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PubMed1990

Haemodynamic effect of endothelin, a novel potent vasoconstrictor in dogs.

1. The effects of endothelin (40 and 400 pmol/kg, intravenous (i.v.), a novel vasoconstrictor, on haemodynamics were evaluated in normal dogs and dogs treated with hexamethonium. 2. The lower dose of endothelin caused no significant changes in mean blood pressure (MBP), heart rate (HR), cardiac output (CO), or total peripheral resistance (TPR) in normal dogs. In dogs treated with hexamethonium MBP decreased transiently associated with decrease in TPR. 3. In both dogs, the higher dose of endothelin caused MBP increase with CO increase in an early phase, and with TPR increase in a later phase. In normal dogs, the CO decreased 60 min after endothelin, but in dogs treated with hexamethonium the decrease in CO was not significant. 4. Electrocardiograms showed ST changes and arrhythmias. 5. Thus, endothelin has dual effects on both the vasculature and the heart, its effect depending on its dose and the time after its administration: initial vasodilation followed by prolonged vasoconstriction, and cardiostimulation followed by cardiosuppression. The cardiosuppression appears to be mediated in part by a neural mechanism.

Animals↗

PubMed1994

Comparative haemodynamic effects of verapamil, flecainide, amiodarone and sotalol in the conscious rabbit.

1. The effect of intravenous boluses of verapamil (0.15 mg/kg), flecainide (2 mg/kg), amiodarone (5 mg/kg), and sotalol (1.5 mg/kg) on mean arterial pressure, heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and peak rate of change of left ventricular pressure (LV dP/dt) were assessed in the conscious rabbit. 2. All four drugs had negative inotropic effects: verapamil reduced peak LV dP/dt by 19 +/- 4% (mean +/- s.e.m.; P < 0.01), flecainide by 27 +/- 9% (P < 0.001), amiodarone by 11 +/- 2% (P < 0.01) and sotalol by 13 +/- 3% (P < 0.01). 3. The drugs had different effects on CO as a result of differences in their actions on peripheral blood vessels: verapamil and amiodarone produced, respectively, a 12 +/- 4% (P < 0.03) and 16 +/- 6% (P < 0.01) increase in CO associated with a substantial vasodilatory effect (TPR reduced 15 +/- 7% [P < 0.05] and 20 +/- 5% [P < 0.01], respectively). Flecainide caused only a small (6 +/- 1%; P < 0.01) increase in CO and sotalol had no effect on either CO or TPR. 4. Bolus intravenous injections of verapamil, flecainide and amiodarone produced an increase in HR, while sotalol reduced HR by 10 +/- 2% (P < 0.01). The increase in HR and cardiac output seen with verapamil, flecainide and amiodarone was in part secondary to reflex increase in sympathetic tone and these changes were abolished after total cardiac autonomic blockade. 5. The modest reduction in cardiac performance associated with sotalol was abolished by cardiac autonomic blockade, suggesting that the predominant effect of sotalol on contractility was mediated through its beta-adrenoceptor blocking effect.

Amiodarone↗

PubMed1997

Effects of one-clip, one-kidney hypertension in chronically catheterized pregnant ewes.

1. Hypertension secondary to renal disease was studied in non-pregnant and pregnant ewes to determine whether there were any changes in arterial pressure and the distribution of cardiac output and, in particular, whether uteroplacental blood flow was affected. 2. In six non-pregnant, chronically catheterized, uninephrectomized ewes, a reduction in renal blood flow (RBF) to 40-50% of control caused hypertension within 3 h. This was maintained for as long as RBF was reduced (72 h) and returned to control 24 h after the occluder around the renal artery was released. When this experiment was repeated in 16 uninephrectomized pregnant ewes (118-134 days gestation) hypertension occurred within 3 h and was sustained for as long as RBF was reduced (between 24 and 72 h). Arterial pressure returned to control within 24-72 h of restoring RBF. 3. Compared with non-pregnant ewes, pregnant ewes had similar arterial pressures, higher cardiac outputs (CO; P < 0.001) and heart rates (HR; P < 0.001), lower total peripheral resistances (TPR; P < 0.001) and similar blood flows to brain, ovary, pancreas, kidney and spleen. Splenic vascular resistance (VR) was greater (P = 0.006), gut blood flow was greater (P < 0.05) and gut VR was less (P < 0.05). Myoendometrial blood flow/g was greater (P < 0.005) and myoendometrial VR was less (P = 0.006). 4. In pregnant sheep with renal clip hypertension, there was no change in CO and HR, but TPR increased (P < 0.01), as did plasma renin activity. Gut, brain, pancreatic and myoendometrial VR were increased as long as RBF was reduced; in addition, myoendometrial VR remained high for the rest of the experiment. Placental blood flow was unchanged at 3 h; 24-72 h later it was reduced (P < 0.05) and remained low. Placental VR was increased 24-72 h after RBF was restored when ewes were again normotensive. 5. Thus, one-clip, one-kidney renal hypertension in the pregnant ewe was due to increased TPR associated with a fall in uteroplacental blood flow that persisted even when RBF was restored and ewes were normotensive. This reduction in uteroplacental blood flow could account for the high foetal morbidity and mortality that occurs in pregnant women with renovascular hypertension.

Animals↗

PubMed1990

Hemodynamic and cardiac effects of spiraprilat in normal and sodium depleted conscious dogs.

The cardiac and hemodynamic effects of 3 doses (0.1, 0.3 and 1 mg/kg, iv) of spiraprilat, the diacid active metabolite of the new angiotensin I converting enzyme inhibitor spirapril, have been investigated and compared to those of saline in chronically implanted conscious dogs at rest. Under a normal sodium diet, spiraprilat, 1 mg/kg, induced significant (at least P less than 0.05) decreases in mean arterial pressure (MAP, -11%), total peripheral resistance (TPR, -21%), left ventricular end diastolic pressure (LVEDP, -15%) and increases in heart rate (HR, +12%) and cardiac output (CO, +16%) whereas dP/dtmax remained unchanged. Spiraprilat-induced tachycardia was not modified by propranolol pre-treatment but was abolished by previous administration of the propranolol-N-methylatropine combination. Spiraprilat, 0.1 mg/kg, did not affect any parameter, but spiraprilat, 0.3 mg/kg, showed intermediate effects. Finally, sodium depletion strongly potentiated spiraprilat effects on MAP, TPR, LVEDP, HR and CO. We conclude that: a), in conscious dogs under normal sodium diet, spiraprilat reduces TPR and MAP through peripheral vasodilating properties; b), spiraprilat-induced tachycardia is mainly related to parasympathetic tone withdrawal, possibly in relation with high and low pressure baroreceptors deactivation; and c), sodium depletion considerably potentiates spiraprilat cardiac and hemodynamic effects.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

Pharmacokinetic-pharmacodynamic modeling between pinacidil or pinacidil-N-oxide plasma levels and systemic and regional hemodynamic effects in healthy volunteers.

Pinacidil (P) lowers blood pressure through peripheral vasodilation, but also induces dose-dependent side-effects. In a previous placebo-controlled, randomized, double-blind and crossover study, performed in six healthy male volunteers, we investigated the systemic and regional hemodynamic effects of a single oral administration of 25 mg of P (sustained-release form) and measured the plasma concentrations of P and of its active metabolite, pinacidil-N-oxide (PO). In the present study, our goal has been to investigate the relationships between P and/or PO plasma concentrations and P administration effects on systolic, diastolic and mean arterial pressures (SAP, DAP, MAP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), brachial and carotid arteries' diameters (BAD, CAD), flows (BAF, CAF) and vascular resistances (BVR, CVR) which were assessed before and at different time intervals after drug intake. Concentration-effect relationships were investigated using both linear and log-linear multiple regression models with P, PO or both P and PO as independent variables (six models). Significant linear relationships were observed between P and/or PO and SAP, DAP, MAP, TPR, BAD, BAF, BVR, CAD and CVR. For example, TPR (dynes.s/cm5) = 1308-3.031 x P (ng/ml), R = 0.57, P = 0.0037; BVR (mmHg.s/ml) = 58-0.261 x P (ng/ml), R = 0.56, P = 0.0042. Almost similar R values were obtained using P, PO, or both P and PO. The use of log-linear models did not improve the fittings.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Acute hemodynamic effects of combined inhibition of neutral endopeptidase and angiotensin converting enzyme in spontaneously hypertensive rats.

Neutral endopeptidase inhibitors (NEPI) potentiate the hypotensive effect of converting enzyme inhibitors (CEI) in conscious spontaneously hypertensive rats (SHR) but the mechanism of this potentiation remains unknown. The present study assesses the hemodynamic effects of a CEI (enalaprilat 1 mg/kg; n = 9), a NEPI (retrothiorphan 25 mg/kg + 25 mg/kg/h; n = 9) and the combination (CEI+NEPI; n = 9) versus a control group (n = 9) in anesthetized spontaneously hypertensive rats. CEI alone induced a significant hypotensive effect due to a decrease (-35.1%) in total peripheral resistance (TPR), with no significant increase in cardiac output (CO). NEPI alone had a slight hypotensive effect due to a small decrease in CO. CEI+NEPI decreased the mean arterial pressure to the same extent (-26.7%) as the CEI-induced hypotensive effect, decreased TPR (-44.4%) and induced an increase in CO (+38.2%) with an increase in heart rate. In summary, NEPI combined with CEI induces large decreases in blood pressure and in TPR which do not significantly differ from the CEI-induced effects. It also induces increases in heart rate and in cardiac output in anesthetized SHR.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1987

Effects of triglycyl-lysine-vasopressin on cardiovascular responses to orthostatic stress.

The influence of triglycyl-lysine-vasopressin (TGLVP) on cardiovascular responses to orthostatic stress was studied. Arterial pressures, heart rate (HR) and stroke volume (SV) were measured in eight healthy males subjected to 20 min 70 degrees head-up tilt. On different days they received either 0.01 mg/kg b.w. of TGLVP or a corresponding volume of 0.9% saline i.v. after 15 min supine rest. After the drug injection, in supine subjects, HR had decreased from 58 to 50 beats min-1, total peripheral resistance (TPR) was elevated by 29%, systolic (SAP) and diastolic pressure (DAP) had increased by 7 and 8 mmHg, respectively. During tilt, values for HR and SAP were similar with and without TGLVP whereas DAP and MAP were elevated 8 and 7 mmHg, respectively, by the drug. 4-8 min into the tilt, TGLVP caused an 8% sustained curtailment of SV. Both with and without the drug TPR increased by about 30% in response to head-up tilt. Thus, the marked peripheral arteriolar constriction after vasopressin in the supine position was not affected by head-up tilt. Tilting also abolished the drug-induced elevation in SAP, most likely explained by the reduction in SV. Although TPR was markedly increased by TGLVP during head-up tilt, reflected in the behaviour of DAP, the response of SV speaks against any beneficial effect of this drug on orthostatic tolerance in healthy subjects.

Adult↗

PubMed1993

Cardioinhibitory-vasodepressor response to head-up tilt without hypoxaemia or myocardial ischaemia.

We evaluated whether hypoxaemia and/or myocardial ischaemia are of importance for development of the bradycardic hypotensive phase (cardioinhibitory-vasodepressor syncope) of central hypovolaemia. Arterial blood gas variables and a twelve-lead electrocardiogram (ECG) were followed during head-up tilt in seven men. During tilt, before presyncopal symptoms appeared, mean arterial pressure (MAP) increased (from 67 +/- 7 to 78 +/- 6 mmHg) (mean +/- SE) as did heart rate (HR) (61 +/- 4 to 99 +/- 8 beats min-1) and total peripheral resistance (TPR) (11 +/- 1 to 17 +/- 1 mmHg min l-1) (P < 0.01), while cardiac output (5.9 +/- 0.5 to 4.6 +/- 0.6 l min-1) and central venous pressure (CVP) (4.2 +/- 0.4 to 1.3 +/- 0.7 mmHg) decreased (P < 0.01). After 40 +/- 7 min of head-up tilt presyncopal symptoms appeared together with a decrease in MAP to 48 +/- 7 mmHg, HR to 71 +/- 11 beats min-1 and TPR to 9 +/- 2 mmHg min l-1 (P < 0.01). Arterial oxygen tension was not changed and there was no ST-segment depression of the ECG. The results indicate that during central hypovolaemia decreases in HR and TPR are elicited during normoxaemia and without electrocardiographic signs of myocardial ischaemia.

Adult↗

PubMed1993

Effect of the platelet-activating factor antagonist, TCV-309, and the cyclo-oxygenase inhibitor, ibuprofen, on the haemodynamic changes in canine experimental endotoxic shock.

1. The present study was conducted in order to examine the effects of the platelet-activating factor (PAF) antagonist, TCV-309, and the cyclo-oxygenase inhibitor, ibuprofen, on the acute haemodynamic responses to endotoxin in anaesthetized dogs. 2. Endotoxin (2 mg kg-1, i.v.) induced a severe hypotension by decreasing both total peripheral resistance (TPR) and cardiac output. Endotoxin also decreased central venous pressure and increased effective vascular compliance (EVC), indicating a blood pooling in the capacitance vessels. 3. The endotoxin-induced hypotension but not the fall in cardiac output, was markedly attenuated by ibuprofen. Ibuprofen abolished the decrease in TPR and even caused a systemic vasoconstriction. Ibuprofen abolished the increase in EVC. 4. The hypotension caused by endotoxin was attenuated by TCV-309 to a lesser extent than ibuprofen. However, the reduction in cardiac output produced by endotoxin was markedly attenuated by the PAF antagonist. TCV-309 also abolished the increase in EVC. In contrast to ibuprofen, TCV-309 did not affect the decrease in TPR caused by endotoxin. 5. Combined treatment with ibuprofen and TCV-309 markedly attenuated the endotoxin-induced hypotension, but not the fall in cardiac output. Nevertheless, when compared with animals treated with ibuprofen alone, treatment with ibuprofen and TCV-309 partly attenuated the endotoxin-induced reduction in cardiac output and systemic vasoconstriction. 6. These data indicate that dilatation of both resistance vessels and capacitance vessels contributes to the endotoxin-induced hypotension. It is suggested that (i) both prostanoids and PAF are involved in dilatation of capacitance vessels, (ii) prostanoids, but not PAF cause dilatation of resistance vessels and(iii) PAF may partly contribute to prostanoid-independent reduction in cardiac output in acute canine experimental endotoxin shock.

Animals↗

PubMed1983

Aging and hypertension: hemodynamic implications of systolic pressure trends.

The progressive rise in systolic pressure throughout life is accepted as a phenomenon of "normative aging," although elevated systolic pressure is established as an independent risk factor for untoward cardiovascular events. An analysis of published data for many thousands of individuals indicates comparable average systolic pressure increments of approximately 20 mm Hg between the ages of 40 and 65 years for both normotensives and hypertensives. In both groups there is a disproportionate rise in systolic pressure, that is, systolic increases more than mean and diastolic pressures. In a young person with a normally elastic arterial system an increase in total peripheral resistance (TPR) produces the same increments in systolic, diastolic, and mean arterial pressures; a decrease in arterial distensibility (AD), on the other hand, increases systolic pressure and decreases diastolic pressure to the same extent, leaving mean pressure unchanged. Thus, the proportion of the systolic pressure rise resulting from increased TPR is equal to the increase in the mean pressure (delta mean); the remainder of the increase (delta systolic minus delta mean) is caused by the only other variable that could account for an additional increase in systolic pressure with advancing age, a decrease in AD. Application of this formulation to published blood pressure data shows that in normotensives the ratio of the contribution toward rising systolic pressure of reduced AD to increased TPR is 1:1 between the ages of 40 and 65 years, whereas in hypertensives it is 2:1. Thus, the natural history of essential hypertension, once established, is one of accelerated arterial stiffening, a mechanism that would contribute importantly to the increasing prevalence of "systolic hypertension" with advancing age.

Adult↗

PubMed1999

Sensitivity to orthostatic stress and beta-receptor activation in patients with isoproterenol-induced vasovagal syncope: a case controlled study.

Cardiomotor and vasomotor responses were assessed during isoproterenol tilt-induced vasovagal reaction in patients with a history of syncope. In a case controlled study, all patients and controls were subjected to a standard protocol: baseline supine (10 min), baseline tilt (70 degrees, 45 min), isoproterenol supine (0.05 microgram/kg per min, 10 min), and isoproterenol tilt (70 degrees, 10 min). The participants were 11 consecutive patients referred for syncope evaluation (5 men, 6 women; mean age, 34.1 +/- 10.4 years; range, 18-56 years) and 11 age and sex matched controls (5 men, 6 women; mean age, 35.5 +/- 12.2 years; range, 19-63 years). On-line, beat-to-beat measurements of cardiomotor functions (heart rate, stroke volume, and cardiac output) and vasomotor functions (systolic, mean, and diastolic blood pressures and total peripheral resistance [TPR]) were detected noninvasively by volume clamp photoplethysmography and impedance cardiography. Patients and controls had similar cardiomotor and vasomotor responses during passive tilt and during isoproterenol infusion in the supine position. Immediately after tilt during isoproterenol infusion and before the onset of symptoms, decreases in vasomotor functions were significant in study patients when compared with those in controls; whereas responses in cardiomotor functions were similar between the two groups. When compared with baseline supine findings, TPR decreased by 56.5% +/- 10.9% and 29.5% +/- 23.3% in the patient population and controls, respectively (P = 0.005). When compared with isoproterenol supine findings, TPR decreased by 27.5% +/- 22.8% in the study patients and increased by 22.6% +/- 48.1% in the controls (P = 0.005). The inability to overcome isoproterenol-induced vasodilation during orthostatic stress played an important role in the initiation of a vasovagal response. These observations hold the key to early detection of hemodynamic changes and potential therapeutic interventions before patients become symptomatic.

Adolescent↗

PubMed1990

Evaluation of blood flow velocity waveform in an animal model.

Blood flow velocity waveforms in the abdominal aorta of three anesthetized pigs were recorded by a combined 3.5-MHz real-time and 2-MHz pulsed-Doppler ultrasound. The flow velocity waveforms were analyzed for pulsatility index, systolic to diastolic ratio, rising slope, descending slope, and the minimum diastolic velocity, and then were compared with volume blood flow measured by electromagnetic flowmeter (Q), mean arterial pressure (MAP), and total peripheral resistance (TPR). Total peripheral resistance was calculated according to the formula TPR = MAP/Q. A total of 111 recordings were performed over a range of heart rate: 90-250 beats/min, of Q: 65-1318 mL/min, of MAP: 72-165 mmHg and of total peripheral resistance 0.10-2.17 mmHg x min/mL. A significant positive correlation was found between pulsatility index and total peripheral resistance (correlation coefficient r ranging 0.64-0.87) and between systolic to diastolic ratio and total peripheral resistance (r: 0.59-0.83). The minimum diastolic velocity showed a negative correlation to TPR(r: -0.68 - -0.76). The pulsatility index was dependent on the heart rate, mean arterial pressure and rising slope; however, the relations were not consistent in all experiments. The results indicate that the pulsatility index is a good indicator of the flow velocity waveform changes depending on changes in the peripheral vascular resistance, and that the relationship between the total peripheral resistance and pulsatility index is linear. The systolic to diastolic ratio proved to be comparable even though it is somewhat less effective in performance than the pulsatility index.

Animals↗

PubMed1991

Acute haemodynamic effects of felodipine, verapamil and hydralazine in the anaesthetized dog.

Felodipine, a potent dihydropyridine calcium antagonist with a pronounced vascular selectivity, was given intravenously (0.006-0.025 mumol kg-1) to anaesthetized, open-chest dogs with denervated hearts. The result was a dose-dependent decrease in mean arterial pressure (MAP) and total peripheral resistance (TPR), while heart rate (HR), stroke volume (SV) and left ventricular end-diastolic pressure remained relatively unchanged. Cardiac tension work (TTI) and oxygen consumption (MVO2) were reduced, probably due to the decrease in afterload. The relative reduction of the coronary vascular resistance (CVR) was greater than that of TPR. The hypotensive effect of verapamil (0.05-0.20 mumol kg-1) was small and MAP decreased mainly via a decrease in HR and SV. Higher doses of verapamil which induced vasodilatation could not be given without the development of complete atrio-ventricular dissociation. Hydralazine (11-45 mumol kg-1) decreased TPR and CVR in parallel but the decrease in MAP was partly counteracted by a powerful increase in HR, SV and cardiac inotropy which was associated with elevated catecholamine levels in plasma. When MAP and HR were maintained constant by means of aortic balloon inflation and atrial pacing, felodipine markedly increased coronary blood flow and coronary sinus oxygen saturation while SV, TTI, inotropy and MVO2 remained relatively unchanged. It is concluded that felodipine markedly dilates peripheral resistance vessels, and in particular those in the coronary vascular bed, without any cardiodepressant effects.

Animals↗

PubMed1975

Arterial pressure, cardiac output and systemic resistance before and after pithing in normotensive and spontaneously hypertensive rats.

After complete cardiovascular denervation mean arterial pressure (MAP) falls to almost equally low levels in spontaneously hypertensive rats (SHR) and normotensive control rats (NCR). This has earlier been suggested to indicate a dominance of neurogenic mechanisms in established SHR hypertension. -- In the present study, total peripheral resistance (TPR) remains, however, some 35 per cent higher in adult SHR than in NCR after pithing while cardiac output (CO), and stroke volume, is 35 per cent lower in SHR. These opposite differences in TPR and CO after denervation, resulting in equal MAP levels in SHR and NCR, seem rather to be a consequence of the rapidly established structural adaptation that affects all SHR high-pressure cardiovascular sections. Thus, the SHR precapillary resistance vessels display thickened walls and luminal narrowing, which keeps TPR higher than in NCR even during maximal vasodilatation. Due to hypertrophy, the SHR left ventricle exhibits a reduced myocardial stretch for a given filling pressure and stroke volume is consequently reduced more than in NCR after complete denervation. -- Paradoxically, therefore, rather than reflecting any dominance of neurogenic mechanisms in established SHR hypertension the MAP equalization in SHR and NCR after cardiovascular denervation emphasizes the hemodynamic importance of cardiovascular structural changes present in hypertension.

Animals↗

PubMedDate not supplied

Tissue phantom ratios for a Clinac 4/100.

Tissue phantom ratios (TPR), based on a normalization depth of 5 cm, have been measured in water for field sizes from 5 x 5 cm2 to approximately 40 x 40 cm2 and for depths from 1 to 40 cm for a Varian Clinac 4/100. These TPR's have been compared with those calculated from percent depth doses measured at the same time, and the two sets of data generally agree to better than 1%, with an average ratio of measured to calculated TPR of 0.999 +/- 0.013. Beam profiles have been measured for open and wedged fields, with particular concern for the often observed "horns," or the increase in dose at the corners of the field. The maximum dose at a depth of 1 cm, along the diagonal of the field for this machine, is approximately 5% higher than at the same depth on the central axis, whereas along the principal plane the maximum dose is only about 3% higher.

Models, Structural↗

PubMed1999

Determination of scatter factor parameters and electron disequilibrium for monoenergetic photon beams.

The tissue-phantom-ratio (TPR) is expressed as the product of the phantom scatter factor (SF), an electron disequilibrium factor, and an attenuation factor, equal to the zero-area TPR. The scatter factor, as a function of depth d and field size s, has been described by two parameters a and w, SF(d,s) = 1 + asd/(ws + d). We have determined the parameters a and w for 20 monoenergetic photon beams between 1 and 20 MeV. Pencil-beam energy-deposition kernels were obtained using Monte Carlo simulations. The kernels were used to calculate broad-beam depth-dose data, which were converted to TPR and fitted to the equation above using an iterative search over a-w space. The parameter a is nearly equal to the attenuation coefficient for all energies while the parameter w increases with energy. The resulting a and w compare favorably to values determined for clinical photon beams, as a function of the measured attenuation coefficient. With the scatter factor determined, we isolated the electron disequilibrium factor for each monoenergetic beam. It can be characterized as a quadratic function of the depth. The coefficients of the quadratic function can be related to the range of the most energetic secondary electron produced.

Computer Simulation↗

PubMed1986

Evolution and spread of IncFIV plasmids conferring resistance to trimethoprim.

Twenty-one IncFIV-group plasmids conferring trimethoprim resistance in Escherichia coli isolates from humans and pigs were examined. Three evolutionary lines of plasmids were identified on the basis of restriction enzyme analysis. One was found exclusively in human isolates and another was found in pig isolates, while the third line consisted of plasmids from both sources. All R plasmids readily transferred to laboratory strains, and evidence was found for transfer to other biotypes of E. coli in the environment. The Tpr genes from representatives of the plasmid lines were cloned and compared by restriction analysis and by hybridization with two characterized Tpr dihydrofolate reductase genes. The sequences flanking the Tpr genes were different for each line, but all showed homology with the type 2 dihydrofolate reductase gene, irrespective of whether they were of human or animal origin. There was no hybridization to the type 1 gene. The remarkable degree of similarity among plasmids of the third line provided clear evidence of the exchange of plasmid-bearing E. coli between humans and pigs.

Animals↗

PubMed1976

Transposition of a deoxyribonucleic acid sequence encoding trimethoprim and streptomycin resistances from R483 to other replicons.

R483, a plasmid of the Ialpha incompatibility group, contained a deoxyribonucleic acid (DNA) sequence encoding resistance to trimethoprim (TpR) and streptomycin (SmR) that could be transposed to other replicons, i.e., to the Escherichia coli chromosome and to related and unrelated plasmids. Each transposition resulted in the acquisition by the recipient replicon of a segment of DNA of about 9 X 10(6) daltons, both resistance genes, but never the colicin Ia or pilus genes of R483. Transposition took place at a single chromosomal site between dnaA and ilv and did not suppress the DnaA phenotype, in contrast to integration of the whole R483 plasmid. The chromosome, having received the transposition, could secondarily act as a transposition donor to another plasmid. Such a plasmid was indistinguishable from one having received a direct transposition from R483. TpR SmR transposition was very site specific and did not require a functional recA+ gene. We postulate that the TpR SmR segment of R483 is a transposon (TnC) with specific boundary sequences.

Base Sequence↗