Search PubMed⌕ Search

Biomedical subjects

D Cavanagh

Publications and source records attributed to D Cavanagh.

At least 235 records · Page 13Linked to original sources

Contractility of endotoxic atria.

Previous studies showed that atria of guinea pigs pretreated with endotoxin had a reduced sensitivity to norepinephrine. Since accumulation of [3H]norepinephrine was reduced in atria from endotoxin-treated guinea pigs, the reduced responsiveness of such atria to norepinephrine cannot be explained on the basis of endotoxin effect on the uptake of the amine. In the present study, the relative enhancement of the contractile force of the atria during paired stimulation in endotoxic and control animals was of equal magnitude. The results indicate that reduced sensitivity to norepinephrine may not be related only to endotoxin effect on the contractility of the myocardium. Endotoxin treatment may induce certain changes in the sequence of steps involved in the process of excitation-contraction coupling in the myocardium. The most likely locus of endotoxin action appears to be the heart cell membrane.

Animals↗

The localization of influenza virus in the respiratory tract of ferrets: susceptible nasal mucosa cells produce and release more virus than susceptible lung cells.

Infectious virus production by ferret nasal mucosa and lung organ cultures has been monitored in both tissue pieces and medium over 24 h following inoculation with an Asian (H2N2) strain of influenza virus. Freshly prepared cultures of nasal mucosa produced approx. 10-fold more virus per cell than fresh lung cultures. Also the nasal mucosa cells liberated into the medium a greater proportion (mean 31%) of the total virus produced than did fresh lung (mean 6%). Maintenance of lung explants for 24 h prior to inoculation resulted in a 20- to 100-fold increase in the amount of virus released. However, total virus production by fresh and maintained lung was similar. Trypsin did not increase the infectivity of virus released from any of the cultures, indicating that the haemagglutinin in the virus particles was cleaved. Similar results were obtained with a Hong Kong (H3N2) virus strain. Hence, one factor operating in the lower susceptibility of the lung compared with the nasal mucosa in vivo may be a lower capacity of lung cells both to produce and release influenza virus.

Animals↗

Early events in the interaction between foot-and mouth disease virus and primary pig kidney cells.

Foot-and-mouth disease virus (FMDV) attached to pig kidney cells at 0 degrees C and could only be recovered in a form with a sedimentation coefficient and buoyant density lower than that of the native virus. Incubation of the virus-cell complex at 37 degrees C caused disruption of about 80% of the particles into a 12S protein sub-unit that had the same polypeptide composition as that produced by reducing the pH of the virus below pH7. The remaining 20% had the same polypeptide and RNA composition as the native virus but it had a lower sedimentation coefficient, buoyant density and specific infectivity. These lower values are probably due to the association of the virus with cell membrane components. The 12S subunits were shown to be located inside the cell, indicating that disruption of the virus had occurred within the cell. The results are discussed in relation to the different cell mediated alteration of other picornaviruses.

Adsorption↗

Association of foetal wastage with influenza infection during ferret pregnancy.

Inoculation of influenza virus into pregnant ferrets during the late gestational period was investigated. Foetal resorption followed intracardial inoculation of a large dose of influenza virus (10(9.4) EBID50) and a 100-fold lower dose caused lower litter sizes at birth. The possible role of fever in foetal resorptions was largely discounted by 2 observations: a non-pyrexic dose inoculated intracardially into the pregnant ferret still had detrimental effects on foetal viability; influenza virus inoculated intranasally caused a pyrexia but did not affect the progeny. The potential of the ferret as a model for studying the possible adverse effects of influenza during pregnancy is discussed.

Animals↗

Sensitivity to pyrexial temperatures: a factor contributing to virulence differences between two clones of influenza virus.

The influence of pyrexia on the differential persistence of a virulent and an attenuated clone of influenza virus in the respiratory tract of ferrets has been further studied. Clone 64d, an attenuated clone of a recombinant virus (A/PR/8/34-A/England/939/69 (H3N2)) grown in organ cultures of ferret nasal turbinates, was inactivated at pyrexial temperatures more readily than a virulent Clone 7a. In addition, replication of Clone 64d was restricted at pyrexial temperatures to a greater extent than that of Clone 7a in organ cultures of both ferret nasal turbinate and lung tissue. The greater adverse effects of pyrexial temperatures on Clone 64d appears to explain the earlier reduction of upper respiratory tract infection seen in ferrets infected with this attenuated clone. Also, the differential influence of pyrexial temperatures may be the reason for the virtual lack of lung infection with Clone 64d in vivo in contrast to the consistent infection found with Clone 7a. The relevance of these findings to human infection and to markers of attenuation of influenza virus is discussed.

Animals↗

Natural family planning. I. The peak symptom and estimated time of ovulation.

The observation of the "Peak" mucus symptom in women using the ovulation method of natural family planning has been correlated with the estimated time of ovulation, as evaluated by indirect hormonal parameters. In 65 cycles of the 73 studied in 24 patients, there was hormonal confirmation of ovulation; in eight cycles, anovulation or luteal dysfunction was suspected. In the 65 normal cycles, 64 exhibited a Peak symptom. In those cycles, ovulation was estimated to occur from 3 days before to 3 days after the Peak symptom with a mean of 0.31 days before the Peak symptom. In 95.4% of these cycles, ovulation was estimated to occur from 2 days before to 2 days after the Peak symptom. The variation between cycles of the same patient ranged from 0 to 4 days with a mean of 1.8 days. The beginning of the mucus symptom preceded the estimated time of ovulation by an average of 5.9 days.

Adult↗

Experimental toxemia in the pregnant primate.

In order to develop a model for the study of eclamptogenic toxemia, a series of experiments were carried out on 31 female baboons. In Group 1, consisting of 10 animals, metal clips were placed around the uterine arteries in order to partially occlude them, and the ovarian vessels were transected. The animals were subsequently mated. Nine developed hypertension and proteinuria, and one aborted. The renal lesions in these animals were indistinguishable from those described in human toxemia. Group 2 consisted of three of the 10 baboons from Group 1, which became pregnant a second time. They again developed hypertension and proteinuria. In Group 3, three baboons at 100 days of gestation were treated as in Group 1 with similar results. Groups 4 and 5 served as pregnant (3) and nonpregnant (15) controls. It is concluded that a toxemia model has been developed in a subhuman primate. This model will prove useful in the further study of eclamptogenic toxemia.

Animals↗

Septic shock in a pregnant or recently pregnant woman.

Septic shock may be classified clinically as primary (reversible) or secondary (irreversible). Primary shock is further distinguished as early ("warm-hypotensive") or late ("cold-hypotensive"). Infected abortion, chorioamnionitis, or pyelonephritis of pregnancy calls for appropriate measures directed toward preventing septic shock, including administration of huge doses of antibiotics. If septic shock ensues, extirpation of the nidus of infection becomes a primary consideration. Surgical extirpation should be carried out if possible, and as soon as possible. Besides antibiotics, patients with septic shock may require glucocorticoids, vasomotor drugs, digitalis, and heparin. Careful monitoring is essential.

Female↗

Immunogenic and cell attachment sites of FMDV: further evidence for their location in a single capsid polypeptide.

Chymotrypsin cleaves only one of the four major polypeptides of foot-and-mouth disease virus (FMDV serotype O) in situ. This polypeptide (VP1, mol. wt. 29 X 10(3) was first cleaved into fragments of mol. wt. 20 and 9 X 10(3) and further cleavage could be prevented by the addition of a large excess of bovine serum albumin. The infectivity of the virus particles at this stage was the same as that of the intact virus although the rate of attachment to BHK 21 cells was slower and the immunogenic activity was reduced. If hydrolysis was allowed to continue, VP1 was cleaved into fragments with mol. wt. 18 and less than 9 X 10(3), similar to those obtained with trypsin and the virus particles then had a greatly reduced infectivity and a lower immunogenicity. Treatment of strains from five other serotypes of the virus with the two enzymes cleaved only VP1 in each instance and there was a corresponding loss of infectivity. The results are discussed in relation to the location and biological activity of the virus polypeptides.

Animals↗

Effect of dopamine infusion on the hemodynamics of normal and sympathectomized rhesus monkeys in endotoxin shock.

Infusion of endotoxin in chemically sympathectomized monkeys caused a fall in the mean aortic pressure, but the cardiac output, stroke volume, and central venous pressure were well maintained. Endotoxin-induced tachycardia in monkeys with functional sympathetics was not seen in the sympathectomized animals. Infusion of dopamine improved the hemodynamic and cardiovascular status, probably by causing vasoconstriction of the splenic and hepatic artery where the pooling of blood is believed to occur in endotoxin shock. However, these beneficial effects were not apparent when dopamine was administered in the chemically sympathectomized animal infused with endotoxin. Since chemical sympathectomy did not affect the endotoxin-induced decline in the systolic and mean aortic pressure or the severity of the endotoxin shock, it is suggested that catecholamines may not be the primary initiator or trigger substances in endotoxin shock.

Animals↗