Search PubMed⌕ Search

Biomedical subjects

S Greenberg

Publications and source records attributed to S Greenberg.

At least 163 records · Page 9Linked to original sources
PubMed1982

Vascular reactivity during the development of two-kidney, one-clip Goldblatt hypertension in conscious dogs.

This study evaluates the sequential changes in vascular reactivity in conscious dogs during the early and late phases of two-kidney, one-clip Goldblatt hypertension (2-KGH) produced by unilateral renal artery constriction (URAC). The in vivo responses to serotonin (5-HT), norepinephrine (NE), angiotensin II (Ang II), prostacyclin (PGI2), acetylcholine (ACH), and nitroglycerin (GTN) were reproducible and stable throughout the 32-day period of study in dogs subjected to sham URAC. The vascular responses to 5-HT, Ang II, and PGI2 were enhanced day 1 post-URAC, before mean arterial pressure (MAP), cardiac output (CO), or total peripheral resistance (TPR) increased. The magnitude of the enhanced reactivity progressed on days 4 and 32 post-URAC, as hypertension developed. The pressor responses to NE did not change from pre-URAC values until CO and MAP were elevated. The vasodepressor responses to ACH and GTN diminished over a 12-day period post-URAC, in parallel with the change in CO, but prior to any increase in TPR. These data suggest that in dogs with 2-KGH changes in vascular reactivity precede the development of the increased MAP and TPR of hypertension. The lack of uniformity of the onset of the reactivity changes to the different agonists suggests that both intrinsic factors and pressure changes modify the vascular wall in the early and later stages of 2-KGH.

Angiotensin II↗
PubMed1982

Effect of an increased cardiac output on vascular responses to vasoactive agents in two-kidney, one-clip Goldblatt hypertension.

The effect of the increased cardiac output of two-kidney, one-clip Goldblatt hypertension (2-KGH) on the altered vascular responses to vasoactive agents was examined in the conscious, chronically instrumented dog. The early stage of 2-KGH is characterized by an increased arterial pressure, an increased aortic flow, a decreased total peripheral resistance, and enhanced responses to angiotensin II and serotonin. As the aortic flow increases the responses to norepinephrine are enhanced, and the dilator responses to acetyl-choline and nitroglycerin are depressed. Aortic flow then returns to control values and the increased arterial pressure is maintained by an increase in peripheral resistance. When the increased aortic flow is prevented by occluding the vena cava to maintain flow at control values, the vascular responses to each of the agonists do not differ from that obtained when the aortic flow is elevated. Moreover, the temporal development and magnitude of the elevation in arterial pressure resulting from the increased vascular resistance is similar in dogs with an increased and normal aortic flows. The results suggest that increased aortic flow is not essential for the increased vascular resistance or the vascular changes in the canine model of 2-KGH.

Acetylcholine↗
PubMed1982

Effect of chronic administration of clonidine and propranolol on the myocardium of spontaneously hypertensive rats.

Chronic administration of clonidine to six month old spontaneously hypertensive rats (SHR) by continuous infusion with Alzet minipumps resulted in a decreased systolic arterial pressure, a decrease in heart weight, protein content and the incorporation of precursors of cellular protein and glycoprotein into the myocardium. Chronic administration of propranolol to SHR for three consecutive weeks by Alzet minipump reduced systolic arterial pressure but did not reverse the indices of myocardial hypertrophy. Chronic administration of propranolol to SHR for three consecutive weeks resulted in myocardial necrosis in each of the SHR tested. Because both clonidine and propranolol inhibit sympathetic activity to the myocardium, whereas propranolol also blocks myocardial beta receptors, the data support the conclusion that the ability of clonidine to reverse myocardial hypertrophy in the SHR cannot result from withdrawal of sympathetic tone to the myocardium. Moreover, since both drugs caused an equivalent reduction in pressure, the effects of clonidine cannot result from a decrease in afterload to the myocardium. The data support the conclusion that clonidine may reverse myocardial hypertrophy by a direct action on the myocardium or by inhibiting the synthesis or release of circulating or trophic factors which may mediate myocardial hypertrophy. Moreover, if propranolol-induced focal myocardial necrosis is found to occur in other species, caution should be utilized in the use of propranolol for the treatment of essential hypertension in man.

Animals↗
PubMed1982

Difference in prostaglandin modulation of arterial and venous smooth muscle responses to bradykinin and norepinephrine.

The role of endogenously synthesized prostaglandins as modulators of canine vascular smooth muscle responses to bradykinin (BK) and norepinephrine (NE) was evaluated in vitro with the use of helical strips of canine arteries and veins and measurement of prostaglandins with bioassay and thin layer chromatography. Inhibition of prostaglandin synthetase with indomethacin (INDO) resulted in a small, but significant, enhancement of the contractile responses of mesenteric and splenic arteries and portal veins to NE. Eicosatetraynoic acid (ETYA), another inhibitor of prostaglandin synthetase, did not affect the contractile responses of canine splenic and mesenteric arteries and portal veins to NE. ETYA (1 x 10(-5) M), inhibited prostaglandin biosynthesis. Addition of INDO to arterial smooth muscle strips, in which prostaglandin synthesis was inhibited with ETYA, also resulted in consistent enhancement of the responses to NE. INDO did not effect the contractile responses of canine mesenteric and splenic veins to NE. BK-induced relaxation of canine mesenteric, but not splenic, arteries was inhibited by INDO, INDO did not effect BK-induced contraction of splenic, mesenteric or portal veins. ETYA was without effect on the responses of either arteries or veins to BK. After inhibition of prostaglandin synthetase with ETYA, INDO was still an effective inhibitor of BK-induced relaxation of arterial smooth muscle. Tranylcypromine (1 x 10(-5) M) inhibited prostacyclin (PGI2) synthesis but did not affect the responses of the vascular smooth muscle to BK or NE. These findings are consistent with the conclusion that in canine vascular smooth muscle in vitro, endogenously synthesized prostaglandins do not modulate the contractile responses to NE or BK. The data also confirm the presence of a direct vascular smooth muscle action for INDO.

Animals↗
PubMed1982

Wheelchair prescription guidelines.

Few physicians are familiar with the components of wheelchairs. Consequently, they may prescribe wheelchairs that limit or impair their patients' functional abilities. Correct ordering requires use of catalogs, patient measurements, assessment of functional needs and a knowledge of the available modifications and accessories. Consultation with a rehabilitation specialist may be required for patients with special needs.

Adolescent↗
PubMed1982

Functional and structural changes in veins in spontaneous hypertension.

Six month old spontaneously hypertensive rats (SHR) and age and sex matched normotensive Wistar-Kyoto rats (WKY) were examined to evaluate the existence of functional and structural changes in the portal vein (PV), inferior vena cavae (IVC) and pulmonary arteries (PA). PV, central nervous and systolic right ventricular pressures did not differ in the anesthetized SHR when compared with WKY, despite elevated systolic arterial pressure. PV, IVC and PA obtained from SHR were less extensible, developed more tension, exhibited an enhanced sensitivity to serotonin and a thromboxane-like prostanoid, accumulated more of the protein precursors 2-14C-leucine, 2-14C-glucosamine, 7-3H-fucose, exhibited a normal rate of uptake of 2-14C-thymidine, and increased protein content and a decreased concentration of DNA. When examined under light and electron microscopy, the veins and PA obtained from SHR demonstrated medial smooth muscle hypertrophy, and increased density of PAS-Schiff positive stain, enlarged and prominent Golgi apparati and an increased cell diameter through the region of the nucleus. These changes were not due to water-logging since the water content of the veins and PA from SHR and WKY did not differ. These data support the conclusion that PV, IC and PA obtained from SHR exhibit functional and structural changes independent of increases in intravenous pressure. These changes may relate to the increase in blood vessel protein.

Animals↗
PubMed1982

Effect of clonidine and propranolol on venous smooth muscle from spontaneously hypertensive rats.

Clonidine and propranolol reverse arterial smooth muscle hypertrophy in hypertensive animals. It is uncertain whether this is mediated by a reduction in pressure or withdrawal of sympathetic nerve activity to the vasculature. Veins obtained from spontaneously hypertensive rats undergo hypertrophy and thereby provide a model for the separation of pressure-dependent and independent effects of antihypertensive drugs. Clonidine (0.075 and 0.3 mg/kg/day) or propranolol (0.75 and 3.0 mg/kg/day), administered by Alzet minipump for three consecutive weeks to SHR and age and sex matched Wistar-Kyoto normotensive rats (WKY), produced dose-related reductions in systolic arterial pressure, without affecting central or portal venous or right ventricular pressure. Clonidine reversed the decreased extensibility and the biochemical correlates of hypertrophy which characterized the portal (PV) and vena caval veins (IVC) and pulmonary arteries (PA) obtained from SHR. Moreover, clonidine decreased the uptake of PAS-Schiff stain for neutral and acidic glycosaminoglycans (GAG's) and decreased the medial wall thickness of the PV, IVC and PA obtained from SHR. Clonidine did not affect these parameters in blood vessels obtained from WKY. Propranolol exerted actions similar to clonidine, but its effects were more variable and less effective than clonidine, despite equivalent reductions in arterial pressure. The data support the conclusion that clonidine can reverse the functional morphological derangements of venous and PA dysfunction in SHR. The effects appear to be independent of both a reduction in pressure and withdrawal of sympathetic tone to the blood vessels. The data suggest that clonidine, and to a lesser extent propranolol, may act directly on the veins, or indirectly by inhibiting the release or synthesis of a trophic nonadrenergic factor, to reverse the functional and structural changes in the veins.

Animals↗
PubMed1981

Adrenergic mechanisms in canine intralobar pulmonary arteries and veins.

The responses of canine intralobar pulmonary arteries (IPA) and veins (IPV) to transmural nerve stimulation (TNS), and exogenously administered norepinephrine (NE) were studied to evaluate the alpha-adrenergic neuroeffector system in the canine pulmonary vasculature. IPA and IPV elicited contractions in response to both NE (10(-10) to 10(-5) M) and TNS (0.5-32 Hz, 2 ms duration and delay). The equilibrium (steady state) contractile responses of IPA and IPV to TNS were abolished with the adrenergic neuronal blocking agents guanethidine and bretylium and the depolarization blocking agent tetrodotoxin in concentrations which did not affect the responses to NE or KCl. The contractile responses of IPA and IPV to TNS and NE were reduced in a concentration-dependent way, by the alpha-adrenergic receptor-blocking agents phentolamine, tolazoline and clonidine. The contractile responses of IPA and IPV to TNS and NE were enhanced after inhibition of neuronal reuptake of NE (uptake1) with cocaine, as well as after blockade of extraneuronal reuptake of NE (uptake2) with hydrocortisone. Analysis of the equilibrium responses of the IPA and IPV to TNS and NE with an Arunlakshana-Schild plot to define the concentration of alpha 1-receptor antagonists necessary to double the ED50 for TNS and NE (defined as the pA2), demonstrated that the postsynaptic alpha-receptors of IPV differed from that of IPA. These data support the conclusions that IPA and IPV 1) contain a functional adrenergic innervation and neuroeffector system, 2) contract in response to both TNS and NE, 3) demonstrate the presence of mechanisms for both uptake1 and uptake2 of NE, and 4) IPV contain postsynaptic alpha-receptors that may differ from each other.

Animals↗
PubMed1981

Pulmonary vascular smooth muscle function in porcine splanchnic arterial occlusion shock.

Pulmonary complications are a major cause of death in patients in various forms of shock. The exact causes of the pulmonary complications are unknown. This study evaluates the functional characteristics of intralobar pulmonary arteries (IPA) and veins (IPV) obtained from swine subjected to splanchnic arterial occlusion (SAO) shock ans subsequent cardiovascular collapse and sham-shocked swine subjected to surgery but no occlusion. The contractile response of pulmonary arteries to norepinephrine (NE) and serotonin (5-HT) were depressed when obtained from pigs subjected to SAO shock. The depression in the sensitivity to 5-HT and maximal tension development to 5-HT and NE was selective, since the responses to potassium ion were not depressed. IPA obtained from swine with SAO shock were more sensitive to the relaxant actions of arachidonic acid, a precursor for bisenoic prostaglandins, than were IPA from sham-shocked swine. This was not observed when prostaglandins were used as agonists. This suggests that synthesis of prostaglandin differs in the pulmonary vasculature of sham-shocked and SAO-shocked animals. IPV obtained from swine in SAO shock were less sensitive to 5-HT and NE but more sensitive to arachidonic acid and 9 alpha, 11 alpha-epoxymethano-PGH2, a thromboxane like compound. IPV obtained from swine in SAO shock converted more arachidonic acid into a substance with the chromatographic mobility of thromboxane B2. The data suggest that alterations in the prostaglandin system within the pulmonary artery and vein may contribute to the pulmonary complications of SAO shock. The alterations appear to include an enhanced synthesis of prostacyclin as well as thromboxane-like substance. Because the veins were more sensitive than the arteries to 9 alpha, 11 alpha-epoxymethano-PGH2, thromboxanes or endoperoxides may elevate venous tone and contribute to the pulmonary edema associated with shock states.

Animals↗
PubMed1981

Evidence for circulating factors as a cause of venous hypertrophy in spontaneously hypertensive rats.

Increased contractility, decreased extensibility, and hypertrophy occur in portal veins (PV) obtained from spontaneously hypertensive rats (SHR). This study evaluates the potential existence of circulating humoral factors as mediators of these changes. SHR were parabiosed with normotensive Wistar-Kyoto rats (WKY) matched for sex and age. Blood pressure increased over a 3-wk to 5-mo period in 2-mo-old WKY parabiosed with SHR. Similar changes were absent in WKY parabiosed with WKY (WKY-WKY) or in SHR parabiosed with SHR (SHR-SHR). The functional blood flows between the parabiosed pairs were 1.4 +/- 0.21%. PV obtained from WKY-WKY developed less spontaneous tension, less tension in response to norepinephrine, potassium chloride, angiotensin II, an 9 alpha, 11 alpha-epoxymethano-prostaglandin H2, and were more extensible than PV obtained from SHR-SHR. In contrast, PV obtained from the WKY member of the WKY-SHR, developed changes similar to PV obtained from the SHR. The wet and dry weight and protein content increased in the PV of WKY-SHR, when compared with these parameters in the PV obtained from WKY-WKY. Light microscopy of the blood vessels demonstrated that PV obtained from the wKY parabiosed to SHR exhibited medial smooth muscle hypertrophy. These data support the conclusion that a circulating humoral factor in the SHR may initiate the venous smooth muscle derangements during the development of spontaneous hypertension.

Animals↗
PubMed1981

Properties of intestinal and cutaneous arteries and veins in two-kidney one-clip Goldblatt hypertension.

This study evaluates whether changes in arterial and venous smooth muscle contractility and extensibility precede or result from the elevated arterial pressure (MAP) and total peripheral resistance (TPR) of two-kidney one-clip Goldblatt hypertension (2-KGH). The experiments measure the contractile and extensibility properties of rings of canine mesenteric, cutaneous, gracilis, and pulmonary arteries and veins (0.4-1.0 mm OD) prior to and days 1 and 32 after the initiation of two-kidney one-clip Goldblatt hypertension (2-KGH), produced by unilateral constriction of the renal artery (URAC). The reactivity (ED50) and tension development to norepinephrine (NE), angiotensin II (ANG II), potassium chloride (KCl), serotonin (5-HT), 9 alpha, 11 alpha-epoxymethano prostaglandin H2 (EMP), prostaglandin B2 (PGB2), and CaCl2 were determined. Mean arterial pressure (MAP) and TPR were unchanged from pre-URAC values 24 h post-URAC but were significantly elevated 32 days post-URAC. The ED50's for 5-HT, ANG II, EMP, and PGB2 were decreased in each of the arteries and veins obtained from dogs with 2-KGH, within 24 h post-URAC, and either became more pronounced (PGB2, EMP, and 5-HT) or returned to pre-URAC values by day 32 post-URAC. The ED50's for NE, KCl, and CaCl2 were unchanged from pre-URAC values. Maximal tension development of the arteries and veins to each of the agonists increased within 24 h post-URAC, prior to an increase in MAP or TRP. Within 32 days post-URAC, maximal tension development of the veins obtained from 2-KGH was increased from pre-URAC values, whereas tension development by the arteries was decreased. Extensibility decreased in each of the arteries and veins obtained from dogs with 2-KGH 24 h post-URAC. The extensibility decreased further by day 32 post-URAC as the level of MAP and TPR increased. These data support the postulate that altered venous and arterial smooth muscle contractility and extensibility precede the elevated MAP and TPR of 2-KGH in dogs. Moreover, since these changes occur in both artery and vein, they must reflect the action of circulating humoral or intrinsic vascular or neural substances. Finally, the decrease in arterial contractility suggests that the enhanced vascular responses in vivo and in situ may reflect the greater mechanical advantage of the hypertrophied blood vessel and not an arterial vasculature with enhanced contractility.

Angiotensin II↗
PubMed1981

Overview: deinstitutionalization of psychiatric patients, a critical review of outcome studies.

The authors performed a critical review of experimental studies on the outcomes for psychiatric patients of 1) alternatives to hospital admission, 2) modifications of conventional hospitalization, and 3) alternatives to continued long-term hospitalization. The internal validity of many of the studies was compromised by shortcomings in design and performance and generalizability limited by selection of patient populations. With these qualifications experimental alternatives to hospital care of patients have led to psychiatric outcomes not different from and occasionally superior to those of patients in control groups. This conclusion is best supported for alternatives to admission and for modifications of conventional hospitalization. The available studies do not permit firm conclusions regarding alternatives to continued long-term hospitalization of chronically ill patients or for a critical analysis of the optimal management of specific subpopulations of psychiatric patients. Satisfactory deinstitutionalization appears to depend on the availability of appropriate programs for care in the community.

Adult↗
PubMed1981

Effect of prostacyclin and 9a, 11a-epoxymethanoprostaglandin H2 on calcium and magnesium fluxes and tension development in canine intralobar pulmonary arteries and veins.

Calcium and magnesium ions modulate the responses of canine vascular smooth muscle to prostaglandins (PGs). This study was designed to evaluate the relationship between the effects of prostacyclin (PGI2) and 9a, 11a-epoxymethanoPGH2 (EMP) on calcium and magnesium fluxes and tension development of the canine intralobar pulmonary arteries (IPA) and veins (IPV). PGI2 produced relaxation of canine IPA and IPV, decreased the uptake of 45Ca and increased the accumulation of 28Mg into an intracellular or tightly bound pool of divalent ion. The efflux of both calcium and Magnesium were not affected by PGI2. 6-Keto-PGF1a, the inactive metabolite of PGI2, did not affect the efflux or uptake of either Calcium or Magnesium, and did not produce any change in the basal tone of IPA or IPV. IPA and IPV contracted when challenged with EMP. The contractile responses of the IPA and IPV to EMP were associated with an increase in the efflux of Calcium from a tightly bound pool of calcium ion and a decrease in the uptake of 28Mg into these blood vessels. These data support the conclusions that: 1) PGI2-induced relaxation of IPA and IPV may be mediated by a decrease in the influx of activator calcium ion and an increase in the influx of modulator magnesium ion; 2) EMP-induced contraction of IPA and IPV appears to result from a release of calcium ion from a tightly bound site within the vascular smooth muscle cell; and 3) the effects of PGI2 and EMP on magnesium ion may result from a direct action of these prostanoids on the mechanisms regulating magnesium fluxes or they may be secondary to the alterations in the fluxes of calcium ion.

Animals↗
PubMed1981

Basic upper extremity orthotics.

Improved hand function after injury or disease is achieved by increasing joint mobility, muscle strength and coordination, while reducing edema and pain. Static and dynamic orthoses assist in correcting deformities, provide strengthening activities and maintain a functional hand position. Many orthotic appliances are commercially available or may be fabricated for specific hand problems. The process of gradually increasing wearing tolerance helps to reduce the risk of skin breakdown or excessive pressure. A program of daily range-of-motion exercises may aid in preventing joint immobilization.

Hand Injuries↗
PubMed1980

Varicella-zoster-associated encephalitis: detection of specific antibody in cerebrospinal fluid.

Varicella-zoster (VZ) antibody measured by indirect immunofluorescence was used to identify patients with encephalitis due to VZ virus. In 15 of 16 (94%) patients with VZ infection and clinical evidence of central nervous system involvement, VZ antibody was present at a titer of 1:2 or greater in cerebrospinal fluid. In contrast, no VZ antibody was detected in the cerebrospinal fluid of seven patients with VZ infections without clinical signs of central nervous system involvement, nor was any detected in the cerebrospinal fluid of 25 patients with malignant or demyelinating disease or encephalitis due to other viral or toxic agents. All of these patients had detectable serum VZ antibody. Thus, in this study the presence of detectable VZ antibody in cerebrospinal fluid measured by indirect immunofluorescence seemed to correlate with clinical evidence of central nervous system involvement due to this virus.

Antibodies, Viral↗