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Biomedical subjects

H M Thomas

Publications and source records attributed to H M Thomas.

At least 91 records · Page 5Linked to original sources
PubMed1982

Strength of hypoxic vasoconstriction determines shunt fraction in dogs with atelectasis.

We investigated the degree to which strength of pulmonary hypoxic vasoconstriction affects perfusion of pulmonary shunt pathways in acute atelectasis. In 17 intact supine dogs (anesthetized, paralyzed, and ventilated) we produced left lower lobe atelectasis by occluding the lobar bronchus during oxygen inhalation. Subsequently, shunt fraction (reflecting perfusion of that lobe) was measured using an SF6 infusion while the dogs breathed room air; the mean was 26% (range 14-40%). Pulmonary pressor response to hypoxia was assessed in 13 dogs using the increase in pulmonary end-diastolic gradient (PDG) produced by inhalation of 10% oxygen. Those animals with the largest increase in pulmonary diastolic gradient had the smallest shunt fraction while breathing room air, whereas those with the smallest response had the largest shunt fraction. The contribution of local hypoxia to vasoconstriction in the shunt pathway was assessed in 13 dogs breathing room air by measuring the increase in shunt fraction produced by infusing prostaglandin E1 (PGE1). Those with the largest increase in shunt fraction had the smallest pre-PGE1 shunt fraction. Thus the strength of pulmonary vascular reactivity to hypoxia markedly influences the degree of vasoconstriction in shunt pathways and is a major determinant of shunt pathway perfusion.

Acute Disease↗
PubMed1982

Experimental studies on the effects of physostigmine and of isoproterenol on toxicity produced by tricyclic antidepressant agents.

The IV infusion of nortriptyline and amitriptyline (0.5 mg/kg/min) in anesthetized cats produced death within 60 min of continuous infusion. The tricyclic antidepressant agents produced a quinidine-like depression of the myocardium characterized by bradycardia, depression of contractile force, conduction defects, bradyarrhythmias, and hypotension. The simultaneous IV infusion of isoproterenol (0.1 microgram/ kg/min) produced significant protection against death produced by the TCA drugs. The results suggested that the positive chronotropic, inotropic, and dromotropic actions of isoproterenol may all be contributory factors in the protection. Pretreatment with a large dose of physostigmine (0.2 mg/kg) produced a rightward shift of the nortriptyline time-mortality curve. The small degree of protection produced by the anticholinesterase drug may be due to a respiratory stimulant action rather than a cardiac action.

Amitriptyline↗
PubMed1980

Chronic persistent pulmonary embolism. Report of three cases.

Nonresolution of acute pulmonary embolism and resultant chronic persistent pulmonary occlusion is uncommon; documentation of its occurrence in patients receiving anticoagulants is sparse. We report three cases with hemodynamic data and follow-up of up to seven years. All patients had mild to moderate dyspnea on exertion. All patients had normal resting pulmonary artery pressures; two patients demonstrated pulmonary hypertension with exercise. One patient underwent successful thromboendarterectomy but had subsequent reocclusion secondary to in situ thrombosis. With all patients receiving long-term anticoagulant therapy, there was no clinical recurrence of embolization or progression of symptoms. Patients with chronic persistent pulmonary embolism should be identified and should receive long-term follow-up. Therapy aimed at prevention of recurrent embolization is required. Pulmonary thromboendarterectomy is indicated for selected patients.

Adult↗
PubMed1978

Echocardiographic manifestation of flail right and noncoronary aortic valve leaflets.

Echocardiographic studies provide information useful in determining the etiology and location of aortic valvular lesions, but assessment of their severity remains difficult. We report the findings in two patients with surgically confirmed right (case 1) and noncoronary (case 2) flail aortic leaflets in whom dense echoes filled the aortic root in systole, only to move from this position into the left ventricular outflow tract during diastole. This echocardiographic finding is a clinically useful noninvasive indicator of rupture of the right or noncoronary aortic cusp and dictates a need for early surgery.

Adult↗
PubMed1977

The effect of granulomatous pulmonary disease in dogs on the response of the pulmonary circulation to hypoxia.

We studied the effect of diffuse granulomatous pulmonary disease on the reponse of the pulmonary circulation to hypoxia in two series of experiments in intact dogs. First, in animals with unilateral disease, vasoconstriction in the diseased lung was compared to that in the contralateral control lung. Second, in animals with bilateral disease, the vasoconstriction of pulmonary shunt pathways was compared to that of the rest of the pulmonary vasculature. We assessed vasoconstriction in each study by measuring the distribution of pulmonary blood flow between the test and control set of vessels during 21 and 12% oxygen breathing. In the first set of experiments, we measured apportionment of the blood flow between the two lungs by bronchospirometry and the krypton bolus method. In normal dogs, hypoxia did not shift blood flow systematically from one lung to the other. In 10 dogs with unilateral disease, general hypoxia increased the proportion of blood flow to the diseased lung. The mean percent of blood flow to the left lung in eight dogs with disease in that lung rose from 29% during air breathing to 32% (P < 0.001). In the second set of experiments, we measured apportionment of the blood flow between shunt pathways and gas-exchanging pathways by a constant infusion of radio-active krypton and the standard shunt formula. In eight dogs with bilateral disease, hypoxia consistently increased the flow through shunt pathways, from a mean value of 10% of pulmonary blood flow to 14% (P < 0.005).Thus, diffuse granulomatous disease causes a decreased vasoconstrictive response to hypoxia both in diseased, gas-exchanging regions and in shunt pathways. In proliferative interstitial pulmonary disease, generalized hypoxia causes shifts in pulmonary blood flow which do not ameliorate but rather worsen the hypoxemia of systemic arterial blood.

Animals↗