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Biomedical subjects

P C Russell

Publications and source records attributed to P C Russell.

7 recordsLinked to original sources
PubMed2000

Provision of influenza and pneumococcal vaccines to injection drug users at a syringe exchange.

The objective of this study was to evaluate the feasibility, acceptance, and utility of administering influenza and pneumococcal vaccines to active injection drug users at a syringe exchange program (SEP) in New York City. Influenza and pneumococcal vaccines were offered for 1 month. Data on demographics, health status, vaccine awareness, and prior vaccination status were collected using a staff-administered questionnaire. Of 199 participants interviewed 167 (86%) agreed to one or both vaccinations; 24% of study participants had a chronic condition for which vaccination was indicated and 53% had no regular source of medical care; 95% were aware of influenza vaccine while 25% were aware of pneumococcal vaccine (p <.0001). Of those offered the influenza vaccine, 86% accepted it and 70% of those offered pneumococcal vaccine accepted it (p <.001). Influenza and pneumococcal vaccinations were well-accepted by active drug users at a syringe exchange although there was both greater awareness of and acceptance of influenza. Many SEP participants with chronic medical conditions for which these vaccines are indicated did not have a regular source of health care. Syringe exchange programs may be valuable sites to administer respiratory vaccines and other public health interventions to drug injectors not engaged in medical care in other settings.

Adult↗
PubMed1998

Pulmonary hypertensive effects of lung inflation in chronic hypoxia: a study in rats.

Lung inflation was compared in isolated perfused lungs of control (C) and chronically hypoxic (CH) rats; in the latter, there is muscularization and loss of compliance in the pulmonary arterial system. During ventilation hypoxia, high alveolar pressure (Palv) elevated the pulmonary artery pressure (Ppa) less in C than in CH rats; Ppa fell during sustained inflation, rose on deflation, and after inflation hypoxic vasoconstriction was attenuated. Opposite changes took place in CH rats; Ppa often rose during inflation, fell on deflation, and after inflation hypoxic vasoconstriction was enhanced. Inflation also increased Ppa more in CH than C rats during air ventilation. Ppa/Palv relations measured during incremental inflation revealed normoxic tone in "extra-alveolar" vessels in both rat groups, which usually increased during hypoxia. In CH, but not C rats, there was also evidence for constriction in "alveolar" vessels during hypoxia. The effects of inflation were not changed by NO synthase blockade in either rat group. Pulmonary hypertensive effects of inflation in chronically hypoxic rats can be attributed to vascular remodelling.

Animals↗
PubMed1994

Histamine induced pulmonary vasodilatation in the rat: site of action and changes in chronic hypoxia.

Histamine constricts postcapillary lung vessels and also causes dilatation, site unknown. In chronically hypoxic rats, pulmonary arterioles are muscularized and histamine-containing mast cells increase. We wanted to determine a) whether vasoreactivity to histamine changes in chronic hypoxia; b) whether dilatation is due to H2 receptors; and c) which vessels dilate. We perfused isolated lungs of normal (C) and chronically hypoxic (CH) rats. Histamine was tested during hypoxic vasoconstriction. To examine effects on arteries alone, we raised alveolar (inflation) pressure above outflow pressure; during inflation, pressure/flow (P/Q) lines were measured during normoxia, and hypoxia, and after histamine during continued hypoxia. Dose-related dilatation was seen, which was abolished by cimetidine and enhanced in CH rats. A mast cell-discharging agent, but not exogenous histamine, caused constriction, which was abolished by chlorpheniramine. P/Q lines differed in C and CH rats in a manner which suggests that hypoxia constricts larger "extra-alveolar" vessels in C rats, but mainly muscularized arterioles exposed to alveolar pressure in CH rats. Histamine restored the P/Q line to nearly its normoxic position; it therefore dilated those vessels which constrict in hypoxia in each rat group. It is concluded that histamine has a strong H2 dilator effect, enhanced in chronic hypoxia, which might be an important attenuating factor in hypoxic pulmonary hypertension.

Animals↗
PubMed1992

Interactions between hypoxic and almitrine-induced vasoconstriction in the rat lung.

1. To test whether almitrine might improve the arterial partial pressure of O2 in patients with chronic obstructive airways disease by improvement of ventilation-perfusion matching, we looked at the interaction between hypoxic and almitrine-induced vasoconstriction in isolated rat lungs perfused with blood at constant flow. Increases in pressure represented increases in resistance. 2. Almitrine, given in increasing doses between challenges with 2% O2, enhanced hypoxic vasoconstriction at low doses but attenuated it at high doses. 3. Stimulus-response curves to hypoxia of increasing severity gave a sigmoid curve. 4. Almitrine solvent caused small changes in pulmonary artery pressure and shifted the stimulus-response curve slightly in a parallel fashion. 5. Small doses of almitrine enhanced the action of mild to moderate hypoxia, medium doses attenuated moderately severe hypoxia, whereas high doses depressed vasoconstriction due to all degrees of hypoxia. 6. These effects of almitrine on hypoxic vasoconstriction were compared with the effect of solvent by analysis of variance; the results substantiated significant enhancement of hypoxia by small doses and attenuation by large doses. 7. In patients, if similar effects apply, small doses of almitrine would assist ventilation-perfusion matching, but large doses might worsen it. 8. Almitrine-induced vasoconstriction was attenuated by a fall in perfusate temperature in a similar manner to hypoxic vasoconstriction. It was also attenuated by three drugs, chlorpheniramine, propanolol and diethylcarbamazine, all of which also decrease hypoxic vasoconstriction. The similarity between hypoxic and almitrine-induced pulmonary vasoconstriction is further confirmed.

Almitrine↗
PubMed1990

Enhanced reactivity to bradykinin, angiotensin I and the effect of captopril in the pulmonary vasculature of chronically hypoxic rats.

We compared the reactivity of pulmonary vessels to bradykinin (BK) and angiotensin I (AI) in normal and chronically hypoxic rats; the latter have pulmonary hypertension and muscularized pulmonary arterioles. These peptides are respectively inactivated and activated by the angiotensin converting-enzyme (ACE) on pulmonary endothelium. Isolated lungs were perfused at a constant flow rate when changes in pulmonary artery pressure (Ppa) reflect changes in vascular resistance. Dose-response curves to BK (1 ng-10 micrograms) were derived during normoxia and pre-constriction by hypoxia; BK both decreased and increased vascular resistance, i.e. vasodilation and vasoconstriction. In normal rats only constriction was seen in normoxia, which reflected low basal vascular tone, whereas in chronically hypoxic rats there was only dilatation which reflected high basal vascular tone. In hypoxia in normal rats, low doses caused dilatation, high doses constriction; in chronically hypoxic rats there was again only dilatation which was larger than in controls. After the ACE-inhibitor captopril, constriction was exaggerated in control rats in both normoxia and hypoxia and took place in chronically hypoxic rats after high doses in both normoxia and hypoxia; oedema often followed. Dose-response curves to AI (1 ng-micrograms) in normoxia showed greatly enhanced pressor responses in chronically hypoxic compared with normal rats, probably attributable to increased sensitivity to angiotensin II (AII) rather than enhanced conversion of AI to AII. Captopril caused a proportionate reduction in responses in both groups of rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1989

Reactivity and site of vasomotion in pulmonary vessels of chronically hypoxic rats: relation to structural changes.

The high pressure muscular pulmonary circulation of chronically hypoxic (CH) rats was compared with the low pressure circuit in control (C) rats; differences were found in the effects of lung inflation, in pressure/flow relations during lung inflation, in reactivity to autocoids, and in responses to pulmonary dilator drugs. Isolated blood-perfused lungs of CH rats (2 to 3 wk in 10% O2) were compared with those of C rats kept in air. High inflation (alveolar) pressure (Palv) caused a rise in pulmonary artery pressure (Ppa) close to delta Palv in both groups; in CH rats, Ppa continued to rise, whereas it adapted to a lower level in C rats. Pressure-flow (P/Q) lines were measured at high and low Palv, all in Zone 2 state. In normoxia, high Palv caused a parallel shift in the P/Q line close to delta Palv in both C and CH rats. However, during hypoxic pulmonary vasoconstriction (HPV), high Palv caused a shift in the P/Q line less than delta Palv in C rats and greater than delta Palv in CH rats. Similar differences between C and CH rats were seen during constriction caused by almitrine, a drug that simulates HPV. Thus, these stimuli affect vessels that are functionally "extra-alveolar" in C rats but functionally "alveolar" in CH rats. We consider whether vasoconstriction by hypoxia and almitrine moves peripherally to the newly muscularized alveolar arterioles that are found in CH rats. Reactivity of lung vessels to bradykinin, angiotensin-1, and platelet-activating factor was greater in CH than in C rats, possibly also associated with muscularization of arterioles in the former.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗