Search PubMed⌕ Search

Biomedical subjects

R Zimlichman

Publications and source records attributed to R Zimlichman.

At least 55 records · Page 3Linked to original sources

Insulin induces medial hypertrophy of myocardial arterioles in rats.

To investigate the effect of hyperinsulinemia on arteriolar hypertrophy, myocardial hypertrophy, and blood pressure, we administered insulin intraperitoneally to SHR and WKY rats for 3 consecutive weeks. To prevent hypoglycemia, the drinking water contained 10% sugar, and to accentuate the blood pressure, their chow contained 8% table salt. Blood pressure was measured by the tail-cuff method. Heart weights were factored with body weights. Arterioles of approximately 100 microns in diameter were examined at the end of the experiment and the vascular wall thickness was factored with the lumen diameter. At the end of 3 weeks, blood pressure rose in the SHR but not in the WKY rats. The heart weights in the WKY normotensive rats did not increase, whereas in the SHR they did. Furthermore, there was a significant rise in vessel wall thickness in the rats that received insulin, whether there was a rise in blood pressure or not and whether they had an increase in heart weight or not. There was a similar rise in blood glucose in all the groups, with slightly more accentuated rise in the SHR that received insulin. Nevertheless the increase in vascular wall thickness occurred only in the groups which received insulin. This seems to preclude the importance of hyperglycemia per se as the causative agent for the increase in vascular wall thickness in this study. The increase was in the form of medial hypertrophy without any sign of atherosclerosis. It seems, therefore, that hyperinsulinemia is associated with hypertrophy of the media of arterioles regardless of the increase in heart weight or the rise in blood pressure.

Animals↗

Hyperinsulinaemia increases blood pressure in genetically predisposed spontaneously hypertensive rats but not in normotensive Wistar-Kyoto rats.

BACKGROUND: There is controversy in the literature concerning the effect of short-term insulin administration on blood pressure in different experimental situations, because in some experiments this association is clear, whereas in others it is nonexistent. OBJECTIVE: To investigate whether there is a difference in the effect of exogenous insulin administration on the blood pressure of normotensive Wistar-Kyoto (WKY) rats and hypertensive spontaneously hypertensive rats (SHR). METHODS: Hyperinsulinaemia was induced in normotensive WKY rats and in hypertensive SHR by the administration of long-acting insulin (insulin retard 0.4 U/kg body weight per day in one group and 0.8 U/kg body weight per day in another group) once a day, intraperitoneally, for 3 weeks. All of the rats drank a 10% sucrose solution, to prevent hypoglycaemia in those receiving insulin. RESULTS. Baseline serum levels were significantly higher in the SHR groups than in the WKY rat groups. At the end of the experiment, after 3 weeks' insulin therapy, systolic blood pressure measured by the tail-cuff method showed a significant increase in the SHR, but not in the WKY rats, possibly because of the genetic predisposition of the SHR to increase their blood pressure. The increase was similar in the SHR given 0.4 U/kg body weight per day insulin retard to that in those given 0.8 U/kg per day. CONCLUSIONS: Exogenous insulin increased systolic blood pressure in the SHR but not in the WKY rats. The rise was similar in rats receiving either 0.4 or 0.8 U/kg body weight per day insulin retard.

Animals↗

Acute hemodynamic effects of nisoldipine in young hypertensive patients.

The hemodynamic effects of oral nisoldiopine in 12 hypertensive patients aged 35-55 years were determined using the impedance cardiography method. Hemodynamic measurements were performed at hourly intervals before and following ingestion of the medication. Nisoldipine significantly decreased systolic and diastolic blood pressure, with a slight increase in heart rate. Stroke volume did not change significantly following the medication. Total peripheral resistance decreased gradually reaching its lowest values 2 h after ingestion of nisoldipine. We conclude that nisoldipine is a potent oral antihypertensive agent that induces peripheral vasodilatation without decrease in cardiac output.

Adult↗

Opioids inhibit endothelin-mediated DNA synthesis, phosphoinositide turnover, and Ca2+ mobilization in rat C6 glioma cells.

Opioid agonists inhibit DNA synthesis in C6 rat glioma cells that express opioid receptors, induced by desipramine (DMI). This inhibition was not observed in cells that were not treated with DMI, and thus did not express opioid-binding sites. Endothelin, a known mitogen, increased thymidine incorporation dose dependently (up to 1.7-fold) in DMI-treated C6 cells. This increase was reversed by an anti-idiotypic antibody to opioid receptors, Ab2AOR, which has opioid agonist properties. The opioid antagonist naltrexone blocked the inhibition caused by Ab2AOR. Endothelin also stimulated phosphoinositide (PI) turnover and this effect was inhibited by morphine (50%) or by Ab2AOR (72%) in DMI-treated but not in DMI-untreated C6 cells. These actions of morphine and Ab2AOR were reversed by naltrexone. The inhibition of PI turnover and of thymidine incorporation by Ab2AOR or morphine was insensitive to pertussis toxin (PTX). Since PI turnover is known to induce Ca2+ mobilization, it was of interest to examine the effects of the applied opioids on intracellular Ca2+ concentrations. Endothelin increased the concentration of cytosolic free Ca2+ in the cells while Ab2AOR, morphine, and beta-endorphin reversed the endothelin-induced Ca2+ mobilization in DMI-treated but not in DMI-untreated C6 cells. The effect of these agonists was also blocked by naltrexone. The results indicate that glial cells can be a target of an opioid receptor-mediated antimitogenic action and that an abatement in PI turnover and Ca2+ mobilization may be associated with this mechanism.

Animals↗

Measurements of cardiac output by impedance cardiography in pacemaker patients at rest: effects of various atrioventricular delays.

OBJECTIVES: The purpose of this study was to evaluate the ability of impedance cardiography to determine the change in cardiac output caused by modifications in the atrioventricular (AV) delay in DDD (dual-chamber) pacing mode while pacing the atrium and ventricle at different programmed rates. BACKGROUND: Impedance cardiography permits continuous noninvasive monitoring of hemodynamic variables on a beat to beat basis. METHODS: Eleven patients with a DDD pacemaker were evaluated by impedance cardiography. Stroke volume, cardiac output and total peripheral resistance were assessed in the supine rest position during both DDD and ventricular (VVI) pacing. Hemodynamic variables were measured during DDD pacing at rates ranging from 60 to 110 beats/min in 10-beats/min increments with programmed AV delay varying from 50 to 250 ms in 50-ms increments. When the pacemaker was reprogrammed to the VVI pacing mode, these measurements were repeated at the same pacing rates. RESULTS: Cardiac output measurements during programmed conditions were found to be highly reproducible. The mean coefficient of variation was 3% during DDD pacing; it was 6% in the VVI pacing mode. A large decrease in cardiac output (approximately 30%) was found when a pacemaker was reprogrammed from the DDD to the VVI pacing mode. At DDD pacing rates between 70 to 110 beats/min, the highest cardiac output occurred at an average AV delay of < 120 ms from atrial stimulus to ventricular stimulus. At an average AV delay of > or = 200 ms, the cardiac output in the DDD and VVI pacing modes was similar. CONCLUSIONS: 1) Impedance cardiography allows highly reproducible noninvasive assessments of cardiac output in pacemaker patients; 2) inappropriate programming of the AV interval in patients with atrial and ventricular pacing can decrease cardiac output significantly, and the extent of the decrease is similar to or less than that observed in ventricular pacing; 3) hemodynamic measurements obtained with impedance cardiography can facilitate optimal programming of pacemaker variables.

Cardiac Output↗

Resolution of hypertensive retinopathy despite persistent high diastolic pressure.

Four patients with exudative retinopathy due to hypertension were observed for periods ranging from 12 to 35 months. Despite multiple drug therapy in high dosage and some clinic attendance, blood pressure was not controlled and remained severely elevated. Even though severe hypertension persisted, however, exudative phenomena disappeared and renal function remained stable during the follow-up period. Neither the pathogenesis nor the natural course of hypertensive retinopathy is yet fully understood. It is accepted that antihypertensive therapy causes gradual regression of the retinal changes of hypertensive retinopathy. There are no data concerning the natural course and progress of hypertensive retinopathy in patients with severe untreated hypertension. It is unclear why the patients in our study had complete regression of hypertensive retinopathy.

Adult↗

Quantitation of thyroid hormone effect on skin perfusion by laser Doppler flowmetry.

Clinical observations have long suggested that skin perfusion (SP), among other factors, depends on thyroid status. However, quantitative data concerning this relationship are rather sparse. This study characterizes SP by means of laser Doppler flowmetry (LDF) in various thyroid dysfunctional states. The data reveal that mean capillary flow velocity, capillary pulse wave amplitude, and capillary flow oscillation amplitude, but not capillary flow oscillation frequency, are increased in hyperthyroid patients and decreased in hypothyroid patients. Regaining the euthyroid state is accompanied by normalization of LDF parameters only in hyperthyroid patients. It is concluded that LDF is useful in monitoring the thyroid effect on SP. However, it may not be used as a biological marker for the thyroid status of a given individual.

Adult↗

Analysis of the diminished skin perfusion in elderly people by laser Doppler flowmetry.

Clinical observations suggest an age-associated decline in skin perfusion but there are few quantitative in vivo data on skin perfusion at various ages. We studied skin perfusion of the dorsum of the foot by determining the capillary blood flow velocity (CBFV) expressed in millivolts (mV), using laser Doppler flowmetry, in ten young and 12 elderly men. Our data revealed that, at 32 degrees C skin temperature, the CBFV oscillations (vasomotions) are of higher median amplitude in young people than in elderly subjects: 9.4 mV (95% CI, 8.8-10.0 mV) and 4.6 mV (95% CI, 4.1-7.4 mV), respectively (p less than 0.05). The vasomotion frequency was similar in both age groups. At 44 degrees C skin temperature, the median CBFV peak in the young was 163 mV (95% CI, 128-192 mV), as opposed to 102 mV (95% CI, 92-124 mV) in the aged subjects (p less than 0.0005). The median increment in CBFV, driven by every heart beat, was also higher in the young age group: 86 mV (95% CI, 76.4-96.0 mV) compared with the elderly group: 63 mV (95% CI, 50-72 mV, p less than 0.005). Considering the fact that the magnitude but not the pattern of skin perfusion varied between the two groups, we conclude that ageing is associated with loss of capillary plexus functional units, and therefore the skin perfusion is lower in aged people.

Adult↗

Murine typhus endocarditis.

We have described a 28-year-old male sheepfarmer who had fever, headache, chills, malaise, and aortic insufficiency. Echocardiography revealed a tricuspid aortic valve with a large vegetation on the right cusp, an enlarged left ventricle, and diastolic flutter of the mitral valve. Repeated blood cultures were negative. Seroconversion of IgG and IgM to Rickettsia typhi was found on the 13th day of hospitalization. The patient was treated with tetracycline for 1 year and remained afebrile and free of symptoms for 9 months, when he was lost to follow-up. IgM and IgG fluorescent antibodies to R typhi remained positive during 8 months of the follow-up period. We believe this to be the second reported case of endocarditis due to R typhi and the first not treated surgically.

Adult↗

Carotid body tumor: diagnostic and therapeutic approach.

Carotid body tumor may be clinically suspected when the only clues are physiologic manifestations of carotid body dysfunction or when a palpable cervical mass is evident upon presentation. In the latter case, the physiologic signs of carotid body dysfunction are usually recognizable. We have presented the case of a patient who was completely disabled by a slowly enlarging carotid body tumor. An attempt at surgical excision of the tumor was unsuccessful because of its proximity and adhesion to vital neck structures. An endocardial pacemaker inserted to ameliorate the episodes of bradycardia and hypotension accompanied by transient complete atrioventricular block resulted in only partial and temporary relief. Finally, irradiation of the tumor induced fast shrinkage and rapid regression of symptoms.

Carotid Body Tumor↗