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Biomedical subjects

S Baez

Publications and source records attributed to S Baez.

7 recordsLinked to original sources
PubMed1978

Microvascular responses to norepinephrine and vasopressin during halothane anesthesia in the rat.

This experiment was designed to determine the microvascular responses to the two known naturally occurring vasoconstrictors, norepinephrine (NE) and vasopressin, at known levels of central vasomotor activity before, during and after halothane anesthesia. The responses to topical application of NE and vasopressin were studied in the microvasculature of the mesentery and cremaster muscle, using microscopic methods. Neural (CNS) stimulation was accomplished through electrodes chronically implanted in vasoactive sites of the forebrain and midbrain. The increase in blood pressure in response to CNS stimulation was decreased during halothane anesthesia (32.4 +/- 5.4 per cent before and 24.7 +/- 6.1 per cent during; P less than 0.001). There was no significant change in the steady-state diameter of the microvasculature under study during or after halothane anesthesia. Marked abatement of arteriolar vasoconstriction in response to CNS stimulation was seen prior to halothane. However, the same target vessel showed increased constriction in response to topically applied NE (from 32.3 +/- 4.7 to 53.2 +/- 7.8 per cent; P less than 0.01) during halothane anesthesia. By contrast, the response to vasopressin decreased (from 42.4 +/- 5.7 to 1.0 +/- 6 per cent; P less than 0.001) with halothane. The precise mechanism(s) underlying the described hypersensitivity to NE and hyposensitivity to vasopressin in the same vascular structure during halothane anesthesia remains undetermined.

Animals↗
PubMed1977

Central neural influence on precapillary microvessels and sphincter.

The responses to central nervous system (CNS) stimulation of consecutive segments of arterioles down to the precapillary sphincter were measured in the mesoappendix and/or cremaster of nine male rats with indwelling electrodes. Under pentobarbital sodium anesthesia, vasoactive sites were stimulated at threshold for maximal constriction or lumen closure of the precapillary sphincter and/or immediately preceding precapillary arteriole (metarteriole). In all experiments, CNS stimulation induced blood pressure elevation and constriction of three consecutive segments of precapillary vessels and of the sphincter. A threefold increase in rate of vasomotion of precapillary sphincter and metarteriole was the rule, but this was noted infrequently in larger arterioles. In addition to an overall influence of the CNS on microcirculation, the data show a gradient of responses to stimulation, the slope of which is negatively related to the size of the vessels and sphincter, in both tissues studied. A complete lumen closure of the metarteriole and precapillary sphincter (when present) in response to CNS stimulation implies active participation in the regulation of local blood flow. No evidence was foun for central neural regulation of the precapillary sphincter independent of arteriolar control.

Abdominal Muscles↗
PubMed1975

On the relationship of brain vasculature to production of neurological deficit and morphological changes following acute unilateral common carotid artery ligation in gerbils.

The known susceptibility of the Mongolian gerbil to cerebral infarction following unilateral carotid artery ligation has been attributed in the past to the demonstrated absences of an anastomotic supply between the anterior and posterior cerebral circulations. In a study of 34 adult gerbils exposed to such a procedure, 11, or 33%, developed severe neurological sequelae and succumbed to the procedure in less than 30 hr, whereas 23 animals survived with only minor or transient neurological signs. All animals displayed the expected lack of an anastomosis between the anterior and posterior circulations, but in addition the animals which survived the procedure were found to have a prominent early cross-connection between the anterior cerebral arteries, whereas the animals which succumbed had no such connection. Neuropathological changes in susceptible animals were apparent as early as 3 and one-half hr after ligation and consisted of edema, initially perivascular and then intraneuronal, slowed by acute necrosis. A variety of other vascular anomalies was encountered. We conclude that the peculiar susceptibility of Mongolian gerbils to cerebral infarction following acute unilateral common carotid artery ligation is not related primarily to lack o adequate collaterals between the anterior and the anterior cerebral arteries, but to the degree of adequate adequacy of communication between the anterior cerebral arteries. The critical difference may be more one of degree, i.e. the point at which the medial branches of the anterior cerebral artery fust to become anazygos vessel, rather than an actual difference in the pattern of distribution of the anterior cerebral arteries. The presence of other variation in vascular supply in a relatively small series suggests that results of similar studies of infarction and response to treatment be interpreted with caution.

Animals↗
PubMed1975

Reactivity of aorta and portal vein in germfree rats.

The responsiveness of conventional and germfree rat aortas and portal veins to vasoactive agents were compared in vitro. The results indicate: (1) aortas and portal veins from germfree rats exhibit an attenuated reactivity to angiotensin, vasopressin and epinephrine but not to KC1; (2) the dose-response curves for epinephrine and the peptides were shifted to the right concomitant with a decrease in maximum contractile tension, and (3) CaC12 dose-response curves obtained on potassium-depolarized aorta were not different from one another, whereas those obtained on portal veins from germfree animals were shifted to the right with a concomitant decrease in maximum response. In addition, aortas and portal veins from germfree rats were found to exhibit a higher total Ca content (but not Mg or water) when compared to conventional animals.

Angiotensin II↗
PubMedDate not supplied

Pial microcirculation in subarachnoid hemorrhage.

Microsurgical and microscopic methods were employed in guinea pigs to expose, observe, and measure response characteristics of cerebral cortical pial microvessels and microcirculation to traumatic and nontraumatic experimental subarachnoid hemorrhage. Bleeding produced by vascular micropuncture was associated with a 44.3% arteriolar constriction. Topical application of homologous blood alone produced a 33.2% vasoconstriction. Observed microcirculatory flow characteristics subsequent to such microvascular changes were consistent with those known to be associated with cerebral cortical infarction. These changes could be prevented or reversed by topical application of the alpha adrenergic blocker, phenoxybenzamine. Topical pretreatment with the beta adrenergic blocker, propranolol, prevented blood-induced spasm, but did not reverse such spasm once it had been established. A chemo-mechanical mechanism is suggested as underlying the vasoconstriction association with rupture of pial microvessels. It is thought that consideration of such microvascular characteristics, in conjunction with those known to be associated with larger intracranial vessels, adds to current knowledge of the pathophysiology of subarachnoid hemorrhage and may be extrapolated to bear future clinical import.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Sodium nitroprusside (SNP) hypotension: intracranial pressure (ICP) and hemodynamics in pial arteriole in the rat.

A detailed description is made of an acute closed cranial window method. The method is used for the study of cerebral pial microcirculation by intravital microscopy in the rat. Using these methods and techniques, the effects of systemic hypotension by SNP, i.v., on pial microvessel hemodynamics and on ICP were simultaneously measured and characterized under normophysiological conditions. The pH, PO2, PCO2 and temperature of the artificial cerebrospinal fluid (CSF) in the closed cranial window, intermittently measured, remained relatively constant, 30 to 60 min following the period of stabilization of the preparation. The infusion of SNP (6.2-35.0 micrograms/kg/min, 0.02% sol., i.v.) significantly decreased BP (52.1 +/- 13.4 mm Hg, mean +/- SD). From measurement of microvessels internal diameter (I. D.) and microhemodynamics, significant increases in pial arteriolar I.D. (from 35.4 +/- 10.1, microns, to 47.1 +/- 5.7, microns, mean and S.D., 33.0%) and estimated bulk flow (51.2%), occurred during the hypotension. The changes in hemodynamic parameter were predominantly in the arteriolar system. Only minimal changes in the venular diameter occurred during the SNP hypotension. The observed moderate (22.0%) increase in ICP during SNP hypotension in pentobarbital anesthetized rat correlates well with the microhemodynamic changes of the cerebral microcirculatory system.

Animals↗