hyporeactivity with advancing age is suggested.

5-Hydroxytryptophan↗
PubMed1982

Pulmonary and systemic vascular actions of tolazoline in anesthetized dogs.

The cardiovascular actions of tolazoline are poorly understood. Therefore, we administered tolazoline (2 mg kg-1, IV) to anesthetized adult dogs and puppies. Tolazoline induced transient pulmonary and systemic pressor responses, transient systemic vasoconstriction and pulmonary vasodilation, and transient hypoxemia and acidosis in pentobarbital anesthetized dogs. None of these responses were evident during a second injection of tolazoline, indicating either the development of tachyphylaxis or a secondary antagonistic property of tolazoline. These responses to tolazoline were also prevented by alpha adrenergic blockade. Histamine H1 - and H2-receptor blockade sustained the transient pulmonary and systemic pressor and systemic vasoconstrictor responses to tolazoline. Thus, tolazoline appears to activate both alpha and histamine receptors in the pulmonary and systemic vascular beds of the anesthetized dog. In anesthetized puppies, tolazoline induced a slight pulmonary pressor response, marked bradycardia, and systemic hypertension. The present findings confirm the pharmacological complexity of tolazoline and suggest that anesthesia, age, and pulmonary vascular tone are important factors in determining the cardiovascular responses to tolazoline.

Anesthesia↗
PubMed1982

Fine structural changes in pulmonary veins of chronically hypoxic mice.

The pulmonary veins of male Swiss albino mice, exposed to simulated high altitude (380 mm Hg) for four weeks were studied for structural alterations. Endothelial cells contained invaginated nuclei and an accumulation of vesicles on the adluminal surfaces. In the subendothelial region, cells which contained filaments and dense bodies were noted. Increased muscular contraction, evidenced by decrease in the width of the I-band of the sarcomere, caveolae formation, sarcolemmal invaginations, and glycogen deposition were the most evident changes in the cardiac muscle layer. These alterations were interpreted as possible morphologically adaptive changes of pulmonary venous pulmonary vasoconstriction in response to increased metabolic demands as a result of changes in pulmonary hemodynamics with chronic hypoxia.

Altitude↗
PubMed1982

Glycogen localization in pulmonary vascular smooth muscle of chronically hypoxic rats.

The pulmonary trunk, muscular arteries, and arterioles of male Sprague-Dawley rats exposed to simulated high altitude hypoxia (380 mm Hg) for six weeks were studied for glycogen localization. As early as three days exposure time, glycogen particles were mobilized in the smooth muscle cells of muscular arteries and arterioles. Weekly sacrifice of animals showed increasing preferential accumulation of glycogen, near the sarcoplasmic reticulum, in the subsarcolemmal region, adjacent to micropinocytotic vesicles, and near the mitochondria in the smooth muscle cells of muscular arteries and arterioles. However, in the smooth muscle cells of the pulmonary trunk and newly muscularized vessels (arteries and arterioles), glycogen storage was not readily noted. These results suggests that the vascular energetics responsible for maintaining the pulmonary hypertensive state differ depending on the class of vessel. Also the muscular pulmonary arteries and arterioles which exhibited the greatest change in glycogen metabolism, may be primarily responsible for the maintenance of pulmonary hypertension.

Altitude↗
PubMed1981

Vascular responsiveness in isolated rat lungs is inversely related to blood flow.

The pulmonary pressor responses to prostaglandin F2 alpha, 5-hydroxytryptamine, angiotensin II, and alveolar hypoxia were significantly increased when blood flow was reduced from 10 to 5 ml/min in isolated perfused rat lungs. When blood flow was increased from 10 to 15 ml/min, the pressor responses to hypoxia and angiotensin II were reduced. We speculated that the changes in pulmonary vascular reactivity with alterations in blood flow were due to vessel distension and changes in vessel wall-to-lumen ratios and consequent effects on mechanical contractile efficiency.

Angiotensin II↗
PubMed1981

Early management of laryngeal injuries.

The results of acute laryngeal trauma sustained by 44 patients are reported. Three major aetiological groups are identified: road traffic accidents, blunt injury and penetrating injury. Road traffic accidents appear to produce severe injury, but the long-term follow-up results are similar to those laryngeal injuries which were not recognized initially and who developed a chronic stenosis. The blunt injury group sustained less forceful trauma; 14 of the 18 were treated conservatively and all patients had a good result. The majority of the penetrating injury group developed good breathing and a good voice following operation. Some of the technical expertise normally used to treat chronic laryngeal stenosis has been included in this series to good effect.

Accidents, Traffic↗
PubMed1980

Pulmonary vascular actions of the antihistamine oxatomide during hypoxia.

The role of histamine in the cardiovascular responses to hypoxia has not been resolved. Oxatomide, an orally active anti-allergic drug, has been reported to inhibit mast cell discharge and to antagonize any histamine which is released. This drug was administered to six dogs to determine the effect of inhibiting histamine release on the pulmonary vascular and cardiac responses to hypoxia. Oxatomide potentiated hypoxic pulmonary vasoconstriction, but reduced the cardiac output and stroke volume responses to hypoxia. These findings suggest that histamine is released during hypoxia and acts to oppose hypoxic vasoconstriction. In addition, histamine released from peripheral tissues may play an important role in mediating the increased cardiac output observed during acute hypoxia. By utilizing infusions of histamine, oxatomide was also found to be a histamine H1-receptor antagonist.

Animals↗
PubMed1979

Pulmonary and systemic vascular responses to hypoxia after chemical sympathectomy.

Mongrel dogs were anesthetised and exposed to acute hypoxia (8% or 10% O2 for 10 min) before and again either 2 or 12 days after 6-hydroxydopamine (6-OHDA, 80 mg . kg-1) pretreatment. Under normoxic conditions, systemic arterial pressure and systemic vascular resistance were reduced 2 days post 6-OHDA, but only systemic resistance was reduced 12 days post 6-OHDA. Pulmonary vascular haemodynamics were unchanged by 6-OHDA under normoxic conditions. No changes in the cardiac output, pulmonary, and systemic haemodynamic or ventilatory responses to hypoxia were observed 2 days post 6-OHDA, although the heart rate response was reduced. Similarly, 12 days post 6-OHDA, reponses to hypoxia were unchanged except for a reduced systemic pressor response. A significant transient fall in systemic arterial pressure was observed at the start of the hypoxic exposure 2 days post 6-OHDA. The ventilatory responses to hypoxia appeared to be influenced very little by the sympathetic nervous system. The results indicate that pulmonary vascular resistance is under little sympathetic influence, and that hypoxic pulmonary vasoconstriction is not mediated by the sympathetic nervous system.

Animals↗
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↗
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

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↗