Bilateral knee effusions in sickle cell crisis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J V Jones.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The haemodynamic shifts during head up and head down tilt were investigated in adult spontaneously hypertensive rats (SHR) and matched normotensive control rats (NCR) under nembutal anaesthesia and autonomic blockage. During head up tilt a greater fall in blood pressure and stroke volume was observed in SHR than in NCR, while the reverse was true when tilted in the opposite direction. This altered cardiac response to venous filling, also observed in patients with essential hypertension, is suggested to be caused by an altered Frank-Starling relationship of the hypertrophied heart in hypertensive individuals.
Isolated hindquarters of rats were perfused at constant flow with a plasma substitute so that pressor responses to various concentrations of noradrenaline (NA) could be measured in consective sections of the vascular bed with normal (greater than 1.5 mM) or low (0.2 mM) Ca2+ in the perfusate. The animals used were 6-week-old spontaneously hypertensive rats of the Okamoto strin (SHRy), normotensive controls of the same age NCRy); 6--7-month-old SHR (SHRA) and NCR (NCRA); and rats made hypertensive by clipping of one renal artery (RHR) plus matched normotensive controls (NCRR). Concentration-response curves to NA showed that constrictor responses to NA become more dependent on external calcium as one proceeds peripherally in the vascular system in both SHRA and NCRA, with responses in proximal vessels being least and small pre- and postcapillary vessels being most dependent in both cases. In low calcium SHRA retained their responses better than NCRA, whereas RHR retained their responses to NA poorer than did NCRR. No significant differences in responses in low calcium were observed in SHRY compared to NCRY though a trend in the same direction as in SHRA could be traced. It is concluded that there is no evidence that altered handling of calcium initiates vascular hyperreactivity in SHR, but that the handling of vascular calcium in SHR differs from RHR and both differ from NCR.
The characteristics of 47 non-medullated and 54 medullated fibres arising from aortic arches of 6 hypertensive rabbits have been investigated. The threshold for activation of the aortic C-fibres lay between 78 and 190 (mean 122) mmHg. The threshold for activation of 54 medullated aortic baroreceptors in the same animals was from 70 to 140 (mean 109) mmHg. At the awake mean arterial blood pressure (MABP) of these hypertensive rabbits (143 mmHg) all the medullated fibres were active as were 78% of the C-fibres. In contrast in a group of normotensive animals 91% of the medullated and only 28% of the non-medullated fibres were active. Pressure response curves were constructed for 19 C-fibres and 12 medullated fibres from the hypertensive animals. At a MABP of 110 mmHg the firing in the non-medullated fibres was 2.0 Hz as compared with 19.0 Hz in the medullated fibres and at the awake MABP mean firing was 9.0 Hz in the non-medullated fibres and 48.0 Hz in the medullated fibres. The firing at awake MABP was considerably higher in the hypertensives (9.0 Hz) as compared with the normotensives (1.1 Hz). Thus these data indicate that although the aortic C-fibres are reset in chronic hypertension, they are reset less than the medullated aortic baroreceptors from the same animal. It is suggested that arterial baroreceptor C-fibres may have an important role in the tonic control of the circulation in hypertension.
To study the dependency of vascular smooth muscle contractions, produced by noradrenaline, on the concentration of extracellular calcium, experiments were performed on adult male Wistar rats. The hemodynamic characteristics of the isolated, perfused hindquarters were investigated from maximal dilatation up to maximal, noradrenaline-induced constriction under constant flow conditions. Pressor responses to noradrenaline in the consecutive segments of the vascular bed ("proximal" and "distal" precapillary resistance vessels and postcapillary resistance vessels) were determined at low (0.2mM) and at normal (1.5-2.0 mM) Ca++ concentrations in the perfusate. Dependence on external calcium is much greater peripherally. The smallest pre- and postcapillary resistance vessels are the most dependent while the larger, "proximal" resistance vessels are the least dependent on the availability of external calcium. The results illustrate the considerable differentiation of smooth muscle, depending on its location along the vascular circuit. They further indicate that it is likely that the hemodynamically so important microvessels are highly dependent on extrinsic Ca++ sources not only concerning their involvement of remote adrenergic control, but also in their maintenance of normally pronounced "myogenic" tone.
To study the extent and time course of arterial baroreceptor threshold resetting to increases in blood pressure, renal hypertension was induced in young normotensive male Wistar rats by unilateral renal artery constriction. At different intervals after operation the extent of baroreceptor threshold resetting in the carotid sinus was examined. Experiments were performed 7, 14 and 25 days after renal artery clipping to enable baroreceptor resetting to be correlated with the rate and extent of cardiovascular changes in rats which had renovascular hypertension of indentical durations (Lundgren et al. 1974). Baroreceptor thresholds in the carotid sinuses were established by progressive clamping of both carotid arteries after partial vascular isolation of the sinuses. The results show that after one week of hypertension baroreceptor resetting is only just apparent but by two weeks resetting is gross and seems to be largely completed. This parallels the adaptive changes in the hindquarters of renal hypertensive rats and it is concluded that baroreceptor resetting is a secondary phenomenon related to the structural changes induced in the vessels by the elevated blood pressure.
The cardiovascular responses to acute mental "stress" were compared in the Milan strain of spontaneously hypertensive rats (MHS) and in normotensive control rats (NR). Blood pressure and heart rate were followed in pairs of awake MHS and NR, while defence reactions were provoked by alerting stimuli (noise, vibration). No differences were noted between the two groups in response to "stress" although resting heart rate in MHS was lower than in NR. Administration of atropine or propranolol to MHS and NR showed the MHS to have a higher resting vagal tone and lower sympathetic tone than the NR. Subsequent (at least two weeks later) hemodynamic investigation, under nembutal anesthesia, showed no difference in cardiac output between MHS and NR but a higher stroke volume, presumably related to the lower heart rate in MHS. Thus, total peripheral resistance was increased in MHS as was the ratio left ventricular weight/body weight, and in good proportion to the blood pressure rise. Thus MHS differ substantially in both their responses to "stress" and also hemodynamically from the Okamoto strain of spontaneously hypertensive rat (SHR), being the so far most studied and best known model of essential hypertension in man. In MHS the hypertension is more of a systolic type and is of primarily renal origin. As such, MHS provide another model for investigating the polygenic nature of hypertension in man.
The characteristics of 40 C-fibres arising from the aortic arches of 15 normotensive rabbits have been investigated. The conduction velocity of the fibres varied between 0.5-1.8 m/s (0.91 +/- 0.05, mean +/- S.E.). The activation threshold for all the fibres lay between 70-140 mmHg. 32 medullated fibres from the same animals had thresholds between 35 and 90 mmHg. After correction for the time delay in conduction the firing in the C-fibres occurs in early systole. Pressure response curves were constructed for 10 medullated and 18 C-fibres. The mean activity at 100 mmHg was, for the C-fibres 5.0 Hz and for the medullated fibres 34 Hz. At 130 mmHg the activity in the C-fibres was 13 Hz and in the medullated fibres 68 Hz. Thus C-fibres from the aortic baroreceptor regions are activated at higher pressures than the medullated fibres and have lower discharge frequencies. Noradrenaline did not influence the pressure response curves of the C-fibres. It is concluded that the arterial baroreceptor C-fibres may exert a weak tonic influence on the vasomotor centre at normal pressures but are likely to be of greater importance when the arterial pressure rises acutely.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.