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Biomedical subjects

R L Kent

Publications and source records attributed to R L Kent.

At least 73 records · Page 4Linked to original sources
PubMed1986

Beta adrenergic receptor blockade of feline myocardium. Cardiac mechanics, energetics, and beta adrenoceptor regulation.

Myocardial oxygen consumption is regulated by interrelated mechanical and inotropic conditions; there is a parallel increase in the aerobic metabolism and inotropic state during beta-adrenergic stimulation under fixed mechanical conditions. In contrast, there is some evidence that beta-blockade may reduce oxygen consumption through effects independent of its influence on mechanical conditions and contractile state, and that prolonged beta-blockade may sensitize the myocardium to beta-adrenergic stimulation. To clarify these two points, the present study examined the relationship of myocardial energetics to mechanics and inotropism during acute beta-blockade and after the withdrawal of long-term beta-blockade, whereupon the basis for any effect observed was sought by characterizing the number, affinity, and affinity states of the beta-receptors as well as the coupling of activated beta-receptors to cyclic AMP generation. Studies of right ventricular papillary muscles from control and chronically beta-blocked cats demonstrated contractile and energetic properties as well as dose-response behavior and inotropic specificity suggestive of an increase in myocardial sensitivity to beta-adrenoceptor stimulation in the latter group. Assays of cardiac beta-adrenoceptors from further groups of control and pretreated cats, both in cardiac tissue and in isolated cardiac muscle cells, failed to define a difference between the two groups either in terms of receptor number and affinity or in terms of the proportion of receptors in the high-affinity state. However, coupling of the activated beta-adrenoceptors to cyclic AMP generation was enhanced in cardiac muscle cells from chronically beta-blocked cats. These data demonstrate that beta-adrenoceptor blockade (a) produces parallel effects on inotropic state and oxygen consumption without an independent effect on either and (b) increases myocardial sensitivity to beta-adrenergic stimulation after beta-blockade withdrawal, not by "up-regulation" of the cardiac beta-adrenoceptors, but instead by more effective coupling of these receptors when activated to cyclic AMP generation.

Adrenergic beta-Antagonists↗
PubMed1986

Evaluation in reconstructive implantology.

Acceptance of implants by dentist, readiness for use, and general indications are described. Individual evaluation for implants is detailed and success of implants defined. Indications for removal are cited and appropriate statistic methodology presented.

Consumer Behavior↗
PubMed1985

Biochemical and structural correlates in unloaded and reloaded cat myocardium.

Cardiocytes of unloaded myocardium rapidly lose structural and functional integrity through a combined loss of myofibrils and contractile activity; both changes are reversible with load restoration. The present study correlates the biochemical composition of unloaded and reloaded myocardium with these alterations in structure and function. Cardiac muscle was unloaded by transecting the chordae tendineae of a cat right ventricular papillary muscle and was reloaded by suturing these same chordae tendineae to the ventricular wall at the base of the valve; an adjacent intact muscle served as the control. Muscles unloaded for 1 to 14 days were assayed for DNA, protein, total creatine and hydroxyproline content. The ratios of wet weight/DNA and creatine/DNA decreased by 30 and 22% respectively, in parallel with a 38% reduction in cardiocyte cross-sectional area. Protein/unit wet weight was decreased by 50% after 14 days of unloading, so that both protein/DNA and protein/creatine were markedly reduced. Reloading of the muscle restored cardiocyte size, protein per unit wet weight and protein/DNA to normal. Parallel reductions in both contractile filaments and contractile proteins after unloading and parallel increases in each following load restoration were demonstrated by morphometric analysis of electron micrographs and analysis of actin and myosin by gel electrophoresis. In summary, the myocardium undergoes marked, parallel changes in structure, function and biochemical composition in response to the removal and restoration of load.

Actins↗
PubMed1985

Resistance to antibiotics in clinical isolates of Klebsiella pneumoniae.

The antibiotic resistance of Klebsiella pneumoniae isolates from 12 medical centers worldwide, over a 1- to 6-year period, were tested. Clinical isolates of K. pneumoniae were resistant to ampicillin and carbenicillin. Resistance to other antibiotics was less frequent with isolates of K. pneumoniae from 5 of 6 US centers than with those from 6 centers outside the US. In nearly all of the centers, resistance to sulfamethoxazole-trimethoprim, gentamicin, tobramycin, or chloramphenicol was more frequent in isolates of K. pneumoniae than in those of Escherichia coli, while the reverse was true for resistance to tetracycline. Resistance to multiple antibiotics declined gradually in isolates of K. pneumoniae at one center, but rose abruptly again with dissemination of a new plasmid.

Ampicillin↗
PubMed1985

Structural analysis of pressure versus volume overload hypertrophy of cat right ventricle.

Pressure overload of cat right ventricle causes progressive abnormalities of in vitro contractile function at a time when in vivo contractile function is normal. In marked contrast, the same degree and duration of volume overload of cat right ventricle results in neither in vitro nor in vivo contractile dysfunction. The purpose of the present quantitative structural study was to determine whether there were any histological alterations in pressure-overloaded myocardium that might be causally related to the contractile dysfunction found only in this model. Four experimental groups of eight cats each were studied: a group with pulmonary arterial banding to create a pressure overload, sham-operated controls for this group, a group with atrial septal defects to create a volume overload, and sham-operated controls for this group. Seven to ten weeks after each operative procedure, right ventricular pressure was elevated only in the pressure-overloaded group, pulmonary-to-systemic blood flow ratio was increased only in the volume-overloaded group, and right ventricle-to-body weight ratio was significantly and comparably increased in both the pressure- and the volume-overloaded groups. There was a single striking histological distinction between myocardium hypertrophying in response to pressure as opposed to volume overload: the volume density of cardiocytes in papillary muscles from pressure-overloaded right ventricles was decreased significantly with a proportional increase in connective tissue. Given the critical importance of these two myocardial components to both systolic and diastolic cardiac function, these data provide a potential structural basis for at least some of the functional abnormalities observed in pressure but not in volume overload hypertrophy of the cat right ventricle.

Animals↗
PubMed1985

Hemodynamic versus adrenergic control of cat right ventricular hypertrophy.

The purpose of this study was to determine whether cardiac hypertrophy in response to hemodynamic overloading is a primary result of the increased load or is instead a secondary result of such other factors as concurrent sympathetic activation. To make this distinction, four experiments were done; the major experimental result, cardiac hypertrophy, was assessed in terms of ventricular mass and cardiocyte cross-sectional area. In the first experiment, the cat right ventricle was loaded differentially by pressure overloading the ventricle, while unloading a constituent papillary muscle; this model was used to ask whether any endogenous or exogenous substance caused uniform hypertrophy, or whether locally appropriate load responses caused ventricular hypertrophy with papillary muscle atrophy. The latter result obtained, both when each aspect of differential loading was simultaneous and when a previously hypertrophied papillary muscle was unloaded in a pressure overloaded right ventricle. In the second experiment, epicardial denervation and then pressure overloading was used to assess the role of local neurogenic catecholamines in the genesis of hypertrophy. The degree of hypertrophy caused by these procedures was the same as that caused by pressure overloading alone. In the third and fourth experiments, beta-adrenoceptor or alpha-adrenoceptor blockade was produced before and maintained during pressure overloading. The hypertrophic response did not differ in either case from that caused by pressure overloading without adrenoceptor blockade. These experiments demonstrate the following: first, cardiac hypertrophy is a local response to increased load, so that any factor serving as a mediator of this response must be either locally generated or selectively active only in those cardiocytes in which stress and/or strain are increased; second, catecholamines are not that mediator, in that adrenergic activation is neither necessary for nor importantly modifies the cardiac hypertrophic response to an increased hemodynamic load.

Animals↗
PubMed1984

Left ventricular performance in patients with coexistent mitral stenosis and aortic insufficiency.

Isolated mitral stenosis and isolated aortic insufficiency impose unique and opposite loading conditions on the left ventricle. To assess these combined effects, hemodynamic and angiographic factors were compared among normal subjects and patients with isolated mitral stenosis, isolated aortic insufficiency or combined mitral stenosis and aortic insufficiency. Left ventricular end-diastolic volume index was lower in patients with combined lesions and severe or moderate aortic insufficiency than in patients with isolated severe or moderate aortic insufficiency (138 +/- 19 versus 206 +/- 20 cc/m2 and 87 +/- 5 versus 145 +/- 22 cc/m2, respectively) (p less than 0.05 for both). Left ventricular end-diastolic and end-systolic volume indexes were normal in two-thirds of patients with combined lesions and moderate or severe aortic insufficiency, whereas these indexes were high in all but one patient with isolated moderate or severe aortic insufficiency. Among patients with moderate or severe aortic insufficiency, 8 of 14 with isolated insufficiency had a reduced ejection fraction or circumferential fiber shortening rate compared with 5 of the 9 patients with combined lesions. Among patients with isolated aortic insufficiency, left ventricular end-systolic wall stress and end-diastolic and end-systolic volume indexes were higher (p less than 0.05) in those with reduced ejection performance than in those with normal ejection performance. These variables did not differ between patients with reduced or normal ejection performance in the group with combined lesions. The contractile index (ratio of end-systolic wall stress to end-systolic volume index) was significantly depressed in patients with severe aortic insufficiency in the groups with isolated aortic insufficiency or combined lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Atrophy reversal and cardiocyte redifferentiation in reloaded cat myocardium.

We have recently described rapid cardiac atrophy in response to decreased load. The present study was designed to determine whether this atrophy is solely a degenerative response of damaged myocardium or is, instead, an adaptive response of viable myocardium. A discrete portion of cat myocardium was unloaded by severing the chordae tendinae of a single right ventricular papillary muscle. One week later, the muscle was reloaded by attachment of its apex to the ventricular free wall. This allowed the load to be removed and restored without altering the blood supply, innervation, or frequency of contraction of the tissue. In myocardium unloaded for 1 week, the cardiocyte cross-sectional area and the volume densities of mitochondria and myofibrils decreased significantly. Large areas of cytoplasm were devoid of organelles, and the few remaining myofilaments were oriented in a variety of directions rather than longitudinally within the cell. Upon reloading for 1 week, the cardiocyte cross-sectional area, volume density of mitochondria, and ultrastructural organization all returned to normal. The volume density of the myofibrils increased toward control, and they reoriented with respect to the long axis of the cardiocyte. The contractile function of the papillary muscles, which was depressed as early as 1 day after unloading and almost absent at times later than 3 days after unloading, returned to normal after 2 weeks of reloading. This study demonstrates that adult mammalian myocardium responds to unloading with a marked loss of cellular differentiation, organization, and function which is fully reversible with reloading. This plasticity in response to load may well be the basic mechanism responsible for the development and maintenance of normal cardiac structure and function.

Aging↗
PubMed1983

Altered coenzyme A and carnitine metabolism in pressure-overload hypertrophied hearts.

Changes in the total content and acylation state of coenzyme A (CoA) and carnitine in the heart result in alterations in fatty acid metabolism that may be associated with ventricular dysfunction. The present study was undertaken to determine whether abnormal myocardial CoA and carnitine metabolism occur in pressure-overload hypertrophy and congestive heart failure. Right ventricular hypertrophy was induced in cats by pulmonary artery (PA) banding. Total tissue CoA was reduced by 50% in the hypertrophied right ventricle and 25% in the nonhypertrophied left ventricle of PA-banded cats in the presence or absence of heart failure. No alterations were observed in long-chain fatty acyl CoA levels in either ventricle of PA-banded cats. In addition, a 20% reduction in total CoA was also observed in hypertrophied hearts of rats subjected to aortic banding. Although the CoA content was reduced in hypertrophied cat hearts, myocardial tissue levels of its precursor, pantothenic acid, were unaltered. Total tissue carnitine and long-chain fatty acyl-carnitine levels were unchanged in both ventricles of PA-banded cats; however, total carnitine was reduced by 25% in hypertrophied rat hearts. This study establishes a marked reduction in myocardial CoA content in pressure-overload hypertrophy.

Animals↗
PubMed1983

The effects of hyperosmolar solutions on isolated vascular smooth muscle examined with verapamil.

Hyperosmotic sucrose solutions elicited tension from rat aortic strips in direct proportion to osmolarity. Norepinephrine-induced tension was reduced in proportion to increases in osmolarity; however, reduction of barium-induced tension by hyperosmolar solutions was minimal. Norepinephrine-induced tension is primarily dependent on intracellular calcium mobilization, while barium-induced tension is primarily dependent on extracellular calcium influx. Therefore, hyperosmolar solutions may alter vasoconstriction associated with intracellular calcium mobilization rather than that associated with extracellular calcium influx. In the presence of verapamil which blocks calcium entry into muscle, barium-induced tension was eliminated while the direct tension elicited by hyperosmolar solutions was slightly affected (6% reduction) and the inhibitory effect of hyperosmolar solutions on norepinephrine-induced tension was still observed. In contrast, the tension elicited by hyperosmolar solutions was greatly reduced by papaverine which promotes sequestration of myoplasmic calcium to cause relaxation. The vascular effects of hyperosmolar solutions may be due to alterations in the intracellular calcium rather than the extracellular calcium utilized by vasoconstricting agents.

Animals↗
PubMed1982

An index for comparing the inhibitory action of vasodilators.

An index for comparing the inhibitory effects of vasodilators was developed to gain insight into their mechanism of action on vascular smooth muscle. Rat aortic strips were bathed in Krebs bicarbonate solution and were initially contracted to a stable tension by either phenylephrine or barium chloride. A vasodilator was then added and the remaining tension was noted; this was repeated for cumulative concentrations of vasodilator. At each concentration of vasodilator, the percent reduction in phenylephrine-induced tension (Phe) was compared to the percent reduction in barium-induced tension (Ba) and was expressed as a ratio (Phe/Ba). This ratio clearly separated verapamil and nifedipine (ratio less than 1), which block calcium influx, from papaverine (ratio = 1) which promotes calcium sequestration regardless of the source of calcium, and from dantrolene (ratio greater than 1) which interferes with intracellular calcium mobilization. This index provides a method for comparing the action of those agents presently classified as non-receptor specific vasodilators which act directly on vascular smooth muscle.

Animals↗
PubMed1982

Molecular epidemiology of antibiotic resistance in salmonella from animals and human beings in the United States.

We collected serotyped isolates of salmonella from reference laboratories in the United States, tested their susceptibility to antibiotics, and extracted plasmids from isolates that were resistant to a different combination of antibiotics from each of three serotypes. Restriction-endonuclease digestion showed that within each of the three groups, plasmid molecules from animal and human isolates were often identical or nearly identical. One serotype-plasmid combination appeared to be endemic in cattle in 20 states and infected 26 persons in two states. The human cases, which were not recognizably related except for their common plasmids, appeared to be clustered in time but geographically dispersed, like cases in previous outbreaks spread by food products. These findings suggest that resistance plasmids may be extensively shared between animal and human bacteria, and that spread of multiresistant strains of salmonella among animals and human beings, as observed in Britain, may have been undetected in the United States for lack of comparable surveillance.

Animals↗
PubMed1982

Synergistic effects of pressure, distal resistance, and vasoconstriction on stenosis.

The synergistic effects of perfusion pressure, distal resistance, and arterial vasoconstriction on stenotic hemodynamics were examined using an in vitro arterial preparation. Canine carotid and coronary arteries were attached to a perfusion apparatus. Perfusion pressure and distal resistance were controlled independently. Arterial vasoconstriction was induced by perfusing the artery with a 100 mM K solution. A stenosis was created by partially inflating a balloon catheter within the artery. Pressure proximal and distal to the arterial segment and flow were measured. For the coronary arteries the combination of high perfusion pressure, high distal resistance, and arterial vasodilation decreased stenotic resistance to 0.79 +/- 0.10 mmHg . ml-1 . min, whereas low perfusion pressure, low distal resistance, and arterial vasoconstriction increased stenotic resistance to 22.40 +/- 4.90 mmHg . ml-1 . min (P less than 0.01). These large changes in stenotic resistance were accompanied by maximum and minimum flow rates of 86.1 +/- 6.0 and 5.5 +/- 1.1 ml/min, respectively (P less than 0.01). Qualitatively similar results were obtained with the carotid arteries. Thus perfusion pressure, distal resistance, and arterial vasoconstriction acted synergistically to greatly influence the severity of the stenosis.

Animals↗